ORIGINAL CONTRIBUTION. Glucose Homeostasis in Huntington Disease. Abnormalities in Insulin Sensitivity and Early-Phase Insulin Secretion
|
|
- Milo Cummings
- 5 years ago
- Views:
Transcription
1 ORIGINAL CONTRIBUTION Glucose Homeostasis in Huntington Disease Abnormalities in Insulin Sensitivity and Early-Phase Insulin Secretion Nebojša M. Lalić, MD, PhD; Jelena Marić, MD; Marina Svetel, MD, PhD; Aleksandra Jotić, MD, PhD; Elka Stefanova, MD, PhD; Katarina Lalić, MD, PhD; Nataša Dragašević, MD, PhD; Tanja Miličić, MD; Ljiljana Lukić, MD; Vladimir S. Kostić, MD, PhD Background: with Huntington disease (HD) develop diabetes mellitus more often than do matched healthy controls. Recent studies in neurodegenerative diseases suggested that insulin resistance constitutes a metabolic stressor that interacts with a preexisting neurobiological template to induce a given disorder. Objective: To investigate possible changes in insulin sensitivity and secretion, major determinants of glucose homeostasis, in a group of consecutive normoglycemic patients with HD. Design: Metabolic investigations. : Twenty-nine untreated, nondiabetic patients with HD and 22 control participants matched by age, sex, and socioeconomic background. Main Outcome Measures: Glucose tolerance, assessed by means of the glucose curve during oral glucose challenge; insulin sensitivity, assessed using homeostasis model assessment and minimal model analysis based on frequent sampling of plasma glucose and plasma insulin during the intravenous glucose tolerance test; and insulin secretion, determined by means of the acute insulin response and the insulinogenic index. Results: The evaluation of insulin sensitivity using homeostasis model assessment demonstrated higher homeostasis model assessment insulin resistance indices, and a lower sensitivity index when the minimal model approach was used, in patients with HD compared with controls (P=.3 and P=.3, respectively). In the assessment of early-phase insulin secretion, the acute insulin response and the insulinogenic index were lower in patients with HD compared with controls (P=.2). The number of CAG repeats correlated significantly only with acute insulin response (P=.3). Conclusions: Besides impairment in insulin secretion capacity, a simultaneous decrease in insulin sensitivity, with an increase in the insulin resistance level, was found in normoglycemic patients with HD compared with controls. These data imply that progression of the insulin secretion defect in HD may lead to a failure to compensate for insulin resistance. Arch Neurol. 28;6(4): Author Affiliations: Institutes of Endocrinology, Diabetes, and Metabolic Diseases (Drs N. M. Lalić, Marić, Jotić, K. Lalić, Miličić, and Lukić) and Neurology (Drs Marić, Svetel, Stefanova, Dragašević, and Kostić), Clinical Center of Serbia, Belgrade. HUNTINGTON DISEASE (HD) is an autosomal dominant progressive neurodegenerative disorder characterized by involuntary movements, especially chorea; frank dementia; behavioral and psychiatric disturbances; and functional disability. It is caused by an unstable expanded CAG trinucleotide repeat in exon 1 on the huntingtin gene (HD [OMIM 1431]) on the tip of the short arm of chromosome 4. 1 with HD develop diabetes mellitus (DM) approximately 7 times more often than matched control participants. 2 Podolsky and Leopold 3 suggested that decreased insulin secretion might be a possible explanation. Recent studies 4 in neurodegenerative diseases suggested that insulin resistance constitutes a metabolic stressor that interacts with a preexisting neurobiologic template to induce a given disorder. Studies with a transgenic HD mouse model that expresses a portion of the human HD gene have shown that these animals develop impaired glucose tolerance and eventually become diabetic, associated with weight loss. The aim of this study was to investigate possible changes in insulin sensitivity (ie, the ability of insulin to exert its biological actions in an individual, whereas insulin resistance was defined as a decrease in insulin sensitivity and signified a defect in the biological action of insulin) and secretion, major determinants of glucose homeostasis, in a group of consecutive normoglycemic patients with HD. The analysis of insulin sensitivity comprised evaluation of the hepatic and pe- (REPRINTED) ARCH NEUROL / VOL 6 (NO. 4), APR Downloaded From: on 1/16/218
2 Table. Characteristics of With Huntington Disease and Subjects ripheral components of insulin sensitivity, and the analysis of insulin secretion was focused on its early phase, the potential failure of which was expected to be the first step in glucose intolerance development in normoglycemic patients. 6,7 METHODS With Huntington Disease (n=29) s (n=22) Sex, M/F, No. 13/16 1/12 Age, mean (SEM), y.4 (11.) 2.4 (9.6) Disease duration, mean (SEM), y 7.1 (1.6) NA BMI, mean (SEM) 2.4 (2.9) 2.7 (3.1) Glucose, mean (SEM), mg/dl 1 (7) 94 (7) HbA 1c, mean (SEM), % 6.2 (.4) 6.1 (.3) Total cholesterol, mean (SEM), mg/dl 21 (8) 22 (19) LDL-C, mean (SEM), mg/dl 12 (8) 124 (12) HDL-C, mean (SEM), mg/dl 46 (12) 8 (4) Triglycerides, mean (SEM), mg/dl 133 (9) 142 (18) Insulin, mean (SEM), µiu/ml 1.6 (.7) a 7.7 (.6) Abbreviations: BMI, body mass index (calculated as weight in kilograms divided by height in meters squared); HbA 1c, hemoglobin A 1c ; HDL-C, highdensity lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; NA, not applicable. SI conversion factors: To convert total cholesterol, LDL-C, and HDL-C to millimoles per liter, multiply by.29; glucose to millimoles per liter, multiply by.; HbA 1c to proportion of total hemoglobin, multiply by.1; insulin to picomoles per liter, multiply by 6.94; triglycerides to millimoles per liter, multiply by.113. a P=.1 vs controls. After providing informed consent, 29 consecutive untreated patients with clinically and genetically verified HD were included in the study from families registered at the Department of Movement Disorders, Institute of Neurology, Clinical Center of Serbia (Table). The study was approved by the ethics committee of the University Clinical Center of Serbia. The inclusion criterion was adult-onset HD confirmed by DNA analysis, as previously described. 8 with intestinal absorption problems or previously diagnosed DM or patients who were confined to a bed or wheelchair were excluded from the study. The control group (n=22) included individuals matched by age (±2 years), sex, and socioeconomic background who were recruited from the hospital staff and spouses of the department s patients. Only nondiabetic patients and controls were included, which was verified by using a 2-hour 7-g oral glucose tolerance test (OGTT) (Figure 1) and the World Health Organization criteria for the diagnosis of DM during recruitment (DM was defined as a 2-hour plasma glucose [PG] level 2 mg/dl [to convert to millimoles per liter, multiply by.]). 9 In patients with HD and controls, body mass index was calculated as weight in kilograms divided by height in meters squared. 1 Metabolic investigations (performed at the Center for Metabolic Disorders in Diabetes of the Institute of Endocrinology in the same manner as performed in DM research in non-hd subjects) included (1) glucose tolerance assessment based on the blood glucose curve during OGTT; (2) insulin sensitivity assessment using 2 different methods: homeostasis model assessment (HOMA) based on basal PG and plasma insulin (PI) levels, 6,11 primarily evaluating hepatic insulin sensitivity, 11 and Plasma Glucose Level, mg/dl with HD participants OGTT, min Figure 1. Mean plasma glucose levels in patients with Huntington disease (HD) and control participants during the oral glucose tolerance test (OGTT). Error bars represent SEM. There were no significant differences between the groups at any point during the test. To convert glucose to millimoles per liter, multiply by.. the minimal model analysis based on frequent sampling of PG and PI during the intravenous GTT (IVGTT), 12 determining predominantly peripheral insulin sensitivity 6,12 ; and (3) insulin secretion evaluation using 2 different methods for estimating earlyphase insulin secretion: the acute insulin response (AIR), determined during the IVGTT, evaluating the response to intravenous glucose challenge, 13 and the insulinogenic index, determined during the OGTT, evaluating the response to oral glucose challenge. 14 In all the participants, the OGTT preceded the IVGTT by 4 to 7 days. The OGTT was used to evaluate the glucose tolerance status and to determine the insulinogenic index, as a measure of insulin secretion, from the values of PG and PI obtained during the test after the glucose load. The OGTT was exerted after a 12-hour overnight fast, with a 7-g oral glucose load in the form of % glucose administered in 3 minutes. Blood samples for the determination of PG and PI levels were collected immediately before and 3, 6, 9, and 12 minutes after the glucose load. The insulinogenic index was determined during the OGTT as the ratio of the increment of PI to that of PG determined 3 minutes after a glucose load, that is, PI (-3 minutes)/ PG (-3 minutes). 14 The IVGTT was performed after a 12-hour overnight fast by infusing.3 g/kg of % glucose in 3 seconds. Blood samples for the testing of PG and PI were drawn immediately before and at multiple intervals after the intravenous glucose load. The PG and PI values obtained from the IVGTT were used to evaluate insulin sensitivity by means of minimal model analysis and to analyze early-phase insulin secretion by determining AIR (described in the third paragraph following). 12,13 Minimal model analysis of insulin sensitivity was performed from the frequently sampled PG and PI levels during the IVGTT. 12 Briefly, after the injection of.3 g/kg body weight of glucose, the blood samples were collected immediately before and 1, 2, 3, 4,, 6, 7, 8, 9, 1, 12, 14, 16, 2, 23, 24, 2, 27, 3, 4,, 6, 7, 8, 9, 1, 12, 16, and 18 minutes after intravenous glucose stimulation. Insulin was injected as a continuous infusion, 4 mu/kg/min, between minutes 2 and 2 to optimize the conditions for calculations of the insulin sensitivity index from the declining curve of PG and PI. 12 The sensitivity index was calculated from the results of PG and PI levels by means of computerized minimal model analysis using the MINMOD program. The HOMA analysis of insulin sensitivity was implemented using fasting PG and PI samples during the IVGTT. The (REPRINTED) ARCH NEUROL / VOL 6 (NO. 4), APR Downloaded From: on 1/16/218
3 A B P <.1 8 A P <. 3 B 2 P <.1 HOMA-IR Index P <. Si, min 1 /mu/l x AIR, mu/l PI3/ PG Figure 2. Evaluation of insulin sensitivity in patients with Huntington disease (HD) and control participants using 2 different methods: the homeostasis model assessment insulin resistance (HOMA-IR) index (A) and the insulin sensitivity index (Si), determined during minimal model analysis (B). Values are given as means. Error bars represent SEM. The HOMA-IR index, describing insulin resistance as a reciprocal value of insulin sensitivity, was significantly higher, whereas the Si was significantly lower, in patients with HD. Figure 3. Analysis of early-phase insulin secretion in patients with Huntington disease (HD) and control participants using 2 different methods: the acute insulin response (AIR) during the intravenous glucose tolerance test (A) and the insulinogenic index ( plasma insulin [PI] 3 / plasma glucose [PG] 3 ) during the oral glucose tolerance test (B). Values are given as means. Error bars represent SEM. The AIR and insulinogenic index values were significantly lower in patients with HD. HOMA insulin resistance (HOMA-IR) index, describing insulin resistance as a reciprocal value of insulin sensitivity, was calculated from the following equation: (PG PI)/ The AIR was determined during the IVGTT as the average increment of PI higher than basal values for samples obtained in the first 1 minutes of the IVGTT. 13 The PG level was determined by means of the glucose oxidase method using a glucose analyzer (Beckman Instruments, Fullerton, California). The PI level was tested by radioimmunoassay using double antibody kits (INEP, Zemun, Serbia). The results were evaluated using a statistical software program (SPSS 1.; SPSS Inc, Chicago, Illinois). Before statistical analysis, the normal distribution and homogeneity of the variances were evaluated using the Kolmogorov-Smirnov test. Comparisons of the mean values between groups were performed using the unpaired t test for continuous variables or the Mann-Whitney test for the insulinogenic index as a variable found to be without normal distribution. Spearman correlations were calculated to determine the relationship between the variables of insulin sensitivity and insulin secretion capacity and genetic features of HD. A P. was considered statistically significant. RESULTS The anthropometric and metabolic characteristics of patients with HD and controls are given in the Table. Only insulin levels were significantly higher in patients with HD compared with controls (P=.). The PG levels during the OGTT did not differ between patients with HD and controls at any point after the oral glucose load (Figure 1). CHANGES IN INSULIN SENSITIVITY Evaluation of insulin sensitivity using HOMA demonstrated that the mean (SEM) HOMA-IR index, describing insulin resistance as a reciprocal value of insulin sensitivity, was significantly higher in patients with HD (2.68 [.33]) compared with controls (1.71 [.18], P=.3) (Figure 2A). Use of the minimal model approach revealed that the mean (SEM) sensitivity index was significantly lower in patients with HD compared with controls (3.49 [.3] vs 6.76 [.9] min 1 /mu/l 1 4, P=.3) (Figure 2B). CHANGES IN EARLY-PHASE INSULIN SECRETION The mean (SEM) AIR values were significantly lower in patients with HD compared with controls (14.69 [1.6] vs 2.71 [2.2] mu/l, P=.2) (Figure 3A). Determination of the insulinogenic index revealed that its mean (SEM) values were significantly lower in patients with HD (7.47 [1.9]) compared with controls (2.9 [4.], P=.2) (Figure 3B). The mean (SEM) number of CAG repeats in patients with HD was 4.6 (7.3) (range, 4-73). The number of CAG repeats correlated only with the AIR (r=.17, P=.3), and no correlation was observed for the HOMA-IR index (r=.32, P=.1), the sensitivity index (r=.29, P=.4), or the insulinogenic index (r=.22, P=.27). COMMENT The main finding of this study was the impairment in insulin sensitivity and insulin secretion in normoglycemic patients with HD. Insulin sensitivity was analyzed using 2 different methodological approaches, HOMA and minimal model analysis, widely used in the evaluation of insulin sensitivity in healthy subjects 1 and in patients with DM 16 and in other diseases presumably caused by impaired insulin sensitivity. 17,18 In these studies, HOMA was found to evaluate primarily hepatic insulin sensitivity, 6 whereas minimal model analysis detected insulin sensitivity on the level of peripheral tissues. 19 Thus, we found a decrease in insulin sensitivity in patients with HD on the level of hepatic (Figure 2A) and peripheral (Figure 2B) tissues. (REPRINTED) ARCH NEUROL / VOL 6 (NO. 4), APR Downloaded From: on 1/16/218
4 The present data of the simultaneous presence of insulin resistance and decreased early-phase -cell secretion were similar to the changes observed in the state of increased risk for type 2 DM. 2 In the prediabetic state and in type 2 DM, the pivotal role in further glucose metabolism impairments was ascribed to the deterioration of insulin secretion capacity. 2 However, the insulin resistance found in our patients was associated with lowerthan-normal body mass index and showed no association with lipid abnormalities (Table), in contrast to patients with pre-dm and the metabolic syndrome who exhibit obesity, low high-density lipoprotein cholesterol levels, and high triglyceride levels. 6 Analysis of early-phase insulin secretion demonstrated the decrease in insulin secretion capacity after intravenous glucose challenge (AIR) (Figure 3A) and after a more potent oral glucose challenge that involved the cephalic phase of hormone release (Figure 3B). 14,21 Only a decrease in AIR weakly correlated with the number of CAG repeats, suggesting that at least the early phase of insulin response to intravenous challenge may be affected by the polymorphism of the mutated HD gene. However, lack of a large CAG expansion range in the present study could be partly responsible for the observed general lack of correlations (except for the AIR). In the R6/2 transgenic mouse model of HD, which expresses exon 1 of the human HD gene containing 1 CAG repeats, mice developed glycosuria and glucose intolerance from age 9 weeks, and by 14 weeks of age more than 7% of them had developed DM. 21 The histopathologic hallmark of HD, intranuclear inclusions, is also present in pancreatic cells. 22,23 In R6/2 mice, the onset of DM followed the formation of ubiquitin-positive huntingtin inclusions in pancreatic cells, 21 suggesting that inclusions might be involved in the development of hyperglycemia and type 1 DM. Indeed, plasmid vaccination against mutant huntingtin dramatically improved the diabetic phenotype. 24 The accumulation of such insoluble nuclear protein aggregates in islets was temporally associated with selective impairment of expression of transcriptional regulatory proteins essential for glucose-responsive insulin gene expression. 23 More recently, Björkqvist et al 2 identified 2 separate pathologic processes that are responsible for DM in R6/2 mice: deficient -cell mass and a loss of insulin-containing secretory granules, abrogating stimulated hormone secretion. In the same animal model, Hunt and Morton 21 attempted pharmacologic treatment of DM and found that mice responded acutely to glyburide (which induces exocytosis of insulin) but not to rosiglitazone maleate (which induces sensitization to insulin). Therefore, they suggested that DM in R6/2 mice was caused by an impairment in insulin release rather than by an impairment in insulin sensitivity. with HD have an increased prevalence of DM and have pathologic GTT findings. 3 Podolsky and Leopold 3 performed OGTTs and intravenous arginine tolerance tests in 14 patients with HD and found that % of them had abnormal glucose tolerance characterized by hyperglycemia and hyperinsulinemia. The etiology of such abnormalities is unknown. with HD are significantly underweight on a population basis, despite the fact that they tend to have adequate caloric intake. 26 It is unlikely that energy expenditure caused by involuntary movements explains this feature because the patients were significantly underweight even at the time of their first neurologic examination, when they had only minimal chorea, 27 suggesting that the low body mass index in HD could be related to a general metabolic derangement. 28,29 Similarly, most animal models of HD are associated with major loss of weight. 3 Recently, Duan et al 31 found that paroxetine, a serotonin reuptake inhibitor, improves survival in a transgenic mouse model of HD while inhibiting weight loss. This drug increases concentrations in brain-derived growth factor, which in turn seems to improve otherwise impaired insulin production and responsiveness in these mice. The same effect on brain-derived growth factor was also found with food restriction, which paradoxically slowed disease progression and weight loss in HD transgenic mice. 3 Yamamoto et al 32 demonstrated that activation of insulin receptor substrate 2, a scaffolding protein that mediates the signaling cascades of growth factors, such as insulin, leads to macroautophagy-mediated clearance of the accumulated polyglutamine proteins, suggesting that an impairment in insulin regulatory mechanisms also affects the insulin signaling pathways important for the pathogenesis of HD. Crocker et al 33 conducted DNA microarray analysis of striatal gene expression in symptomatic transgenic R6/2 mice, and their bioinformatic analysis pointed to insulin and neuroinflammatory mediators as potential key regulators of a variety of differentially expressed genes in the transgenic mice and, consequently, in HD. Neurons share similarities with insulin-producing pancreatic islet cells, possibly owing to the islet s evolution from an ancestral insulin-producing neuron. 34 Therefore, the pathogenetic mechanisms in the pancreatic islets may be relevant for the pathogenesis of neurodegeneration in HD. Data from transgenic HD animals suggested that DM occurs in mice as a result of impairment of the release of insulin, whereas insulin resistance is not a primary factor in the DM occurring in these animals. 21,2 Opposite of experimental findings, in our normoglycemic patients with HD, we found, besides impairment in insulin secretion capacity, a decrease in insulin sensitivity compared with controls. These data imply that progression of the insulin secretion defect may lead to a failure to compensate for insulin resistance, but further analyses are necessary with longer follow-up to elucidate (1) the progression of observed impairments and (2) whether the improvement in insulin sensitivity may have a beneficial effect on HD phenotype. Accepted for Publication: November 28, 27. Correspondence: Vladimir S. Kostić, MD, PhD, Institute of Neurology, Clinical Center of Serbia, Ul. Dr Subotića 6, 11 Belgrade, Serbia (kostic@imi.bg.ac.yu). Author Contributions: All authors had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: N. M. Lalić, Stefanova, and Kostić. Acquisition of data: N. M. Lalić, Marić, Svetel, Jotić, (REPRINTED) ARCH NEUROL / VOL 6 (NO. 4), APR Downloaded From: on 1/16/218
5 K. Lalić, Dragašević, Miličić, and Kostić. Analysis and interpretation of data: N. M. Lalić, Marić, Lukić, and Kostić. Drafting of the manuscript: N. M. Lalić, Marić, Svetel, Stefanova, Dragašević, and Kostić.Critical revision of the manuscript for important intellectual content: N. M. Lalić, Jotić, K. Lalić, Miličić, Lukić, and Kostić. Statistical analysis: N. M. Lalić, Svetel, Stefanova, Lukić, and Kostić. Obtained funding: Kostić. Administrative, technical, and material support: Dragašević, Miličić, and Kostić. Study supervision: N. M. Lalić, Marić, Jotić, K. Lalić, and Kostić. Financial Disclosure: None reported. Funding/Support: This work was funded by projects 147Ð and 1489 from the Ministry of Science, Republic of Serbia. Additional Contributions: Richard Bergman, MD, PhD, of the University of Southern California, Los Angeles, provided the MINMOD program. REFERENCES 1. Huntington s Disease Collaborative Research Group. A novel gene containing a trinucleotide repeat that is unstable in Huntington s disease chromosomes. Cell. 1993;72(6): Farrer LA. Diabetes mellitus in Huntington s disease. Clin Genet. 198;27(1): Podolsky S, Leopold NA. Abnormal glucose tolerance and arginine tolerance tests in Huntington s disease. Gerontology. 1977;23(1): Craft S. Insulin resistance and cognitive impairment: a view through the prism of epidemiology. Arch Neurol. 2;62(7): Hurlbert MS, Zhou W, Wasmeier C, Kaddis FG, Hutton JC, Freed CR. Mice transgenic for an expanded CAG repeat in the Huntington s disease gene develop diabetes. Diabetes. 1999;48(3): Tripathy D, Carlsson M, Almgren P, et al. Insulin secretion and insulin sensitivity in relation to glucose tolerance: lessons from the Botnia Study. Diabetes. 2; 49(6): Del Prato S. Loss of early insulin secretion leads to postprandial hyperglycemia. Diabetologia. 23;46(suppl 1):M2-M8. 8. Major T, Svetel M, Romac S, Kostić VS. DYT1 mutation in primary torsion dystonia in a Serbian population. J Neurol. 21;248(11): World Health Organization. Definition, Diagnosis, and Classification: Diabetes Mellitus. Geneva, Switzerland: World Health Organization; 198:9-2. Technical report series James WP, Ferro-Luzzi A, Waterlow JC. Definition of chronic energy deficiency in adults: report of a working party of the International Dietary Energy Consultative Group. Eur J Clin Nutr. 1988;42(12): Matthews DR, Hasker JP, Rudensky AS, Naylor BA, Treacher DF, Turner RC. Homeostatic model assessment: insulin resistance and -cell function from plasma glucose and insulin concentration in men. Diabetologia. 198;28(7): Bergman RN. Lilly lecture 1989: toward physiological understanding of glucose tolerance: minimal-model approach. Diabetes. 1989;38(12): Bergman RN, Adler M, Huecking K, Van Citters G. Accurate assessment of cell function: the hyperbolic correction. Diabetes. 22;1(suppl 1):S212- S Ahren B, Taborsky GJ. -Cell function and insulin secretion. In: Porte D, Sherwin RS, Baron A, eds. Ellenberg and Riffkin s Diabetes Mellitus. 6th ed. New York, NY: McGraw Hill; 23: Festa A, D Agostino R, Hanley AJG, Karter AJ, Saad MF, Haffner SM. Differences in insulin resistance in nondiabetic subjects with isolated impaired glucose tolerance or isolated impaired fasting glucose. Diabetes. 24;3(6): Haffner SM, D Agostino R, Mykkänen L, et al. Insulin sensitivity in subjects with type 2 diabetes: relationship to cardiovascular risk factors: the Insulin Resistance Atherosclerosis Study. Diabetes Care. 1999;22(4): Inoue T, Matsunaga R, Sakai Y, Yaguchi I, Takayanagi K, Morooka S. Insulin resistance affects endothelium-dependent acetylcholine-induced coronary artery response. Eur Heart J. 2;21(11): Rewers M, Zaccaro D, D Agostino R, et al; Insulin Resistance Atherosclerosis Study Investigators. Insulin sensitivity, insulinemia, and coronary artery disease: the Insulin Resistance Atherosclerosis Study. Diabetes Care. 24;27 (3): Saad MF, Anderson RL, Laws A, et al; Insulin Resistance Atherosclerosis Study Investigators. A comparison between the minimal model and the glucose clamp in the assessment of insulin sensitivity across the spectrum of glucose tolerance. Diabetes. 1994;43(9): Ferrannini E, Gastaldelli A, Miyzaki Y, Matsuda M, Mari A, De Fronzo RA. -Cell function in subjects spanning the range from the normal glucose tolerance to overt diabetes: a new analysis. J Clin Endocrinol Metab. 2;9(1): Hunt MJ, Morton AJ. Atypical diabetes associated with inclusion formation in the R6/2 mouse model of Huntington s disease is not improved by treatment with hypoglycaemic agents. Exp Brain Res. 2;166(2): Sathasivam K, Bobbs C, Turmaine M, et al. Formation of polyglutamine inclusions in non-cns tissue. Hum Mol Genet. 1999;8(): Andreassen OA, Dedeoglu A, Stanojevic V, et al. Huntington s disease of the endocrine pancreas: insulin deficiency and diabetes mellitus due to impaired insulin gene expression. Neurobiol Dis. 22;11(3): Miller TW, Shirley TL, Wolfgang WJ, Kang X, Messer A. DNA vaccination against mutant huntingtin ameliorates the HDR6/2 diabetic phenotype. Mol Ther. 23; 7(, pt 1): Björkqvist M, Fex M, Renström E, et al. The R6/2 transgenic mouse model of Huntington s disease develops diabetes due to deficient -cell mass and exocytosis. Hum Mol Genet. 2;14(): Turner C, Schapira AH. Energy metabolism in Huntington s disease. In: Bates G, Harper P, Jones L, eds. Huntington s Disease. 3rd ed. Oxford, England: Oxford Press; 22: Djoussé L, Knowlton B, Cupples LA, Marder K, Shoulson I, Myers RH. Weight loss in early stage of Huntington s disease. Neurology. 22;9(9): Strand AD, Aragaki AK, Shaw D, et al. Gene expression in Huntington s disease skeletal muscle: a potential biomarker. Hum Mol Genet. 2;14(13): Weydt P, Pineda VV, Torrence AE, et al. Thermoregulatory and metabolic defects in Huntington s disease transgenic mice implicate PGC-1 in Huntington s disease neurodegeneration. Cell Metab. 26;4(): Duan W, Guo Z, Jiang H, Ware M, Li X, Mattson MP. Dietary restriction normalizes glucose metabolism and BDNF levels, slows disease progression, and increases survival in huntingtin mutant mice. Proc Natl Acad Sci U S A. 23; 1(): Duan W, Guo Z, Jiang H, et al. Paroxetine retards disease onset and progression in Huntingtin mutant mice. Ann Neurol. 24;(4): Yamamoto A, Cremona L, Rothman JE. Autophagy-mediated clearance of huntingtin aggregates triggered by the insulin-signaling pathway. J Cell Biol. 26; 172(): Crocker SF, Costain WJ, Robertson HA. DNA microarray analysis of striatal gene expression in symptomatic transgenic Huntington s mice (R6/2) reveals neuroinflammation and insulin associations. Brain Res. 26;188(1): Rulifson EJ, Kim SK, Nusse R. Ablation of insulin-producing neurons in flies: growth and diabetic phenotypes. Science. 22;296(7): (REPRINTED) ARCH NEUROL / VOL 6 (NO. 4), APR Downloaded From: on 1/16/218
Neurodegenerative disorders and diabetes: common underlying impairments. N.M. Lalic (Serbia)
Neurodegenerative disorders and diabetes: common underlying impairments N.M. Lalic (Serbia) Neurodegenerative disorders and diabetes: common underlying impairments Professor Nebojsa M. Lalic Faculty of
More informationAssociations among Body Mass Index, Insulin Resistance, and Pancreatic ß-Cell Function in Korean Patients with New- Onset Type 2 Diabetes
ORIGINAL ARTICLE korean j intern med 2012;27:66-71 pissn 1226-3303 eissn 2005-6648 Associations among Body Mass Index, Insulin Resistance, and Pancreatic ß-Cell Function in Korean Patients with New- Onset
More informationClinical Study 1-Hour OGTT Plasma Glucose as a Marker of Progressive Deterioration of Insulin Secretion and Action in Pregnant Women
Hindawi Publishing Corporation International Journal of Endocrinology Volume 2012, Article ID 460509, 5 pages doi:10.1155/2012/460509 Clinical Study 1-Hour OGTT Plasma Glucose as a Marker of Progressive
More informationSpecific insulin and proinsulin in normal glucose tolerant first-degree relatives of NIDDM patients
Brazilian Journal of Medical and Biological Research (1999) 32: 67-72 Insulin and proinsulin in first-degree relatives of NIDDM ISSN 1-879X 67 Specific insulin and proinsulin in normal glucose tolerant
More informationElevated Serum Levels of Adropin in Patients with Type 2 Diabetes Mellitus and its Association with
Elevated Serum Levels of Adropin in Patients with Type 2 Diabetes Mellitus and its Association with Insulin Resistance Mehrnoosh Shanaki, Ph.D. Assistant Professor of Clinical Biochemistry Shahid Beheshti
More informationORIGINAL INVESTIGATION. C-Reactive Protein Concentration and Incident Hypertension in Young Adults
ORIGINAL INVESTIGATION C-Reactive Protein Concentration and Incident Hypertension in Young Adults The CARDIA Study Susan G. Lakoski, MD, MS; David M. Herrington, MD, MHS; David M. Siscovick, MD, MPH; Stephen
More informationDiabetes: Definition Pathophysiology Treatment Goals. By Scott Magee, MD, FACE
Diabetes: Definition Pathophysiology Treatment Goals By Scott Magee, MD, FACE Disclosures No disclosures to report Definition of Diabetes Mellitus Diabetes Mellitus comprises a group of disorders characterized
More informationPREVALENCE OF INSULIN RESISTANCE IN FIRST DEGREE RELATIVES OF TYPE-2 DIABETES MELLITUS PATIENTS: A PROSPECTIVE STUDY IN NORTH INDIAN POPULATION
PREVALENCE OF INSULIN RESISTANCE IN FIRST DEGREE RELATIVES OF TYPE-2 DIABETES MELLITUS PATIENTS: A PROSPECTIVE STUDY IN NORTH INDIAN POPULATION Arvind Kumar, Poornima Tewari, Sibasis S. Sahoo and Arvind
More informationNeuroscience 410 Huntington Disease - Clinical. March 18, 2008
Neuroscience 410 March 20, 2007 W. R. Wayne Martin, MD, FRCPC Division of Neurology University of Alberta inherited neurodegenerative disorder autosomal dominant 100% penetrance age of onset: 35-45 yr
More informationThe enteroinsular axis in the pathogenesis of prediabetes and diabetes in humans
The enteroinsular axis in the pathogenesis of prediabetes and diabetes in humans Young Min Cho, MD, PhD Division of Endocrinology and Metabolism Seoul National University College of Medicine Plasma glucose
More information2011, Editrice Kurtis
J. Endocrinol. Invest. : -, 2011 DOI: 10.2/902 The role of visfatin in the pathogenesis of gestational diabetes mellitus D.E. Gok 1, M. Yazici 1, G. Uckaya 1, S.E. Bolu 1, Y. Basaran 2, T. Ozgurtas, S.
More informationChanges and clinical significance of serum vaspin levels in patients with type 2 diabetes
Changes and clinical significance of serum vaspin levels in patients with type 2 diabetes L. Yang*, S.J. Chen*, G.Y. Yuan, D. Wang and J.J. Chen Department of Endocrinology, Affiliated Hospital of Jiangsu
More informationNGS in neurodegenerative disorders - our experience
Neurology Clinic, Clinical Center of Serbia Faculty of Medicine, University of Belgrade Belgrade, Serbia NGS in neurodegenerative disorders - our experience Marija Branković, MSc Belgrade, 2018 Next Generation
More informationThe term impaired glucose tolerance
Cardiovascular and Metabolic Risk O R I G I N A L A R T I C L E Risk of Progression to Type 2 Diabetes Based on Relationship Between Postload Plasma Glucose and Fasting Plasma Glucose MUHAMMAD A. ABDUL-GHANI,
More informationObesity and Insulin Resistance According to Age in Newly Diagnosed Type 2 Diabetes Patients in Korea
https://doi.org/10.7180/kmj.2016.31.2.157 KMJ Original Article Obesity and Insulin Resistance According to Age in Newly Diagnosed Type 2 Diabetes Patients in Korea Ju Won Lee, Nam Kyu Kim, Hyun Joon Park,
More informationPeople Living with And Inspired by Diabetes
People Living with And Inspired by Diabetes IMPERFECTLY MOVING TOWARDS & FAINTING GOATS Vol. 2 No. 2 Fall 2016 Vol. 2 No. 2 Fall 2016 1 Review PARTNERING WITH SCIENCE: New Hope for the Effective Treatment
More informationAssociation between Raised Blood Pressure and Dysglycemia in Hong Kong Chinese
Diabetes Care Publish Ahead of Print, published online June 12, 2008 Raised Blood Pressure and Dysglycemia Association between Raised Blood Pressure and Dysglycemia in Hong Kong Chinese Bernard My Cheung,
More informationARIC Manuscript Proposal # 985. PC Reviewed: 12/15/03 Status: A Priority: 2 SC Reviewed: 12/16/03 Status: A Priority: 2
ARIC Manuscript Proposal # 985 PC Reviewed: 12/15/03 Status: A Priority: 2 SC Reviewed: 12/16/03 Status: A Priority: 2 1.a. Full Title: Association between family history of type 2 Diabetes Mellitus, the
More informationInsulin release, insulin sensitivity, and glucose intolerance (early diabetes/pathogenesis)
Proc. Natl. Acad. Sci. USA Vol. 77, No. 12, pp. 7425-7429, December 1980 Medical Sciences nsulin release, insulin sensitivity, and glucose intolerance (early diabetes/pathogenesis) SUAD EFENDt, ALEXANDRE
More informationTRIGLYCERIDE/HIGH-DENSITY LIPOPROTEIN CHOLESTEROL CONCENTRATION RATIO IDENTIFIES ACCENTUATED CARDIO-METABOLIC RISK
ENDOCRINE PRACTICE Rapid Electronic Article in Press Rapid Electronic Articles in Press are preprinted manuscripts that have been reviewed and accepted for publication, but have yet to be edited, typeset
More informationThe American Diabetes Association estimates
DYSLIPIDEMIA, PREDIABETES, AND TYPE 2 DIABETES: CLINICAL IMPLICATIONS OF THE VA-HIT SUBANALYSIS Frank M. Sacks, MD* ABSTRACT The most serious and common complication in adults with diabetes is cardiovascular
More informationIntroduction ORIGINAL RESEARCH. Bilal A. Omar 1, Giovanni Pacini 2 & Bo Ahren 1. Abstract
ORIGINAL RESEARCH Physiological Reports ISSN 2051-817X Impact of glucose dosing regimens on modeling of glucose tolerance and b-cell function by intravenous glucose tolerance test in diet-induced obese
More informationInsulin Resistance. Biol 405 Molecular Medicine
Insulin Resistance Biol 405 Molecular Medicine Insulin resistance: a subnormal biological response to insulin. Defects of either insulin secretion or insulin action can cause diabetes mellitus. Insulin-dependent
More informationORIGINAL INVESTIGATION. Fasting Triglyceride and the Triglyceride HDL Cholesterol Ratio Are Not Markers of Insulin Resistance in African Americans
ORIGINAL INVESTIGATION Fasting Triglyceride and the Triglyceride HDL Cholesterol Ratio Are Not Markers of Insulin Resistance in African Americans Anne E. Sumner, MD; Karl B. Finley, MD; David J. Genovese,
More informationBariatric Surgery versus Intensive Medical Therapy for Diabetes 3-Year Outcomes
The new england journal of medicine original article Bariatric Surgery versus Intensive Medical for Diabetes 3-Year Outcomes Philip R. Schauer, M.D., Deepak L. Bhatt, M.D., M.P.H., John P. Kirwan, Ph.D.,
More informationRole of fatty acids in the development of insulin resistance and type 2 diabetes mellitus
Emerging Science Role of fatty acids in the development of insulin resistance and type 2 diabetes mellitus George Wolf Insulin resistance is defined as the reduced responsiveness to normal circulating
More informationWhat is Diabetes Mellitus?
Normal Glucose Metabolism What is Diabetes Mellitus? When the amount of glucose in the blood increases, After a meal, it triggers the release of the hormone insulin from the pancreas. Insulin stimulates
More information300 Biomed Environ Sci, 2018; 31(4):
300 Biomed Environ Sci, 2018; 31(4): 300-305 Letter to the Editor Combined Influence of Insulin Resistance and Inflammatory Biomarkers on Type 2 Diabetes: A Population-based Prospective Cohort Study of
More informationMETABOLIC SYNDROME IN REPRODUCTIVE FEMALES
METABOLIC SYNDROME IN REPRODUCTIVE FEMALES John J. Orris, D.O., M.B.A Division Head, Reproductive Endocrinology & Infertility, Main Line Health System Associate Professor, Drexel University College of
More informationDiabetes: Staying Two Steps Ahead. The prevalence of diabetes is increasing. What causes Type 2 diabetes?
Focus on CME at the University of University Manitoba of Manitoba : Staying Two Steps Ahead By Shagufta Khan, MD; and Liam J. Murphy, MD The prevalence of diabetes is increasing worldwide and will double
More informationImpact of Physical Activity on Metabolic Change in Type 2 Diabetes Mellitus Patients
2012 International Conference on Life Science and Engineering IPCBEE vol.45 (2012) (2012) IACSIT Press, Singapore DOI: 10.7763/IPCBEE. 2012. V45. 14 Impact of Physical Activity on Metabolic Change in Type
More information28 Regulation of Fasting and Post-
28 Regulation of Fasting and Post- Prandial Glucose Metabolism Keywords: Type 2 Diabetes, endogenous glucose production, splanchnic glucose uptake, gluconeo-genesis, glycogenolysis, glucose effectiveness.
More informationValidation of a novel index to assess insulin resistance of adipose tissue lipolytic activity in. obese subjects
Validation of a novel index to assess insulin resistance of adipose tissue lipolytic activity in obese subjects Elisa Fabbrini, MD, PhD; Faidon Magkos, PhD; Caterina Conte, MD; Bettina Mittendorfer, PhD;
More informationYiying Zhang, PhD Research Scientist. Research Summary:
Yiying Zhang, PhD Research Scientist Research Summary: Address: Naomi Berrie Diabetes Center at Columbia University Medical Center Russ Berrie Medical Science Pavilion 1150 St. Nicholas Avenue New York,
More informationSupplementary Material 1. Statistical methods used to conduct power calculations.
Supplementary Material 1. Statistical methods used to conduct power calculations. Post-hoc power calculations and patient numbers needed to detect changes were conducted considering (i) the observed partial
More informationFrequency of Dyslipidemia and IHD in IGT Patients
Frequency of Dyslipidemia and IHD in IGT Patients *Islam MS, 1 Hossain MZ, 2 Talukder SK, 3 Elahi MM, 4 Mondal RN 5 Impaired glucose tolerance (IGT) is often associated with macrovascular complications.
More informationORIGINAL INVESTIGATION. Prediction of Incident Diabetes Mellitus in Middle-aged Adults
ORIGINAL INVESTIGATION Prediction of Incident Diabetes Mellitus in Middle-aged Adults The Framingham Offspring Study Peter W. F. Wilson, MD; James B. Meigs, MD, MPH; Lisa Sullivan, PhD; Caroline S. Fox,
More informationElectronic Supplementary Material to the article entitled Altered pattern of the
Electronic Supplementary Material to the article entitled Altered pattern of the incretin effect as assessed by modelling in individuals with glucose tolerance ranging from normal to diabetic Integrated
More informationCardiovascular Risk Factors among Diabetic Patients Attending a Nigerian Teaching Hospital. O Alao, S Adebisi, G Jombo, D Joseph, O Damulak, F Puepet
ISPUB.COM The Internet Journal of Endocrinology Volume 6 Number 1 Cardiovascular Risk Factors among Diabetic Patients Attending a Nigerian Teaching Hospital. O Alao, S Adebisi, G Jombo, D Joseph, O Damulak,
More informationMetabolic Syndrome. DOPE amines COGS 163
Metabolic Syndrome DOPE amines COGS 163 Overview - M etabolic Syndrome - General definition and criteria - Importance of diagnosis - Glucose Homeostasis - Type 2 Diabetes Mellitus - Insulin Resistance
More informationThe oral meal or oral glucose tolerance test. Original Article Two-Hour Seven-Sample Oral Glucose Tolerance Test and Meal Protocol
Original Article Two-Hour Seven-Sample Oral Glucose Tolerance Test and Meal Protocol Minimal Model Assessment of -Cell Responsivity and Insulin Sensitivity in Nondiabetic Individuals Chiara Dalla Man,
More informationLetter to the Editor. Association of TCF7L2 and GCG Gene Variants with Insulin Secretion, Insulin Resistance, and Obesity in New-onset Diabetes *
814 Biomed Environ Sci, 2016; 29(11): 814-817 Letter to the Editor Association of TCF7L2 and GCG Gene Variants with Insulin Secretion, Insulin Resistance, and Obesity in New-onset Diabetes * ZHANG Lu 1,^,
More informationSupplementary Online Content
Supplementary Online Content Larsen JR, Vedtofte L, Jakobsen MSL, et al. Effect of liraglutide treatment on prediabetes and overweight or obesity in clozapine- or olanzapine-treated patients with schizophrenia
More informationUNIVERSITY OF PNG SCHOOL OF MEDICINE AND HEALTH SCIENCES DIVISION OF BASIC MEDICAL SCIENCES DISCIPLINE OF BIOCHEMISTRY AND MOLECULAR BIOLOGY
1 UNIVERSITY OF PNG SCHOOL OF MEDICINE AND HEALTH SCIENCES DIVISION OF BASIC MEDICAL SCIENCES DISCIPLINE OF BIOCHEMISTRY AND MOLECULAR BIOLOGY GLUCOSE HOMEOSTASIS An Overview WHAT IS HOMEOSTASIS? Homeostasis
More informationISSN X (Print) Original Research Article
Scholars Journal of Applied Medical Sciences (SJAMS) Sch. J. App. Med. Sci., 2017; 5(11F):4737-4741 Scholars Academic and Scientific Publisher (An International Publisher for Academic and Scientific Resources)
More informationImpaired glucose tolerance and growth hormone in chronic liver disease
Gut, 1981, 22, 3135 Impaired glucose tolerance and growth hormone in chronic liver disease W J RILY* AND V J McCANN From the Department of Biochemistry and Diabetic Unit, Royal Perth Hospital, Perth, Western
More informationResearch Article Associated Factors with Biochemical Hypoglycemia during an Oral Glucose Tolerance Test in a Chinese Population
Hindawi Diabetes Research Volume 2017, Article ID 3212814, 5 pages https://doi.org/10.1155/2017/3212814 Research Article Associated Factors with Biochemical Hypoglycemia during an Oral Glucose Tolerance
More informationCardiovascular Complications of Diabetes
VBWG Cardiovascular Complications of Diabetes Nicola Abate, M.D., F.N.L.A. Professor and Chief Division of Endocrinology and Metabolism The University of Texas Medical Branch Galveston, Texas Coronary
More informationType 2 DM in Adolescents: Use of GLP-1 RA. Objectives. Scope of Problem: Obesity. Background. Pathophysiology of T2DM
Type 2 DM in Adolescents: Use of GLP-1 RA Objectives Identify patients in the pediatric population with T2DM that would potentially benefit from the use of GLP-1 RA Discuss changes in glycemic outcomes
More informationDecreased Non-Insulin Dependent Glucose Clearance Contributes to the Rise in FPG in the Non-Diabetic Range.
Diabetes Care Publish Ahead of Print, published online November 13, 2007 Decreased Non-Insulin Dependent Glucose Clearance Contributes to the Rise in FPG in the Non-Diabetic Range. Rucha Jani, M.D., Marjorie
More informationSerum uric acid levels improve prediction of incident Type 2 Diabetes in individuals with impaired fasting glucose: The Rancho Bernardo Study
Diabetes Care Publish Ahead of Print, published online June 9, 2009 Serum uric acid and incident DM2 Serum uric acid levels improve prediction of incident Type 2 Diabetes in individuals with impaired fasting
More informationReach2HD Phase 2 Clinical Trial Top Line Results. Investor Conference Call 19 th February 2014
Reach2HD Phase 2 Clinical Trial Top Line Results Investor Conference Call 19 th February 2014 Safe Harbour This presentation may contain some statements that may be considered Forward-Looking Statements,
More informationPlasma fibrinogen level, BMI and lipid profile in type 2 diabetes mellitus with hypertension
World Journal of Pharmaceutical Sciences ISSN (Print): 2321-3310; ISSN (Online): 2321-3086 Published by Atom and Cell Publishers All Rights Reserved Available online at: http://www.wjpsonline.org/ Original
More informationDecreased -Cell Function in Overweight Latino Children With Impaired Fasting Glucose
Metabolic Syndrome/Insulin Resistance Syndrome/Pre-Diabetes O R I G I N A L A R T I C L E Decreased -Cell Function in Overweight Latino Children With Impaired Fasting Glucose MARC J. WEIGENSBERG, MD 1
More informationPREVALENCE OF METABOLİC SYNDROME İN CHİLDREN AND ADOLESCENTS
PREVALENCE OF METABOLİC SYNDROME İN CHİLDREN AND ADOLESCENTS Mehmet Emre Atabek,MD,PhD Necmettin Erbakan University Faculty of Medicine, Department of Pediatrics, Division of Pediatric Endocrinology and
More informationCardiometabolic Risk in Patients With First-Episode Schizophrenia Spectrum Disorders Baseline Results From the RAISE-ETP Study
Research Original Investigation Cardiometabolic Risk in Patients With First-Episode Schizophrenia Spectrum Disorders Baseline Results From the RAISE-ETP Study Christoph U. Correll, MD; Delbert G. Robinson,
More informationWeek 3, Lecture 5a. Pathophysiology of Diabetes. Simin Liu, MD, ScD
Week 3, Lecture 5a Pathophysiology of Diabetes Simin Liu, MD, ScD General Model of Peptide Hormone Action Hormone Plasma Membrane Activated Nucleus Cellular Trafficking Enzymes Inhibited Receptor Effector
More informationAssociation of acanthosis nigricans with race and metabolic disturbances in obese women
Brazilian Journal of Medical and Biological Research (2002) 35: 59-64 Acanthosis nigricans, race and metabolic disturbances ISSN 0100-879X 59 Association of acanthosis nigricans with race and metabolic
More informationDiabetes mellitus. Treatment
Diabetes mellitus Treatment Recommended glycemic targets for the clinical management of diabetes(ada) Fasting glycemia: 80-110 mg/dl Postprandial : 100-145 mg/dl HbA1c: < 6,5 % Total cholesterol: < 200
More informationDevelopment and Validation of a Method to Estimate Insulin Sensitivity in Patients With and Without Type 1 Diabetes
ORIGINAL ARTICLE Development and Validation of a Method to Estimate Insulin Sensitivity in Patients With and Without Type 1 Diabetes Lindsey M. Duca, David M. Maahs, Irene E. Schauer, Bryan C. Bergman,
More informationThe number of diabetic patients in Japan
Metabolic Syndrome/Insulin Resistance Syndrome/Pre-Diabetes O R I G I N A L A R T I C L E Glucose Intolerance Is Common in Japanese Patients With Acute Coronary Syndrome Who Were Not Previously Diagnosed
More informationMetabolic changes in menopausal transition
Metabolic changes in menopausal transition Terhi T. Piltonen M.D., Associate Professor Consultant, Clinical Researcher for the Finnish Medical Foundation Department of Obstetrics and Gynecology PEDEGO
More informationDecreased Non Insulin-Dependent Glucose Clearance Contributes to the Rise in Fasting Plasma Glucose in the Nondiabetic Range
Pathophysiology/Complications O R I G I N A L A R T I C L E Decreased Non Insulin-Dependent Glucose Clearance Contributes to the Rise in Fasting Plasma Glucose in the Nondiabetic Range RUCHA JANI, MD MARJORIE
More informationThe Many Faces of T2DM in Long-term Care Facilities
The Many Faces of T2DM in Long-term Care Facilities Question #1 Which of the following is a risk factor for increased hypoglycemia in older patients that may suggest the need to relax hyperglycemia treatment
More informationAdditional Water Intake after Meal Reduced 2-h Postprandial Blood Glucose Level in Healthy Subjects
International Journal of Diabetes Research 2018, 7(1): 18-22 DOI: 10.5923/j.diabetes.20180701.03 Additional Water Intake after Meal Reduced 2-h Postprandial Blood Glucose Level in Healthy Subjects Vanessa
More informationStatus of LDL Oxidation and antioxidant potential of LDL in Type II Diabetes Mellitus
Biomedical Research 2010; 21 (4): 416-418 Status of LDL Oxidation and antioxidant potential of LDL in Type II Singh N, Singh N, Singh S K, Singh A K, Bhargava V. Department of Biochemistry, G. R. Medical
More informationPsych 3102 Lecture 3. Mendelian Genetics
Psych 3102 Lecture 3 Mendelian Genetics Gregor Mendel 1822 1884, paper read 1865-66 Augustinian monk genotype alleles present at a locus can we identify this? phenotype expressed trait/characteristic can
More informationEugene Barrett M.D., Ph.D. University of Virginia 6/18/2007. Diagnosis and what is it Glucose Tolerance Categories FPG
Diabetes Mellitus: Update 7 What is the unifying basis of this vascular disease? Eugene J. Barrett, MD, PhD Professor of Internal Medicine and Pediatrics Director, Diabetes Center and GCRC Health System
More informationAssociation of serum adipose triglyceride lipase levels with obesity and diabetes
Association of serum adipose triglyceride lipase levels with obesity and diabetes L. Yang 1 *, S.J. Chen 1 *, G.Y. Yuan 1, L.B. Zhou 2, D. Wang 1, X.Z. Wang 1 and J.J. Chen 1 1 Department of Endocrinology,
More informationCut-Off Fasting Plasma Glucose Level To Determine Impaired Glucose Metabolism In Obesity
ISPUB.COM The Internet Journal of Internal Medicine Volume 4 Number 1 Cut-Off Fasting Plasma Glucose Level To Determine Impaired Glucose Metabolism In Obesity S Guldiken, A Tugrul, G Ekuklu, E Arikan,
More informationDiabetes Mellitus in the Pediatric Patient
Diabetes Mellitus in the Pediatric Patient William Bryant, M.D. Chief of Section Pediatric Endocrinology Children s Hospital at Scott & White Texas A&M University Temple, Texas Disclosures None Definitions
More informationTHE ROLE OF INSULIN RECEPTOR SIGNALING IN THE BRAIN. COGS 163 By: Pranav Singh Alexandra Villar
THE ROLE OF INSULIN RECEPTOR SIGNALING IN THE BRAIN COGS 163 By: Pranav Singh Alexandra Villar INTRODUCTION Insulin is a hormone produced in the pancreas by the islets of Langerhans that regulates the
More informationSupplementary Online Content
Supplementary Online Content Anagnostou E, Aman MG, Handen BL, et al. Metformin for treatment of overweight induced by atypical antipsychotic medication in young people with autistic spectrum disorder:
More informationDiabetes and Cardiovascular Risks in the Polycystic Ovary Syndrome
Diabetes and Cardiovascular Risks in the Polycystic Ovary Syndrome John E. Nestler, M.D. William Branch Porter Professor of Medicine Chair, Department of Internal Medicine Virginia Commonwealth University
More informationElevated serum levels of visfatin in gestational diabetes: a comparative study across various degrees of glucose tolerance
Diabetologia (2007) 50:1033 1037 DOI 10.1007/s00125-007-0610-7 SHORT COMMUNICATION Elevated serum levels of visfatin in gestational diabetes: a comparative study across various degrees of glucose tolerance
More informationDiabetes Care 24:89 94, 2000
Pathophysiology/Complications O R I G I N A L A R T I C L E Insulin Resistance and Insulin Secretory Dysfunction Are Independent Predictors of Worsening of Glucose Tolerance During Each Stage of Type 2
More informationMETABOLISMO E VITAMINA D
CONVEGNO NAZIONALE GIBIS ROMA 14-15 MAGGIO 2015 METABOLISMO E VITAMINA D Alfredo Scillitani UO Endocrinologia Ospedale Casa Sollievo della Sofferenza Holick MF, NEJM 2007 Sindrome Metabolica E un cluster
More informationThe investigation of serum lipids and prevalence of dyslipidemia in urban adult population of Warangal district, Andhra Pradesh, India
eissn: 09748369, www.biolmedonline.com The investigation of serum lipids and prevalence of dyslipidemia in urban adult population of Warangal district, Andhra Pradesh, India M Estari, AS Reddy, T Bikshapathi,
More informationAdjusting Glucose-Stimulated Insulin Secretion for Adipose Insulin Resistance: An Index of b-cell Function in Obese Adults
Diabetes Care 1 Adjusting Glucose-Stimulated Insulin Secretion for Adipose Insulin Resistance: An Index of b-cell Function in Obese Adults DOI: 10.2337/dc13-3011 Steven K. Malin, 1,2 Sangeeta R. Kashyap,
More informationR. Leibel Naomi Berrie Diabetes Center 19 March 2010
Pathophysiology of type 2 diabetes mellitus R. Leibel Naomi Berrie Diabetes Center 19 March 2010 Body Mass Index Chart 25-29.9 29.9 = overweight; 30-39.9= 39.9 obese; >40= extreme obesity 5'0" 5'2" 52
More informationBerson and Yalow 1 defined insulin resistance (IR) as a
A Study to Evaluate Surrogate Markers of Insulin Resistance in Forty Euglycemic Healthy Subjects AK Gupta*, SK Jain** Original Article Abstract Objective : Insulin resistance (IR) is increasingly being
More informationInflammation markers and metabolic characteristics of subjects with onehour plasma glucose levels
Diabetes Care Publish Ahead of Print, published online November 16, 2009 Inflammation markers and metabolic characteristics of subjects with onehour plasma glucose levels Gianluca Bardini, MD, PhD, Ilaria
More informationCordoba 01/02/2008. Slides Professor Pierre LEFEBVRE
Cordoba 01/02/2008 Slides Professor Pierre LEFEBVRE Clinical Research in Type 2 Diabetes : Current Status and Future Approaches Pierre Lefèbvre* University of Liège Belgium Granada, Spain, February 2008
More informationLaboratory analysis of the obese child recommendations and discussion. MacKenzi Hillard May 4, 2011
Laboratory analysis of the obese child recommendations and discussion MacKenzi Hillard May 4, 2011 aka: What to do with Fasting Labs The Obesity Epidemic The prevalence of obesity in adolescents has tripled
More informationRELATIONS AMONG OBESITY, ADULT WEIGHT STATUS AND CANCER IN US ADULTS. A Thesis. with Distinction from the School of Allied Medical
RELATIONS AMONG OBESITY, ADULT WEIGHT STATUS AND CANCER IN US ADULTS A Thesis Presented in Partial Fulfillment of the Requirements to Graduate with Distinction from the School of Allied Medical Professions
More informationDuring the hyperinsulinemic-euglycemic clamp [1], a priming dose of human insulin (Novolin,
ESM Methods Hyperinsulinemic-euglycemic clamp procedure During the hyperinsulinemic-euglycemic clamp [1], a priming dose of human insulin (Novolin, Clayton, NC) was followed by a constant rate (60 mu m
More informationIschemic Heart and Cerebrovascular Disease. Harold E. Lebovitz, MD, FACE Kathmandu November 2010
Ischemic Heart and Cerebrovascular Disease Harold E. Lebovitz, MD, FACE Kathmandu November 2010 Relationships Between Diabetes and Ischemic Heart Disease Risk of Cardiovascular Disease in Different Categories
More information902 Biomed Environ Sci, 2014; 27(11):
902 Biomed Environ Sci, 2014; 27(11): 902-906 Letter to the Editor Curcuminoids Target Decreasing Serum Adipocyte-fatty Acid Binding Protein Levels in Their Glucose-lowering Effect in Patients with Type
More informationSERUM VISFATIN LEVELS IN PATIENTS WITH SUBCLINICAL AND NEWLY DIAGNOSED TYPE 2 DIABETES MELLITUS
Acta Medica Mediterranea, 2017, 33: 197 SERUM VISFATIN LEVELS IN PATIENTS WITH SUBCLINICAL AND NEWLY DIAGNOSED TYPE 2 DIABETES MELLITUS ASLAN ÇELEBI * MUJGAN GURLER **, DENIZ ÖGÜTMEN KOC *, ALI ABBAS OZDEMIR
More informationDiabetes Day for Primary Care Clinicians Advances in Diabetes Care
Diabetes Day for Primary Care Clinicians Advances in Diabetes Care Elliot Sternthal, MD, FACP, FACE Chair New England AACE Diabetes Day Planning Committee Welcome and Introduction This presentation will:
More informationJournal of the American College of Cardiology Vol. 48, No. 2, by the American College of Cardiology Foundation ISSN /06/$32.
Journal of the American College of Cardiology Vol. 48, No. 2, 2006 2006 by the American College of Cardiology Foundation ISSN 0735-1097/06/$32.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2006.03.043
More informationInsulin and Neurodegenerative Diseases: Shared and Specific Mechanisms. Cogs 163 Stella Ng Wendy Vega
Insulin and Neurodegenerative Diseases: Shared and Specific Mechanisms Cogs 163 Stella Ng Wendy Vega Overview A. Insulin and the Brain B. Alzheimer s Disease and Insulin C. Other neurodegenerative disease:
More informationCommon Diabetes-related Terms
Common Diabetes-related Terms A1C An A1C test measures a person's average blood glucose level over two to three months. Hemoglobin is the part of a red blood cell that carries oxygen to the cells and sometimes
More informationNAFLD AND TYPE 2 DIABETES
NAFLD AND TYPE 2 DIABETES Sonia Caprio, MD STOPNASH Symposium on the Origin and Pathways of Nonalcoholic Steatohepatitis Washington 7, 215 Global Projection of Diabetes Hossain P et al. N Engl J Med 27;356:213
More informationWelcome and Introduction
Welcome and Introduction This presentation will: Define obesity, prediabetes, and diabetes Discuss the diagnoses and management of obesity, prediabetes, and diabetes Explain the early risk factors for
More informationMETABOLIC SYNDROME IN OBESE CHILDREN AND ADOLESCENTS
Rev. Med. Chir. Soc. Med. Nat., Iaşi 2012 vol. 116, no. 4 INTERNAL MEDICINE - PEDIATRICS ORIGINAL PAPERS METABOLIC SYNDROME IN OBESE CHILDREN AND ADOLESCENTS Ana-Maria Pelin 1, Silvia Mǎtǎsaru 2 University
More informationGlucagon secretion in relation to insulin sensitivity in healthy subjects
Diabetologia (2006) 49: 117 122 DOI 10.1007/s00125-005-0056-8 ARTICLE B. Ahrén Glucagon secretion in relation to insulin sensitivity in healthy subjects Received: 4 July 2005 / Accepted: 12 September 2005
More informationWhat systems are involved in homeostatic regulation (give an example)?
1 UNIVERSITY OF PNG SCHOOL OF MEDICINE AND HEALTH SCIENCES DIVISION OF BASIC MEDICAL SCIENCES DISCIPLINE OF BIOCHEMISTRY AND MOLECULAR BIOLOGY GLUCOSE HOMEOSTASIS (Diabetes Mellitus Part 1): An Overview
More informationTotal risk management of Cardiovascular diseases Nobuhiro Yamada
Nobuhiro Yamada The worldwide burden of cardiovascular diseases (WHO) To prevent cardiovascular diseases Beyond LDL Multiple risk factors With common molecular basis The Current Burden of CVD CVD is responsible
More informationStudy of the correlation between growth hormone deficiency and serum leptin, adiponectin, and visfatin levels in adults
Study of the correlation between growth hormone deficiency and serum leptin, adiponectin, and visfatin levels in adults Z.-P. Li 1, M. Zhang 2, J. Gao 3, G.-Y. Zhou 3, S.-Q. Li 1 and Z.-M. An 3 1 Golden
More information