Relationship of insulin resistance with Lipid profile markers in cigarette smoker

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1 ISS Pishkar Leila et al., IJALS, Volume (7) Issue (4) ovember RESEARCH ARTICLE Relationship of insulin resistance with Lipid profile markers in cigarette smoker Pishkar Leila*, Taheri Saba and aghibzadeh Tabatabaei aeeni eda Department of Biology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran leilapishkar@gmail.com Corresponding Author Pishkar Leila Department of Biology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran leilapishkar@gmail.com Article History Received on 11 August, 2014; Received in revised form 14 September, 2014; Accepted 03 October, 2014 Abstract The evidence supports an important contribution of smoking in systemic inflammation and to the development of cardiovascular diseases. The aim of our work was to study the relation of insulin resistance with lipid profile markers as cardiovascular risk factors in smoking. To achieve this outcome, fasting blood samples were collected from the antecubital vein of 28 sedentary men smokers between 8:00 and 9:00 am. Blood was used to measure, glucose, insulin, triglyceride (TG), total cholesterol (TC) LDL and HDL-Cholesterol. Insulin resistance was calculated by fasting glucose and cholesterol. Pearson s correlation coefficient was run for testing of correlation analysis. There were no correlations between insulin resistance with TC (p = 0.223), LDL (p = 0.242) and HDL-cholesterol (p = 0.161). But insulin resistance was strongly and positively associated with triglyceride (p = 0.01). Lack of a significant relationship between them can be attributed to the normal fasting levels of lipid profile markers in smokers that supported by previous studies. Keywords: Exercise, diabetes, insulin resistance and smoking Introduction According to the statistics of the last few years, 47% of the American men, and 10% of the American women were smokers. However, statistics and figures show that about 50% of men and 5% of women in developing countries have turned to smoking in the previous years (ACS, 2000 and Dilyara et al., 2007). The literature suggests that smok decreases the high density lipoprotein (HDL) and increases triglyceride (TG) and also increases insulin resistance which is an early sign of cardiovascular disease and diabetes ( Gould et al., 1998 and Stamler et al., 2000). Some studies suggested that quitting smoking delays the risk of cardiovascular disease for 5 to 10 years in smokers. However, the immediate effects of quitting smoking on inflammatory biomarkers and cardiovascular risk factors are not fully understood yet (Virginia et al., 2011). Increased blood glucose levels in smokers compared to non-smokers was reported by some studies (Al Mutairi et al., 2008). Previous studies also reported a direct relationship between smoking and total cholesterol (TC), low density lipoprotein (LDL) and TC/HDL, and an inverse relationship between smoking and HDL (Tsujii and Kuzuya, 2004). These findings suggest that smoking is associated with the increased abdominal fat, increased waist to hip ratio (Eliasson et al., 1994 and Chiolero et al., 2008), increased free fatty acid and glycerol stimulation, the dyslipidemia phenomenon, i.e., increased LDL Int. J. Adv. Lif. Sci., Available online on at www. ijals.com Page 628

2 ISS Pishkar Leila et al., IJALS, Volume (7) Issue (4) ovember RESEARCH ARTICLE and decreased HDL, endothelial dysfunction, and the increased blood viscosity (Pinto et al., 2007; Weitzman et al., 2005). Despite the observations on the increased insulin resistance and cardiovascular risk factors in smokers compared to non-smokers, there are limited studies on the relationship between them. Hence, the present study aimed at determining the relationship between insulin resistance and each cardiovascular risk factor in smokers. Materials and Methods Human Subjects and study inclusion The participants included 28 sedentary adult men smokers aged 35 to 48 years and weight kg. The main objective of the study was to determine the relationship between insulin resistances with lipid profile markers. The study protocol was approved by the Research Ethics Committee of Islamic Azad University and written informed consent was obtained. Participants were included if they had not been involved in regular physical activity in the previous 6 months. one of the subjects used drugs or therapies for chronic diseases. In fact, a history of chronic diseases was of exclusion criteria. Anthropometric measures Height of the barefoot subjects was measured to the nearest 0.1 cm. Weight was measured by an electronic balance and height by a stadiometer. BMI was calculated as weight (kg)/height (m2). Waist and hip circumferences were measured with the subject standing erect with arms at the sides and feet together, wearing only underwear. The measurer placed an inelastic tape around the subject. Percentage body fat was measured using body composition monitor (OMRO, Finland). Blood biochemistry examination Blood samples were collected, via the cannulated antecubital vein, between 8:00-9:00 a.m. after an overnight fasting for all subjects. Blood samples were analyzed for glucose, insulin, cholesterol, LDL cholesterol, HDL cholesterol, triglycerides with COBAS MIRA. Insulin resistance was derived using the HOMA method (Afreen and Krishnananda, 2013) using the following formulae: Insulin resistance (HOMA-IR) = [fasting insulin (μ/ml) fasting glucose (mmol/l)] / Statistics After calculation of the mean and the standard deviation, the statistical analysis was conducted using the SPSS software version All data were tested for normal distribution by the Kolmogorov- Smirnov test. The bivariate associations between insulin resistances with lipid profile markers were examined with the Pearson correlation analysis. Data were considered significant at P< Results The association of insulin resistance with lipid profile markers in adult males with smoking were determined in this study. Body weight, other anthropometrical markers and blood chemistry parameters of studied subjects are shown in Table 1. Data showed that most of the smokers were obese or overweight. Based on this data, we can confirm previous findings that smoking is associated with abdominal obesity. Although, smoking is associated with both insulin resistance and cardiovascular risk factors, no significant correlation was found between insulin resistances with lipid profile markers as cardiovascular risk factors in this population. On the other hand, insulin resistance was not related with TC, LDL and HDL-cholesterol in studing smokers ( Table 2). Insulin resistance positively correlated with serum triglyceride in studing subjects (Table - 1 and Fig.- 1). Int. J. Adv. Lif. Sci., Available online on at www. ijals.com Page 629

3 ISS Pishkar Leila et al., IJALS, Volume (7) Issue (4) ovember RESEARCH ARTICLE Table 1. Mean and SD of anthropometrical and metabolic markers in studied smokers Variable Mean SD Age (year) Height (cm) Weight (kg) Abdominal (cm) Hip (cm) WHO BMI (kg/m2) Body fat (%) Glucose (mg/dl) Insulin (µiu/ml) Insulin Resistance (HOMA-IR) Total cholesterol (mg/dl) Triglyceride (mg/dl) Low density lipoprotein (mg/dl) High density lipoprotein (mg/dl) Triglyceride (mg/dl) Insulin Resistance (HOMA- IR) 8.00 Fig.- 1: Significant positive correlation of insulin resistance with triglyceride in smokers Table 2. Relationship of insulin resistance with lipid profile markers in studied subjects Table2: Relationship of insulin resistance with lipid profile markers in studied subjects. Insulin Resistance (HOMA-IR) Total cholesterol (mg/dl) Triglyceride (mg/dl) Low density lipoprotein (mg/dl) High density lipoprotein (mg/dl) *. Discussion Correlation is significant at the 0.05 level (2-tailed). Many studies support insulin dysfunction and cardiovascular risk factors in the presence of smoking and often emphasized on the increased insulin resistance and cardiovascular risk factors in response to Insulin Total Low density High density Resistance cholesterol Triglyceride lipoprotein lipoprotein (HOMA-IR) (mg/dl) (mg/dl) (mg/dl) (mg/dl) * * smoking. However, evidence suggests that these metabolic variables do not affect the levels of each other because in the present study, apart from the serum levels of TG, no significant relationship was observed Int. J. Adv. Lif. Sci., Available online on at www. ijals.com Page 630

4 ISS Pishkar Leila et al., IJALS, Volume (7) Issue (4) ovember RESEARCH ARTICLE between the levels of other cardiovascular risk factors (TC, LDL, HDL) and insulin resistance in smokers. These findings somehow support the hypothesis that blood glucose levels and cardiovascular risk factors are directly affected by smoking. The importance and the effects of smoking is so considerable that the literature indicate that even those who are exposed to cigarette smoke may also become a type 2 diabetic (Foy et al., 2005). It has been reported that cigarette smoking has also a potential role in the formation of oxidative stress and beta-cell dysfunction (Ding and Hu, 2007). The literature also supports the inverse relationship between the total antioxidant capacity and C - reactive protein (CRP), as one of the cardiovascular risk factors (Eizadi et al., 2014). On the other hand, the direct relationship between smoking and total cholesterol TC, LDL, and total cholesterol to high density lipoprotein (TC/HDL) and the inverse relationship between smoking and HDL have also been reported (Tsujii and Kuzuya, 2004). The evidence from clinical studies reported that smoking was associated with the increased abdominal fat, increased waist to hip ratio (Eliasson et al., 1994 and Chiolero et al., 2008), increased free fatty acid and glycerol stimulation, the dyslipidemia phenomenon, i.e., increased LDL and decreased HDL, endothelial dysfunction, and increased blood viscosity (Pinto, 2007 and Weitzman et al., 2005). Some recent studies showed that 8 weeks of reduced smoking dramatically changes the blood levels of LDL, HDL and TC/HDL (Rahman et al., 1996). But it is also noted that although some of the changes caused by smoking are reversible after quitting, the levels of CRP, as a cardiovascular risk factor, maintains its high levels even after 10 to 20 years of quitting smoking (Dilyara et al., 2007). In the present study, the only significant direct relationship was observed between insulin resistance and fasting triglyceride levels. These findings indicated that although the causal relationship between insulin resistance and TG in smokers cannot be confidently emphasized, it is hypothesized that the increase in the blood triglyceride levels somehow affects the insulin resistance in this population. In this regard, some studies also pointed to some kind of interaction between them in smokers. Lack of a significant relationship between insulin resistance and other cardiovascular risk factors may be attributed to the low number of studied samples. A recent study showed that the mean postprandial triglyceride levels in smokers are much higher compared to non-smokers (Mero and Syvanne, 1997). However, the findings of another study showed no significant differences between the fasting levels of triglycerides, HDL, and vldl in smokers and nonsmokers. The difference in fasting total cholesterol and LDL levels in smokers and non-smokers was not significant (Gupta et al., 2006). Since some studies support the normal levels of cardiovascular risk factors in smokers in the fasting state, the lack of a significant relationship between insulin resistance and cardiovascular risk factors can be attributed to the normal fasting levels of these variables. References Afreen, A.C. and Krishnananda, P An Association of High Sensitive C Reactive Protein and Lipid Profile Parameters in South Indian Population. International Journal of Scientific and Research Publications., 3(7) : 1-3. Al Mutairi, S.S., Mojiminiyi, O.A., Shihab-Eldeen, A.A., Al Sharafi, A. and Abdella Effect of smoking habit on circulating adipokines in diabetic and non-diabetic subjects. Ann. utr. Metab., 52(4): Chiolero, A., Faeh, D., Paccaud, F. and Cornuz, J Consequences of smoking for body weight, Int. J. Adv. Lif. Sci., Available online on at www. ijals.com Page 631

5 ISS Pishkar Leila et al., IJALS, Volume (7) Issue (4) ovember RESEARCH ARTICLE body fat distribution, and insulin resistance. Am. J. Clin. utr., 87 : Dilyara, G., Yanbaeva., Mieke, A., Dentener. and Eva, C Creutzberg, Geertjan Wesseling and Emiel, F.M. Wouters. Systemic Effects of Smoking. CcChest., 3: Eizadi, M., Dadgan, M.H. and Bagheri, G Association of C-Reactive protein and total antioxidant capacity in smoker. International Journal of Biosciences., 5(12): Eliasson, B., Attvall, S., Taskinen, M.R. and Smith, U The insulin resistance syndrome in smokers is related to smoking habits. Arterioscler Thromb Vasc Biol., 14 : Foy, C.P., Bell, R.A., Farmer, D.F., Goff, D.C. and Wagenknecht, L.E Smoking and Incidence of Diabetes Among U.S. Adults. Findings from the Insulin Resistance Atherosclerosis Study. Diabetes Care., 28 : Gould, A.L., Rossouw, J.E., Santanello,.C., Heyse, J.F. and Furberg, C.D Cholesterol Reduction Yields Clinical Benefit, Impact of Statin Trials. Circulation., 97(10) : Gould, A.L., Rossouw, J.E., Santanello,.C., Heyse, J.F. and Furberg, C.D Cholesterol reduction yields clinical benefit: impact of statin trials. Circulation., 97(10): Gupta, V., Tiwari, S., Agarwal, C.G., Shukla, P., Chandra, H. and Sharma, P Effect of short-term cigarette smoking on insulin resistance and lipid profile in asymptomatic adults. Indian J Physiol Pharmacol., 50(3): Mero,. and Syvanne, M Post prandial elevation of Apo B48 containing triglyceride rich particles and retinyl esters in normolipemic males who smoke. Arterio Scler, Thromb. Vasc. Biol., 17 (10) : Pinto, E.R.C Associação Entre Dislipidemia, Fumo e Perda Óssea Alveolar Radiográfica Em Uma População Brasileira. [Dissertação de mestrado] Duque de Caxias (RJ): Universidade do Grande Rio. Rahman, I. and Macee, W Oxidant/antioxidant imbalance in smokers and chronic obstructive pulmonary disease. Thorax., 51: 348. Stamler, J,, Daviglus, M.L., Garside, D.B., Dyer, A.R., Greenland, P. and eaton, J.D Relationship of baseline serum cholesterol levels in 3 large cohorts of younger men to long-term coronary, cardiovascular, and all-cause mortality and to longevity. JAMA., 284(3) : Tsujii, S. and Kuzuya, H The significance of lifestyle as a factor for the metabolic syndrome. ippon Rinsho., 62(6) : Virginia, R., Xiangying, X., Diane, B., Daniel, J., Christine, F., Patricia, F A Pilot Study To Examine the Effects of Smoking Cessation on Serum Markers of Inflammation in Women at Risk for Cardiovascular Disease. Chest., 3: Weitzman, M., Cook, S., Auinger, P., Florin, T.A., Daniels, S., guyen, M Tobacco Smoke Exposure Is Associated With the Metabolic Syndrome in Adolescents. Circulation., 112: Corresponding Author : Pishkar Leila, Department of Biology, Islamshahr Branch, Islamic Azad University, Islamshahr, Iran, leilapishkar@gmail.com 2014, IJALS. All Rights Reserved. Int. J. Adv. Lif. Sci., Available online on at www. ijals.com Page 632

Figure S1. Comparison of fasting plasma lipoprotein levels between males (n=108) and females (n=130). Box plots represent the quartiles distribution

Figure S1. Comparison of fasting plasma lipoprotein levels between males (n=108) and females (n=130). Box plots represent the quartiles distribution Figure S1. Comparison of fasting plasma lipoprotein levels between males (n=108) and females (n=130). Box plots represent the quartiles distribution of A: total cholesterol (TC); B: low-density lipoprotein

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