Ingestive Behavior: Feeding & Weight Regulation. Hypovolemic vs. Osmotic Thirst

Transcription

1 Ingestive Behavior: Feeding & Weight Regulation 1 Hypovolemic Thirst Receptors, CNS, Responses Salt Appetite Digestive components Glucose Homeostasis: Insulin & Glucagon Diabetes Mellitus 1 & 2 CNS Hypothalamic feeding centers Lateral, Ventromedial, Paraventricular Nuclei Weight Regulation: Satiety Chemicals Eating Disorders Where are we going today? Hypovolemic vs. Osmotic Thirst 2 Osmotic thirst triggered by increase in solute ( solute or in H 2 O) Hypovolemic thirst triggered by decrease in pressure due to fluid loss Not mutually exclusive 2 1

2 Hypovolemic Thirst 3 Hypovolemic pressure is monitored by the Subfornical Organ in the 3 rd Ventricle In the periphery, baroreceptors on major vessels & in the heart measure small drops in blood pressure due to fluid loss 3 Hypovolemic Thirst 4 Kidney regulation of salt and water balance in body Low water volume Subfornical Organ 4 2

3 Synergistic Effect 5 Summary of Systems Synergy = combined effect is greater than the sum of two separate effects = 4 additive, = 6 synergistic When both baroreceptors & angiotensin are activated the effect is greater than the sum of either effect 5 separately. Vasopressin Vasopressin, the antidiuretic hormone (ADH) is responsible for regulating water excretion from kidneys Diabetes Insipidus is a disease state of no vasopressin production Treatment nasal spray of vasopressin 6 Genetic Model to study Diabetes Insipidus People with diabetes insipidus may excrete up to 25 L or 66.5 gallons of water per day. 3

4 The Kidneys Salt Balance 7 Kidneys primary function: balance salt & H 2 O levels Acts as a filtering system: Filters everything & then allows selective reabsorption Renal artery supplies blood to nephron for filtering Renal vein for blood return & ureters for bladder excretion 7 Salt Appetite 8 Kidneys receive hormonal input from: Adrenal cortex: aldosterone increases salt reabsorption Posterior Pituitary: vasopressin decreases water excretion Angiotensin and Vasopressin receptors are also found in the gustatory areas of the brain and salt deprivation changes the peripheral taste neural signals 8 4

5 Digestive System 9 Stomach - Vagus Nerve stomach distension (fullness) - Splanchnic Nerve nutritional value (contents) Liver - makes fuel for use by cells - WHY?: blood level of glucose varies little under normal circumstances Pancreas - regulates glucose storage / use 10 Eating provides nutrients and fuel for our body. Nutrients - vitamins, salts (salt appetite) Fuel - carbohydrates, proteins, fats absorbed and converted by the liver to glucose for use by cells Glucose homeostasis 5

6 Glucose Homeostasis 11 Cells either use glucose for energy or store glucose as glycogen Determined by the circulating levels of 2 hormones released by the pancreas: Insulin glucose entry into cells, signals storage of glucose as glycogen Glucagon signals liver to convert glycogen to glucose Think of it as a thermostat 12 Less Insulin, More Glucagon More Insulin, Less Glucagon LOW GLUCOSE HIGH GLUCOSE Set Point Level of Glucose needed High glucose in blood pancreas secretes more insulin, less glucagon results in glucose entering cells & storage Low glucose in blood pancreas secretes less insulin, more glucagon results in glycagen converted to glucose 6

7 Glucose Homeostasis System 13 Liver converts glycogen to glucose More glucagon, less insulin Increase hunger more eating Low Blood Glucose High Blood Glucose More insulin, less glucagon Decrease hunger less eating Glucose enters cell used or stored Diabetes Mellitus 14 There are two types of diabetes mellitus: Type 1 - immune system destroys insulin producing cells in the pancreas Type 2 - insulin can not be used by the cells related to obesity If untreated: Kidney failure, amputation, blindness, or stroke Type 2 Diabetes is on the increase, probably because people are living longer, getting fatter and leading increasingly inactive lifestyles. 7

8 Type 1 Diabetics lack the insulin loop: Liver converts glycogen to glucose 15 More glucagon, less insulin Increase hunger more eating Low Blood Glucose High Blood Glucose More insulin, less glucagon Decrease hunger less eating Glucose enters cell used or stored Type 1 Diabetics have low insulin levels 16 Liver converts glycogen to glucose More glucagon, less insulin More insulin, less glucagon Glucose cannot be used by cells! Low Blood Glucose High Blood Glucose Glucose enters cell used or stored Increase hunger more eating Glucose in blood is unusable so it is excreted. 8

9 Diabetes Type 1 & 2 17 Type 1 symptoms: High levels of sugar in the blood and urine. Frequent urination & extreme hunger, thirst, weight loss Type 1 treatment: Insulin injections, exercise, monitor blood sugar levels (glucose) Type 2 symptoms: Repeated or hard-to-heal infections of the skin, gums, or bladder. Dry, itchy skin. Blurred vision. Tingling or loss of feeling in the hands or feet. Type 2 Treatment: Diet and Exercise Ingestive CNS Areas 18 Lateral Hypothalamus role in the control of feeding Ventromedial Hypothalamus role in the weight gain Paraventricular Nucleus role in over-eating Arcuate Nucleus role in appetite regulation of LH and VMH How do we know this? Largely through lesion & stimulation studies. 9

10 Lateral Hypothalamus 19 Wide-spread connections in the brain Damage = no eating Aphagia Stimulation = increase eating & eating responses even without food present Ventromedial Nucleus 20 Damage = increase in number of meals Satiety center? Too simplistic Insulin regulation Hyperphagia = over + to eat 10

11 Paraventricular Nucleus 21 Damage = increase in size of meals Satiety center? Too simplistic Part of bigger feedback loop 22 Satiety & Sensory Systems Hunger and Satiety both influence your perception of sensory stimuli Hunger increases the hedonic quality of stimuli Satiety decreases the hedonic quality of stimuli Sensory Specific Satiety: the effects of satiety are sometimes confined to the specific satiation 11

12 Sensory Specific Satiety 23 Specific decrease in pleasantness due to satiation Satiation & OFC response 24 Decrease in responsiveness of OFC neurons (flavor area) based on the amount of tastant consumed Decrease is specific to fresh cream *not shown* Decrease in preference from acceptance to active avoidance 12

13 Obesity Epidemic 25 The Obesity Epidemic 26 Abdominal Obesity versus 2000: men: 12.7 to 38.3% women: 19.4 to 59.9% Body Mass Index (BMI = weight / height 2 ) scores = overweight > 30 obese 58% US population is overweight 21% US population is obese (44.3 million) Overweight was the second leading cause of preventable death in 2000 (16.6% US deaths) 13

14 What is driving OBESITY? Genetics 2. Physical Inactivity 3. Over-consumption of high-fat, high-caloric foods If we know that eating high fat foods causes obesity, why do we continue to consume high fat foods? FAT TASTE!!! Obese Gene? Gene codes the production of a chemical leptin Leptin produced by fat cells the more fat cells the more circulating leptin Satiety Chemicals Disrupt leptin gene, body loses fat feedback signal 28 14

15 Obese Gene? Gene codes the production of a chemical leptin Leptin produced by fat cells the more fat cells the more circulating leptin Satiety Chemicals Disrupt leptin gene, body loses fat feedback signal Leptin injections = weight loss Zucker Rats Most obese humans have plenty of leptin Receptor or feedback pathway deficit 29 Satiety Chemicals 30 Leptin = signal for fat cell levels Neuropeptide Y (NPY) - released by the hypothalamus inhibited by high circulating leptin NPY inhibits the PVN - increases meal size? There are lots of other chemicals: bombesin, CCK Each chemical plays a role in the regulation of satiety and hunger. 15

16 Gut Signals - Neuropeptides 31 Ghrelin released by endocrine cells of the stomach as a powerful appetite stimulant During fasting Ghrelin rises with immediate drops right after eating Obese individuals may have lower Ghrelin baseline levels with little change after eating PYY 3-36 secreted by small & large intestine Low between meals; high levels after meal Injections curb appetite 32 16

17 Arcuate Nucleus 33 Peptide signals from the gut provide inhibition and excitation to regulate feeding / appetite POMC/CART Inhibit appetite & increase metabolism AgRP/NPY stimulate appetite & reduce metabolism Weight Loss 34 There is a special group of neurotransmitters (leptin, PPY, NPY, Bombesin, CCK) that play a role in controlling both feeding and weight Feeding / Weight regulation is a complicated system with no magic pill that can regulate it. Fenphen 2 chemicals that are agonists for serotonin (5HT) and (NE) norepinepherine Systemic side-effects 17

18 35 Weight Loss Drug Strategies Appetite control: Circulating PYY 3-36 (inhibits appetite) may be lower than normal in obese people injections appear to cut caloric consumption by 1/3 Increased metabolism: Many common weight loss drugs (nutritional supplements) stimulate metabolism but also impact cardiovascular Inhibition of fat tissue: Angiogenesis inhibitors are drugs that inhibit new blood vessels from forming in fat tissue 36 Weight Loss Drug Strategies Reduced absorption: Orlistat interferes with digestive absorption / Olestra is an oil that cannot be digested or absorbed gastric distress is a common side effect Reduced CNS reward value: Many foods provide a CNS release of reward neurotransmitters to increase emotion and reduce stress hormones comfort food Drugs that block the reinforcement effects 18

19 Eating Disorders 37 Physiological, psychological, and social factors all contribute to the formation of eating disorders such as Anorexia and Bulimia. Anorexia Nervosa = no appetite + origin in CNS Anorexics often are preoccupied with thoughts of food but deny themselves Distorted body image and self-imposed condition We don t fully understand the condition and it may end up not being either no appetite or primarily a CNS disorder Up to 10% diagnosed eventually die from anorexia Eating Disorders 38 Physiological, psychological, and social factors all contribute to the formation of eating disorders such as Anorexia and Bulimia. Bulimia = great hunger drastically alternating between dieting & overeating binge eating & purging after a meal is common self-image and distorted body-image Both Anorexia & Bulimia deny important nutrients to our organs and immune system Organ failure & mild diseases (immunodeficiency) 19

20 39 Treatment of Eating Disorders Antidepressant medications may be effective in treating bulimia Not as effective for anorexia. Cognitive-behavioral therapies, Changing perceptual distortion of body image Anorexia may require hospitalization 40 Summary of Hypothalamic Areas Hypothalamic Area Preoptic Area Posterior Hypo Lateral Preoptic Area Lateral Hypothalamus Ventromedial Hypothalamus Paraventricular Nucleus Function Temperature regulation Thirst (osmotic & hypovolemic) Control initiation of eating behavior Controls number of meals, insulin regulation Controls meal size, satiety Arcuate Nucleus Receives peripheral digestive signals / regulates LH, VMH, & PVN 40 20

21 For next time 41 Read 10: Sexual Behavior Lab report due tonight at 10pm Study for Exam 2! 41 21