1. 1 Chapter 9 Motivation: Hunger

2. 2 Internal Regulatory Systems Usually Work, But… The percentage of obese Americans jumped from 12% in 1991 to 21% in 2001. At the same time, 1 – 3% of Americans are diagnosed with anorexia nervosa or bulimia nervosa. © Annebicque Bernard/CORBIS SYGMA

3. 3 Cultural Factors Can Override Biological Systems Prior to the introduction of American television programs in 1996, a “robust, well-muscled body” represented the Fijian ideal. Anne Becker reports that dieting and eating disorders are now increasing among young women in Fiji. © Craig Lovell/CORBIS

4. 4 Why do we eat? Repair & maintain body “building blocks” Get energy Movement Warmth

5. 5 Absorption of Nutrients Carbohydrates are broken down into simpler sugars (ex. glucose). Proteins are broken down into amino acids. Fats are broken down into fatty acids.

6. 6 Immediately used Glucose (needs insulin to get into cells) Fatty acids Amino acids Energy Stores Short-term Carbohydrates (glycogen) Located in liver & muscles Long-term Fats (triglycerides) Located in fat tissue Metabolism

7. 7 Creating Energy Stores Fatty acids/amino acids turned into fats, stored in adipose tissue (fat cells) Insulin: A pancreatic hormone Converts glucose into glycogen. Metabolism

8. 8 Diabetes Mellitus Failure to move glucose out of blood supply due to insulin dysfunctions. Type I: results from destruction of insulin-producing cells. Type II: obesity leads to insulin resistance. Symptoms include extreme thirst, frequent urination, fatigue and weight loss

9. 9 Using Energy Stores Absorptive phase: The phase of metabolism during which nutrients are absorbed from the digestive system Glucose principal source of energy for cells during this phase Excess nutrients stored as triglycerides. Metabolism

10. 10 Using Energy Stores Absorptive phase: The phase of metabolism during which nutrients are absorbed from the digestive system Glucose principal source of energy for cells during this phase Insulin: A pancreatic hormone Helps entry of glucose into cells Metabolism

11. 11 Copyright © 2004 Allyn and Bacon Metabolism

12. 12 Using Energy Stores Fasting phase: The phase of metabolism during which nutrients are not available from the digestive system Glucose and fatty acids made from glycogen, protein, and adipose tissue are used during this phase. Metabolism

13. 13 Using Energy Stores Glucagon: A pancreatic hormone Short-term storage Converts glycogen into glucose in the liver. Triglyceride: Fat Long-term storage Storage in adipose cells Metabolism

14. Copyright © 2004 Allyn and Bacon Metabolism

15. 15 Hunger Cues External cues Sight and smell of delicious food Time of day Other habits (e.g. must eat while watching TV) Internal cues Stomach growling Lack of glucose availability to cells Low quantities of stored fats

16. 16 Physiological Hunger Signals Glucoprivation: A dramatic fall in the level of glucose available to cells Lipoprivation: A dramatic fall in the level of fatty acids available to cells. What Starts a Meal?

17. 17 Detectors (“thermostat”) Liver: Receptors in liver detect glucose and fatty acid deficiency, send a signal to the brain through the vagus nerve Brain: Receptors in the hindbrain for glucose (near 4 th ventricle). What Stops a Meal?

18. Copyright © 2004 Allyn and Bacon Detectors

19. 19 The signals that stop a meal (satiety signals) are different from the signals that start a meal Satiety Signals Short-term (during act of eating) Long-term (from adipose tissue) What Stops a Meal?

20. 20 Short-term satiety Head factors Taste and odor of food Act of swallowing Appearance of food Gastric factors Receptors in stomach (detect nutrients) Fullness What Stops a Meal?

21. 21 Short-term satiety Intestinal Factors Duodenum: Receptors for glucose and fatty acids Entry of food into space Cholecystokinen (CCK): A hormone secreted by the duodenum that regulates gastric motility and causes the gallbladder (cholecyst) to contract and produce bile Provides a satiety signal sent to brain through the vagus nerve. What Stops a Meal?

22. 22 The Lateral Hypothalamus (LH) and Hunger Animals with LH lesions do not initiate eating, and starve if not force-fed initially. Electrical stimulation of the LH produces eating behavior. However, it is overly simplistic to view the LH as a “feeding center.”

23. 23 Ventral medial hypothalamus Lesions of the VMH produce weight gains. VMH lesions may disrupt pathways linking other hypothalamic nuclei. VMH lesions result in excess insulin production.

24. 24 Long-term satiety Adipose Tissue Ob mouse (obese): A strain of mouse whose obesity and low metabolic rate is caused by a mutation that prevents the production of leptin. Leptin: A hormone secreted by adipose tissue Decreases food intake and increases metabolic rate, primarily by inhibiting neurons in the hypothalamus. What Stops a Meal?

25. 25 Copyright © 2004 Allyn and Bacon Physiological Regulatory Mechanisms Thermostat Metaphor