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Homeostasis: Your Body’s Constant Drive to Stay in Balance

Homeostasis: Your Body’s Constant Drive to Stay in Balance. Homeostasis. A tendency to maintain a balanced or constant internal state The regulation of any aspect of body chemistry, such as blood glucose, around a particular level

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Homeostasis: Your Body’s Constant Drive to Stay in Balance

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  1. Homeostasis:Your Body’s Constant Drive to Stay in Balance

  2. Homeostasis • A tendency to maintain a balanced or constant internal state • The regulation of any aspect of body chemistry, such as blood glucose, around a particular level • Any change in levels, up or down, results in being motivated to bring the level back to normal.

  3. Homeostatic RegulationAn Example

  4. Homeostatic Regulation

  5. Homeostatic Regulation

  6. Homeostatic Regulation

  7. Homeostatic Regulation

  8. Homeostatic Regulation

  9. Homeostatic Regulation

  10. Homeostatic Regulation

  11. Homeostatic Regulation

  12. ENERGY BALANCE BASAL METABOLIC RATE SET POINT

  13. Basal Metabolic Rate • The rate at which the body uses energy for vital functions while at rest • Factors that influence BMR • Age • Sex • Size • Genetics • Food intake

  14. There is a steep decline in the rate at which your body uses energy for vital functions, such as heartbeat, breathing, and body heat. Your BMR continues to decrease by about 2 to 3 percent during each decade of adulthood. At all points in the lifespan, women’s metabolic rate is 3 to 5 percent lower than men’s

  15. Basal Metabolic Rate (BMR) • BMR = The body’s resting rate of energy expenditure • BMI = Measure of your weight • Want to calculate your own Body Mass Index? Click here to try

  16. Energy Balance • Positive energy balance occurs when caloric intake exceeds calories expended for energy. The excess glucose is converted to body fat. • Negative energy balance occurs when caloric intake falls short of the calories expended for energy. Body fat stores shrink as the reserve energy in fat cells is used

  17. Set Point • The point at which an individual’s long-term “weight thermostat” is supposedly set. • When the body falls below this weight, increased hunger and a lower basal metabolic rate (BMR) may act to restore the lost weight. • Slow, sustained changes in body weight can alter a person’s set point.

  18. Set Point

  19. Physiology of Hunger

  20. Hypothalamus – The Control Center

  21. Cerebral cortex Hypothalamus Portion of limbic system Pituitary gland Brainstem Drives as States of the Brain • The hub of many central drive systems lies in the hypothalamus

  22. Self-Stimulation in Rats An electrode has been placed in the lateral hypothalamus of this rat’s brain. By accident, the animal presses the lever at the far end of the cage, which stimulates the electrode and the animals reward system. He presses the lever at a constant rate, neglecting to eat and drink. Click here to view

  23. Hypothalamus Hypothalamus Hunger Drive • Two areas of the hypothalamus, the lateral and ventromedial areas, play a central role in the hunger drive

  24. Hypothalamus Hypothalamus Lateral Area • Increases Hunger • Chemical lesions to specific cell bodies reduce hunger drive as well as general arousal

  25. Hypothalamus Hypothalamus Ventromedial Area • Decreases Hunger • Lesions alter digestive and metabolic processes & cause unstoppable hunger • Food is converted into fat rather than energy molecules, causing animal to eat much more than normal and gain weight

  26. Hypothalamus & Hunger:Remembering the Difference • Lateral Hypothalamus = Start Eating • Ventromedial Hypothalamus = Stop Eating • L comes before V just like Eat comes before Full • L is for Lunch. V is Vomit (I’m so full I could vomit)

  27. Appetite Hormones See chart on page 399

  28. Glucose • Form of sugar which circulates through the body • Glucose is converted by the liver and stored as glycogen • One feels hunger when the levels become low.

  29. Insulin • Hormone which allows the body to use glucose for energy or fat production • Secreted by the pancreas • Controls blood levels of glucose and promotes the uptake of glucose by the muscles and other body tissues • As insulin levels increase, glucose levels decrease.

  30. Satiation signals: Sensing when to stop • Satiation is the feeling of fullness and diminished desire to eat that accompanies eating a meal Satiation signals include: • taste buds that activate chemical signals in the stomach and intestine to prepare for digesting food • stretch receptorsin the stomach that communicate sensory information to the brainstem • hormone cholecystokinin (CCK)that is secreted by the intestines; it promotes satiation and reduces or stops eating by slowing the rate at which stomach empties • sensory-specific satiety - the reduced desire to continue consuming a particular food

  31. Long-Term Signals That Regulate Body Weight • Leptin is secreted by the body’s adipose (fat) tissue, and insulin is secreted by the pancreas, both in direct proportion to the amount of body fat. • Coordinated fluctuations in leptin and insulin levels, acting on receptor sites in the hypothalamus, influence chemical signals in the brain like neuropeptide Y (start eating) and corticotropin-releasing hormone (stop eating).

  32. Long-Term Signals That Regulate Body Weight • During periods of negative energy balance and weight loss, decreased leptin and insulin levels promote the secretion of neuropeptide Y (NPY) by the hypothalamus. NPY triggers eating behavior, reduces body metabolism, and promotes fat storage. • When leptin and insulin levels increase, corticotropin-releasing hormone (CRH) activity increases in the hypothalamus and surrounding areas. CRH reduces food intake and increases body metabolism.

  33. The Appetite Hormones • Insulin: Hormone secreted by pancreas; controls blood glucose. • Leptin: Protein secreted by “bloated” fat cells; when abundant, sends a message to “stop eating” to brain that increases metabolism and decreases hunger. • Orexin: Hunger - triggering hormone secreted by hypothalamus. As glucose levels drop, orexin levels increase and person feels hungry • Ghrelin: Hormone secreted by empty stomach; sends "I'm hungry" signals to the brain. • Neuropeptide Y – Start eating hormone released by HT • Corticotropin-Releasing Hormone (CRH): hormone in hypothamalus that sends "I'm not hungry" signals to the brain.

  34. Regulating Appetite & Body Weight Appetite is stimulated (+) by increased levels of ghrelin, orexin, and neuropeptide Y. • My stomach is ghrelin (growling) • Girls (Grehlin) Night (NPY) Out (Orexin) – go out to eat! Appetite is suppressed (-) by increased levels of leptin, insulin, CCK, and CRH

  35. Psychological factors that trigger eating • Through classical conditioning, the time of day at which you normally eat acts as a conditioned stimulus and elicits reflexive internal physiological changes (the CR), which increases your hunger • Positive reinforcement plays a role in eating; voluntary eating behaviors are followed by the addition of a reinforcing stimulus—food • Due to prior learning experiences, certain tastes, especially sweet, salty, and fatty tastes, hold greater positive incentive value

  36. Variety of Factors Influence Hunger

  37. Environment and Hunger

  38. External Incentives • Include the sight, sound, and smell of food

  39. Cultural Influences on Eating • Cultural views on obesity can vary • Eating disorders are more prevalent in the West than in East although the more developed a country becomes the more people are seen to develop them. • Culture influences the foods we like and dislike.

  40. Genetics vs. Environment In countries with poorly developed economies and food supplies, the prevalence of underfed people (BMI < 17) is higher than the prevalence of obesity (BMI > 30). But in countries with established or well-developed economies, such as most Western countries, food is plentiful and easily attainable, creating high-risk conditions for obesity.

  41. The Obesity Epidemic

  42. Excess Weight and Obesity • Obesity—condition characterized by excessive body fat and a BMI equal to or greater than 30.0 • Overweight—condition characterized by BMI between 25.0 and 29.9

  43. Factors Contributing to Being Overweight • Highly palatable food—we eat because it tastes so good • SuperSize It—food portions are larger than necessary for health • Cafeteria Diet Effect—more food and more variety leads us to eat more • Positive Incentive Value – eat a certain food because you know it will be pleasurable • Snacking—does not cause us to eat less at dinner • BMR—changes through the lifespan • Sedentary lifestyles

  44. Factors in Obesity • Genetic susceptibility—some people are more likely to be predisposed to obesity • Leptin resistance—condition where higher-than-normal levels of leptin do not produce desired physiological response (Body ignores the high leptin levels) • Weight cycling—repeated dieting, weight loss and weight gain tends to result in higher weight and reduced BMR.

  45. We’re # 1!

  46. Epidemic of Overweight and Obese Americans • The problem of being overweight escalates during young and middle adulthood. • Males outpace females in being overweight in each age group. • However, although the data are not shown, more women than men are obese in each age group.

  47. Research on Weight Regulation and Dieting • No consistent personality trait differences found between obese and non-obese people (e.g., willpower, anxiety) • Dieters and obese are more likely to eat in response to stress than non-dieters • Snacking between meals does not help to decrease calories – actually increases them. • Family environment of little importance in determining body weight; genetics plays a large role • Number of fat-storage cells is a major determinant of body weight • See page 403 Close-Up for helpful hints on weight management.

  48. Fat cells Normal diet High-fat diet Return to normal diet Research on Weight Regulation and Dieting • Fat cells are determined by genetics and food intake • They increase with weight gain, but merely shrink with weight loss; may stimulate hunger • Weight loss causes a decline in basal metabolism

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