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Lect 9. (dietary balances)

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GIT 9

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Lect 9. (dietary balances)

  1. 1. Dietary Balances; Regulation of Feeding; Obesity and Starvation;
  2. 2. Dietary Balances: • Energy Available in Foods: • The Average Daily Requirement for Protein Is 30 to 50 Grams. • Carbohydrates and Fats Act as “Protein Sparers.” • Methods for Determining Metabolic Utilization of Carbohydrates, Fats, and Proteins: by means of “Respiratory Quotient,” : is the ratio of carbon dioxide production to oxygen utilization.
  3. 3. REGULATION OF FOOD INTAKE AND ENERGY STORAGE: • Stability of the body’s total mass and composition over long periods requires that energy intake match energy expenditure
  4. 4. NEURAL CENTERS REGULATE FOOD INTAKE: • The sensation of hunger is associated with a craving for food and several other physiological effects, such as rhythmical contractions of the stomach and restlessness, which cause the person to seek food. • A person’s appetite is a desire for food, often of a particular type, and is useful in helping to choose the quality of the food to be eaten. • If the quest for food is successful, the feeling of satiety occurs.
  5. 5. The Hypothalamus Contains Hunger and Satiety Centers: A) The lateral nuclei of the hypothalamus serve as a feeding center. 1. Stimulation of this area causes an animal to eat voraciously (hyperphagia). 2. Destruction of the lateral hypothalamus causes lack of desire for food and progressive inanition, a condition characterized by marked weight loss, muscle weakness, and decreased metabolism. • The lateral hypothalamic feeding center operates by exciting the motor drives to search for food.
  6. 6. B) The ventromedial nuclei of the hypothalamus serve as a major satiety center. • This center is believed to give a sense of nutritional satisfaction that inhibits the feeding center. 1. Electrical stimulation of this region can cause complete satiety, and even in the presence of highly appetizing food, the animal refuses to eat (aphagia). 2. destruction of the ventromedial nuclei causes voracious and continued eating until the animal becomes extremely obese, sometimes weighing as much as four times normal.
  7. 7. C) The paraventricular, dorsomedial, and arcuate nuclei of the hypothalamus also play a major role in regulating food intake. • lesions of the paraventricular nuclei often cause excessive eating. • lesions of the dorsomedial nuclei usually depress eating behavior. • the arcuate nuclei are the sites in the hypothalamus where multiple hormones released from the gastrointestinal tract and adipose tissue converge to regulate food intake, as well as energy expenditure
  8. 8. The hypothalamus receives: (1) Neural signals from the gastrointestinal tract that provide sensory information about stomach filling. (2) Chemical signals from nutrients in the blood (glucose, amino acids, and fatty acids) that signify satiety. (3) Signals from gastrointestinal hormones. (4) Signals from hormones released by adipose tissue. (5) Signals from the cerebral cortex (sight, smell, and taste) that influence feeding behavior.
  9. 9. The hypothalamic feeding and satiety centers have a high density of receptors for neurotransmitters and hormones that influence feeding behavior, and are generally categorized as (1) orexigenic substances that stimulate feeding. (2) anorexigenic substances that inhibit feeding.
  10. 10. Neurons and Neurotransmitters in the Hypothalamus That Stimulate or Inhibit Feeding:
  11. 11. Orexigenic substances Anorexigenic substances
  12. 12. Neural Centers That Influence the Mechanical Process of Feeding: • If the brain is sectioned below the hypothalamus but above the mesencephalon, the animal can still perform the basic mechanical features of the feeding process. • It can salivate, lick its lips, chew food, and swallow. • Therefore, the actual mechanics of feeding are controlled by centers in the brain stem.
  13. 13. • Neural centers higher than the hypothalamus also play important roles in the control of feeding, particularly in the control of appetite. • These centers include the 1. Amygdala. 2. prefrontal cortex, which are closely coupled with the hypothalamus. Destructive lesions in the amygdala have demonstrated that some of its areas increase feeding, whereas others inhibit feeding. In addition, stimulation of some areas of the amygdala elicits the mechanical act of feeding. “psychic blindness”: destruction of the amygdala on both sides of the results in loses or at least partially loses the appetite control that determines the type and quality of food it eats.
  14. 14. FACTORS THAT REGULATE QUANTITY OF FOOD INTAKE: 1. Short-term regulation, which is concerned primarily with preventing overeating at each meal. 2. Long-term regulation, which is concerned primarily with maintenance of normal quantities of energy stores in the body.
  15. 15. 1- Short-Term Regulation of Food Intake: 1. Gastrointestinal Filling Inhibits Feeding. 2. Gastrointestinal Hormonal Factors Suppress Feeding: (CCK, Peptide YY, Glucose Like Peptide). 3. Ghrelin, a Gastrointestinal Hormone, Increases Feeding. 4. Oral Receptors Meter Food Intake: • When an animal with an esophageal fistula is fed large quantities of food several “oral factors” related to feeding, such as chewing, salivation, swallowing, and tasting, “meter” the food as it passes through the mouth, and after a certain amount has passed, the hypothalamic feeding center becomes inhibited (20 to 40 min).
  16. 16. 2- Intermediate- and Long-Term Regulation of Food Intake 1. Effect of Blood Concentrations of Glucose, Amino Acids, and Lipids on Hunger and Feeding: (Glucostatic, Aminostatic, Lipostatic theory of hunger and feeding regulation). (A) A rise in blood glucose level increases the rate of firing of glucoreceptor neurons in the satiety center in the ventromedial and paraventricular nuclei of the hypothalamus, (B) The same increase in blood glucose level simultaneously decreases the firing of glucosensitive neurons in the hunger center of the lateral hypothalamus.
  17. 17. 2. Temperature Regulation and Food Intake: • When an animal is exposed to cold, it tends to increase feeding; when it is exposed to heat, it tends to decrease its caloric intake. 3. Feedback Signals From Adipose Tissue Regulate Food Intake: • Stimulation of leptin receptors in these hypothalamic nuclei initiates multiple actions that decrease fat storage, including: (A) decreased production in the hypothalamus of appetite stimulators, such as NPY and AGRP. (B) Activation of POMC neurons. (C) increased production in the hypothalamus of substances, such as corticotropin-releasing hormone, that decrease food intake; (D) increased sympathetic nerve activity. (E) decreased insulin secretion by the pancreatic beta cells.
  18. 18. Pathophysiological in FOOD INTAKE AND ENERGY EXPENSION:
  19. 19. Obesity • As an excess of body fat. • BMI greater than 30 kg/m2. • The impact of obesity on the risk for various disorders such as cirrhosis, hypertension, heart attack, stroke, and kidney disease. • Obesity Results From Greater Intake Than Expenditure of Energy. • Hyperplastic obesity (in children). • Hypertrophic obesity (in adults). • Decreased Physical Activity and Abnormal Feeding Regulation as Causes of Obesity. 1. Sedentary Lifestyle Is a Major Cause of Obesity. 2. Abnormal Feeding Behavior Is an Important Cause of Obesity. 3. Childhood Overnutrition as a Possible Cause of Obesity. 4. Neurogenic Abnormalities as a Cause of Obesity. 5. Genetic Factors as a Cause of Obesity. Cause of Obesity.
  20. 20. Inanition, Anorexia, and Cachexia • Inanition: is a extreme weight loss. • It can be caused by inadequate availability of food or by pathophysiological conditions that greatly decrease the desire for food, including psychogenic disturbances, hypothalamic abnormalities, and factors released from peripheral tissues. • Anorexia: a reduction in food intake caused primarily by diminished appetite. • pain and nausea, may also cause a person to consume less food. • Cachexia: is a metabolic disorder of increased energy expenditure leading to weight loss greater than that caused by reduced food intake alone.
  21. 21. Starvation: • Depletion of Food Stores in the Body Tissues During Starvation. • the tissues prefer to use carbohydrate rather than either fat or protein for energy, the quantity of carbohydrate normally stored in the entire body is only a few hundred grams. • the rate of fat depletion continues unabated, until most of the fat stores in the body are gone. • Protein undergoes three phases of depletion: rapid depletion at first, followed by greatly slowed depletion, and finally rapid depletion again shortly before death.
  22. 22. Vitamins:

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