PSYCH 460--Eating

• source of food - 99% of dry body mass is made up of only four elements: carbon and oxygen (derived from the air), hydrogen (derived from water), and nitrogen (derived from soil); using sunlight as a source of energy, plants biosynthesize these elements into complex biological molecules
• nutrients in food
  1. vitamins and minerals
  2. carbohydrates (starches and complex sugars) - broken down into glucose (and other sugars), which are used for energy metabolism, are stored as glycogen in the liver, or are converted to and stored as fat; requirement: about 100 g/day to prevent ketosis and protein breakdown
  3. proteins - broken down into amino acids, which can be converted to glucose, converted to fatty acids, or used for the biosynthesis of peptides and proteins (hormones, neurotransmitters, enzymes, receptor sites, transporters, membrane pumps, etc.); requirement: 0.8-0.9 g/kg body weight per day
  4. fats (triglycerides) - broken down into glycerol (which is converted to glucose) and fatty acids, which can be used for energy metabolism by the body (but not the brain), can be converted to ketones for energy metabolism in the brain (ketosis), or can be stored as triglycerides in fat cells; requirement: some fatty acids are essential (i.e., must be obtained in the diet)
• two phases of metabolism (see diagram and discussion in text)
  1. absorptive phase - glucose used as fuel by entire body; insulin (secreted by the pancreas) promotes glucose uptake outside the brain and also promotes storage of fats
  2. fasting phase - absence of insulin prevents body cells from using glucose, thus sparing glucose for the brain; glucagon (also secreted by the pancreas) promotes the breakdown of fats and use of fatty acids for energy metabolism in the body
• energy requirement of the brain - the brain uses energy at a fairly constant rate regardless of activity (about 10% more during REM sleep and 10% less during SWS)
  1. when the body is at rest, the brain is the most expensive tissue in the body to operate (if the body becomes active, muscles become much more expensive)
  2. BMR for a 70 kg man is about 1600-1700 kcal/day
     Kleiber equation: kcal/day = 70W^0.75, W = body wgt. in kg (kg = lbs/2.2)
  3. 20-25% of this, or about 350 kcal/day, is used by the brain
  4. this is a rate of energy expenditure of about 4 cal/sec or, roughly, 15 watts

• hunger - eating must be turned on before the body begins to starve
• satiety - eating must be turned off before nutrients have had time to reach the tissues
• homeostasis - some system variable is monitored and compared to a set point
• the conscientious objecter study (WWII) - volunteers agreed to be starved; caloric intake cut to 50% of baseline for 6 months
  1. adaptive thermogenesis
  2. semistarvation neurosis
• Vermont State Prison study (1966) - volunteers agreed to overeat by 1000 kcal/day
• caloric equilibrium - the basic formula still holds: calories in = calories out results in a stable body weight (as long as the body's generation of heat is taken into account)

• leptin - a peptide hormone released by fat cells circulates in the blood and regulates food intake over the long term (may establish the set point for body fat)
  1. due to a spontaneous genetic mutation, some mice in a breeding colony starting becoming obese (1950) - the gene has come to be called the obese gene
  2. the ob gene turns on in fat cells and directs the biosynthesis of leptin, which then circulates in the blood and is monitored by the brain
  3. when the obese mice were injected with leptin, they lost 30% of their body weight (normal mice lost 12%)
  4. a second strain of obese mice failed to respond to leptin injection - they apparently can produce leptin but lack the cell surface receptor for it
  5. leptin injection into the lateral ventricle reduced food intake
• glucostatic theory - there are blood glucose receptors in the brain (glucostats)
  1. cells in the hypothalamus change their firing rate depending upon how much glucose they can take up from the blood - this is probably an emergency backup system (why? - if the brain isn't getting its glucose, this is a dire situation)
  2. this is not adequate to regulate blood glucose available to cells outside the brain (why not? - because uptake of glucose by cells in the brain is not insulin dependent!)
  3. there are also glucostats outside of the brain (Russek, 1971) - IV injection of glucose had no effect on food intake (rats), but IP injection suppressed food intake (why? - IP inj. allowed glucose to be carried directly to the liver via the hepatic portal vein)
  4. experiments by Novin, et al (1973, 1983)
     1. fed rats a high carbohydrate diet then injected 2-DG into the hepatic portal vein - blocked cellular uptake of glucose and stimulated eating
     2. glucose injection into the hepatic portal vein suppressed eating but injection into the jugular vein did not
     3. liver glucostats signal both hunger and satiety
• lipostatic theory
  1. Friedman, Tordoff, and Ramirez (1986) - injected rats with drugs that block either glucose metabolism (2-DG) or fat metabolism (methyl palmoxirate) or both
     1. either drug alone had little effect
     2. both drugs together induced eating
     3. rats on a low carbohydrate-high fat diet ate in response to the fat-blocking drug alone
     4. proposed two hunger systems:
           glucoprivic hunger
           lipoprivic hunger
• there is substantial evidence that the peripheral glucostats and lipostats are the same cells - they respond when their metabolic rate falls (i.e., when ATP production falls)

• various hormonal signals have been proposed (e.g., CCK), but these have largely been discounted
• the signal to the brain cannot be nutrients in the blood - Tordoff & Friedman (1988)
  1. infused small amounts of glucose or fructose into the hepatic portal vein - both suppressed food intake
  2. fructose does not cross the blood-brain barrier - therefore, signal must be neural

• Hetherington & Ranson (1942) - VMH lesions cause rats to overeat and become obese (the VMH syndrome)
  1. finicky eaters
  2. primarily overeat carbohydrates (why?)
  3. the role of the paraventricular nucleus (PVN)
• Anand & Brobeck (1951) - LH lesioned rats stop eating (the LH syndrome)

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