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Hunger.docx

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Department
Psychology
Course
PSYCH 1XX3
Professor
Joe Kim
Semester
Winter

Description
Hunger & Chemical Senses • Seeking out food and drink is a fundamental goal-directed behavior; much of day scheduled around feeding • In many ways, life is dominated by consumption of food and drink (think of human history) • Evolutionarily driven behaviors may now seem out of place in modern society where calories are consumed cheaply and easily • Food does not taste the same without sense of smell • Feeding behaviors are motivated by hunger and satiety signals, but are guided by interaction of taste and smell Hunger and Satiety • When fasting, one of the main reasons you feel hungry is low blood glucose • Glucose is preferred source of energy for the brain • Unlike other organs and tissues, brain cannot use fat energy stores for fuel • Body is very sensitive to glucose levels- directly relates to feeling of hunger* • Not always eating so to give brain constant energy supply, your body stores glucose in from of glycogen to be released between meals • Some glycogen stored in muscles, but main supply in liver • In liver, glycogen can be readily converted back to glucose when blood glucose levels are low • This balance = mediated by liver and pancreatic hormone, insulin • You eat a meal = increase in blood sugar  pancreas secretes insulin to promote uptake of glucose by cells (in order for body to immediately use, but also to stimulate storage of excess glucose as glycogen) • As time from meal increases, blood glucose levels correspondingly begin to drop • When levels get low enough, liver breaks down stored glycogen into glucose, releasing it back into blood • Another hungry cue you are likely experiencing comes from Neuropeptide Y or NPY • High levels of NPY activity in hypothalamus associated w/ increased appetite & food-seeking behaviors • NPY affects feeding behavior similarly in fish, birds, reptiles and other mammals • Just as liver sends signals to brain for hunger, also sends signals for saiety • Therefore, if you take a dog that is eating and inject glucose in a vein going straight to the liver, the dog will stop eating • If you inject same glucose dose to a different vein, one not connected directly to liver, dog will continue eating • Low glucose = hunger; high glucose = saiety (control is in LIVER) • Small intestine also plays role in saiety • Small intestine produces CCK (Cholecystokinin) or CCK, a hormone responsible for feelings of saitety/fullness after a meal • Receptors in brain detect CCK- signal to stop eating • If you inject people with CCK – report feeling full sooner • Astudy: Rats who received CCK had shorter average meal durations, compared to controls. • The rats who received CCK ate more total meals per day than the controls • Therefore, total daily food intake was same for both groups • *This shows that CCK is a short-term society signal • *CCK regulates short-term feeding behaviors, but not long-term energy consumption Long-Term Weight Regulation • Animals, unlike humans, need to consider long-term nutrition incase food is scarce • Some store excess energy for use in times where food is scarce • Whenever possible, long-term energy storage takes place in form of fat • Both short-term and long-term mechanisms interact to regulate overall energy & balance body weight • Adipose tissue secretes (hormone) which is involved in long-term energy balance and correlated with fat mass • When leptin levels rise, they act on receptors in hypothalamus to reduce appetite and food consumption decreases • Leptin production controlled by OB Gene • In genetically altered knock-out mice, lacking OB gene, leptin productoion stops  mice are missing a key hormone signal to regulate appetite and become obese • This condition can be reversed if mice are given regular injections of leptin, causing their eating behavior and weight to return to normal • ^ Studies suggest that a contributing factor for obesity in humans may involve OB genes or receptors, however, this inference is not supported in clinical findings • Very few obese people have known defects in leptin signalling system • What you give leptin to an obese animal who has normal leptin levels, it does not reliably result in weight lostt to return to normal levels • Humans and other animals can become leptin-resistant- beyond a certain point, leptin’s ability to inhibit appetite is reduced • Access to calories was a limited resource for most human evolutionary history • Taking in too many calories was a rare luxury • It is more likely that primary adaptive function of leptin was to serve as an indicator of low energy stores, rather than as a signal to directly reduce food intake • Low leptin levels would signal to increase foraging effort or minimize activity in order to conserve enrgy • Rarely would an individual have very high levels of leptin or suffer from negative effects associated with excess adipose • Mechanism of action: • NPY activity in hypothalamus as ON switch for appetite, letpin acts to inhibit actions of NPY • NPY mediated increase is appetite is prevented by leptin, leading to decreased appetite and energy consumption • Together Leptin & NPY interact to regulate your weight • In one series of expts, NPY was injected directly into brain of rats who were satiated by previous food consumption • This revealed: there is an increase in intake of sucrose, rats will begin to work harder for a cue associated with sucrose, rats increase consumption of saccharin (similar taste to sucrose but without calories), and the rats will preferentially chose a diet of carbohydrates over fat/protein • NPY action promotes unconditional and conditional behaviors that specifically lead to increased carbohydrate consumption • Rat’s preexisting preference plays imp. role in NPY-induced increase in carbohydrate preference: Rats that showed higher baseline preference for carbohydrates showed greatest preference for carbohydrates following BPY injection • Endogenous Opoids: - Naturally occurring chemical substances that have morphine-like analgesic actions in the body - Contributes to palatability & reward-driven feeding - Naloxone reduces intake of sacchar sucrose and saline • Consistent with this hypothesis, knock-in mice which have been genetically modified to lack the opoid receptor show lower preference for saccharin than normal mice • Some researchers have speculated that overeating in some people may be reflective of a maladaptive opoid-mediated reward-driven feeding • Mice with opoid receptor deficiency have lower preference for saccharin than control mice • Energy balance and body weight regulation by the hormones and medicines is asymmetric: • The body defends itself against weight loss more strongly than it does against weight gain • This tendency supports a very lucrative global dieting market • The asymmetry can be understood from an evolutionary
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