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Psych 1XX3 Hunger and Chemical Senses Lecture Notes.pdf

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Department
Psychology
Course
PSYCH 1NN3
Professor
Joe Kim
Semester
Fall

Description
Psych 1XX3 – Hunger and Chemical Senses Notes – Mar 26, 2010 Introduction:  Human evolutionary past: food sources were scarce and behaviours were motivated by the constant need to obtain energy and nutrients essential to survival  Feeding behaviours may be motivated by hunger and satiety signals, but are guided by the interaction of the senses of taste and smell Hunger and Satiety: Glucose and Glycogen Balance:  One of the main reasons that you feel hungry is low blood glucose levels.  Glucose is important for keeping your body's functions operating and is the preferred source of energy for the brain; unlike other organs and tissues, the brain cannot use fat energy stores for fuel which makes regulating glucose availability a top priority.  You are very sensitive to the level of glucose in your blood, and this directly relates to your feelings of hunger.  To keep your brain constantly supplied with energy, your body can store glucose in the form of glycogen which can be released in between meals.  Some glycogen is stored in the muscles, but the main supply is in your liver where it can be readily converted back into glucose.  This glucose-glycogen balance is mediated to a large degree by the liver and a pancreatic hormone called insulin  The pancreas secretes insulin to promote the uptake of glucose by cells in your body for immediate use, but also to stimulate storage of excess glucose as glycogen.  When these levels get low enough, the liver begins to break down 'its stored glycogen into glucose, releasing it back into circulation.  In this way, the liver and pancreas help to buffer extreme swings in blood glucose levels. As this cycle continues and the time since your feast increases, your glycogen reserves in the liver will decrease and a status signal is sent to the brain.  At some point, the glucose and glycogen levels get too low and you will feel hungry. (See chart below.) Neuropeptide Y:  Another hunger cue comes from Neuropeptide Y or NPY.  High levels of NPY activity in the hypothalamus are associated with increased appetite and food seeking behaviours - such as heading to the kitchen.  NPV affects feeding behaviour similarly in fish, reptiles, birds, and other non- human mammals. Satiety and the Liver:  What makes you stop after eating?  Just as your liver can send signals to your brain to trigger hunger it also sends signals to the brain that trigger satiety.  If you take a dog that is eating and you inject glucose into a vein that connects directly to the liver, the dog will stop eating.  However, when the same glucose dose is injected into a different vein, say one that does not directly connect to the liver; the dog will continue eating. CCK and Meal Duration:  The small intestine also has a role to play in feelings of satiety.  food moves from your stomach to your gut, the small intestine produces Cholecystokinin, or CCK, a hormone that is responsible for feelings of satiety or fullness after a meal.  Receptors in the brain detect CCK, which serve as a signal to stop eating.  How do we know this? Well, scientists have found that if you inject individuals with CCK, they report feeling satiated sooner.  In another study researchers administered CCK to rats leading to shorter than average meal durations, compared to controls.  Interestingly, these rats who received CCK ate more total meals per day than the controls, and the total daily intake was the same for both groups.  This shows that CCK is a short-term satiety signal. Long-Term Weight Regulation:  Whenever possible, long-term energy storage takes place in the form of fat (i.e. adipose tissue).  Both short-term and long-term mechanisms interact to regulate overall energy balance and body-weight.  Why do animals store most of their excess energy in the form of fat? Why not store it all as glycogen, which is a quickly transferable source of energy? o Fat has more than twice the energy that carbohydrates, like glycogen, have. For every 1 gram of fat, there are 9 units of kilocalories. Compare that with carbohydrates which contain only 4 kilocalories per gram. o And unlike glycogen, fat is found in virtually all parts of the body. If you took a 70 kg man, he has about 1200 kcal of energy stored in the form of glycogen. This would be enough to fuel his activities for 12-18 hours. o However, that same man has approximately 120 000 kcal stored in fat - that‘s  enough  energy  to  live off of for a couple of months! o So for the long-term, fat is the better choice for storing more energy. But the fat or adipose tissue is so much more than just a passive energy storehouse. It is an active component of your regulatory physiology and was fairly recently classified as an endocrine organ as well. Leptin:  Adipose tissue secretes a hormone called leptin, which is involved in long-term energy balance and correlated with fat mass.  When leptin levels rise, they act on receptors in the hypothalamus to reduce appetite  food consumption decreases.  Leptin production is controlled by the OB Gene  in genetically altered knock- out mice lacking an OB Gene, leptin production stops; in this state, mice are missing a key hormonal signal to regulate appetite and become extremely obese.  This condition can be reversed if the mice are given regular injections of leptin, causing their eating behaviour and weight to return to normal. OB Gene Revisited:  These  studies  suggest  that  a  contributing  factor  for  obesity  in  humans  ‘may   involve defective OB genes or receptors.  However, this inference is not supported in clinical findings; very few obese people have known defects in the leptin signalling system.  What happens if you give leptin to an obese animal who happens to have normal leptin levels? In this case, giving additional leptin actually does not reliably result in weight loss to return to normal levels.  It appears that humans and other animals are capable of becoming leptin resistant: that is, at beyond a certain point, leptin's ability to inhibit appetite is reduced.  Consider that access to calories was a limited resource for most of human evolutionary history;' taking in too many calories must have been a rare luxury.  It is more likely that the primary adaptive function of leptin was to serve as 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 energy.  Rarely would an individual have had very high levels of leptin or suffered from the negative effects associated with excess adipose tissue. NPY:  What is the mechanism of leptin action? If you think of NPV activity in the hypothalamus as the ON switch for appetite, leptin acts to inhibit the actions of NPY.  And so, the NPV mediated increase is appetite is prevented by leptin, leading to decreased appetite and energy consumption.  Together leptin and NPV interact to regulate your weight to optimal levels. Maladaptive Feeding and NPY:  Evidence in rats suggests that NPYergic neurons can specifically affect reward- driven feeding for high calorie foods such as sucrose. o In one series of experiments, NPY was injected directly into the brain of rats who were satiated by previous food consumption. This revealed some interesting results: first, there is an increase in the intake of sucrose. o Second, rats will begin to work harder for a cue associated with sucrose o Third, rats also increased the consumption of saccharin (similar taste to sucrose but without calories) o Finally, these rats will also preferentially choose a diet of carbohydrates over protein, or fat.  This line of research suggests that NPV action promotes unconditional and conditional behaviours that specifically lead to increased carbohydrate consumption.  A  rat‘s  preexisting  preferences,  plays  an  important  role  in  this  NPV-induced increase in carbohydrate preference; rats that showed a higher baseline preference for carbohydrates showed the greatest preference for carbohydrates following the NPY injection.  These studies suggest an interesting implication for genetic predisposition toward carbohydrate consumption. Endogenous Opioids:  Another interesting hypothesis on overeating is related to endogenous opioids.  Endogenous opioids have morphine-like actions within the body and also contribute to palatability and reward driven feeding.  Interestingly, blocking the opioid receptors with a drug called naloxone reduces intake of rewarding foods such as saccharin and sucrose.  Consistent with this hypothesis, knock-in mice which have been genetically modified to lack the opioid receptor show lower preference for saccharin than do control mice.  Some researchers have speculated that overeating in some people may be reflective of a maladaptive opioid-mediated reward-driven feeding. Conclusion:  Energy balance and body weight regulation by hormones and mechanisms are asymmetric.  That is, the body defends itself against weight loss more strongly than it does against weight gain.  This asymmetry can be understood from an evolutionary perspective, where calories and nutrition were less certain. However, this asymmetry may have an unintentional maladaptive expression in a modern, fast-food nation where calories are cheap and physical exertion is minimal.  Taste Preferences and Food Selection:  Through the course of evolution, foods that are bitter or sour are associated with flavours not commonly enjoyed, because they are often indicative of toxins or noxious foods.  Sp
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