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Chapter 4e - Hunger & Chemical Senses Video Lecture Psych 1XX3

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McMaster University
Joe Kim

Psych 1XX3 Chapter 4: Sensory Systems Hunger & The Chemical Senses  Feeding behaviours o Motivated by hunger and satiety signals o Guided by interaction of the senses of taste and smell Hunger and Satiety Glucose and Glycogen  Low blood glucose levels – cause the sensation of hunger o Glucose – the preferred source of energy for the brain; is important for keeping the body’s functions operating  The brain cannot use fat energy stores for fuel – makes regulating glucose availability a top priority  Body stores glucose in the form of glycogen which can be released between meals o Some glycogen stored in muscles o Main supply of glycogen is in the liver – can be readily converted back into glucose when circulating blood glucose levels are low o Insulin and the liver mediate the glucose-glycogen balance  Glucose and Glycogen Cycle o When you eat you supply the body with an influx of sugars o The pancreas  Secretes insulin to promote the uptake of glucose by cells in the body for immediate use  Stimulates storage of excess glucose as glycogen o When blood glucose levels get low, the liver begins to breakdown its stored glycogen into glucose, releasing it back into circulation Neuropeptide Y (NPY)  High levels of NPY activity in the hypothalamus are associated with increased appetite and food seeking behaviours  Affects feeding behaviour in fish, reptiles, birds and other non-human mammals  The liver monitors the glycogen stores and blood sugar levels o Low blood glucose and low glycogen levels serve as hunger signals o High glucose levels and high glycogen stores are signals of satiety  Ex/ If you inject glucose into a dogs vein that goes directly to the liver – dog stops eating  Ex/ If you inject glucose into a dogs vein that does not connect to the liver – dog continues eating Psych 1XX3 CCK and Meal Duration  Small intestine produces Cholecystokinin (CCK) – hormone that is responsible for feelings of satiety or fullness  Receptors in the brain detect CCK, which serves as a stop eating signal  Ex/ Inject individuals with CCK – they report being satiated sooner  Ex/ Rats administered with CCK – shorter than average meal durations, compared to controls o Rats who received CCK ate more total meals per day than controls – daily food intake was the same  CCK is a short-term satiety signal Long-Term Weight Regulation Long-Term Energy Storage  Adipose Energy Stores o Animals store most excess energy in the form of fat o Fat has more than twice the energy that carbohydrates (like glycogen) have  1 g of fat = 9 kcal  1 g of carbohydrates = 4 kcal o Fat is found in all parts of the body o Eg/ 70 kg man has  1200 kcal of energy as glycogen – enough to fuel activities for 12-18 hours  120 000 kcal of energy as fat – enough to fuel activities for a couple months o Adipose Tissue is an active component of the regulatory physiology o Classified as an endocrine organ  Leptin o Leptin – a hormone secreted by adipose tissue; involved in long-term energy balance and correlated with fat mass o When leptin levels rise – leptin acts on receptors in the hypothalamus to reduce appetite and food consumption decreases o OB Gene – controls leptin production o Ex/ Genetically altered knockout mice lacking an OB gene – leptin production stops; mice are missing a key hormonal signal to regulate appetite and become obese  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 o Obesity may involve defective OB genes or receptors – supported by experiments, not clinical findings  Giving leptin to an obsess animal with normal leptin levels does not result in weight loss o Animals are capable of becoming leptin resistant – leptin’s ability to inhibit appetite is reduced o The primary adaptive function of leptin was o serve as indicator of low energy stores (rather than a signal to directly reduce food intake)  Low leptin levels would signal to increase foraging effort or minimize activity in order to conserve energy  High levels of leptin or negative effects associated with excess adipose tissue would be rare in the past human evolutionary history  NPY activity in hypothalamus stimulates appetite  High levels of leptin inhibit NPY – decreases appetite and energy consumption Maladaptive Feeding and Neuropeptide Y  Ex/ NPY injected into brain of rats who were satiated by previous food consumption Psych 1XX3 o Increase in the intake of sucrose o Rats begin to work harder for a cue associated with sucrose o Rats increase the consumption of saccharin (similar taste to sucrose but without calories) o Preferentially chose a diet of carbohydrates over protein or fat  Suggests that NPY actin promotes unconditional and conditional behaviours that specifically lead to increased carbohydrate consumption o Preexisting preferences played an important role in NPY-induced increase in carbohydrate preference  Rats that showed a higher baseline preference for carbohydrates showed the greatest preference for carbohydrate following the NPY injection  Suggests implication for genetic predisposition toward carbohydrate consumption Endogenous Opioids  Endogenous Opioids o Naturally occurring chemical substances that have morphine-like analgesic actions in the body o Contributes to palatability and reward-driven feeding
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