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Lecture 16

Lecture 16 Hunger and the Chemical Senses.docx

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Joe Kim

1 Lecture 16: Hunger and the Chemical Senses Introduction to Hunger and Satiety  Seeking out food and drink is a fundamental goal-directed behaviour because your moving body needs regular nourishment to function optimally  During most of the human evolutionary past, food sources were scarce and behaviours were motivated by the constant need to obtain energy and nutrients essential for survival  Feeding behaviours may be motivated by hunger and satiety signals, but are guided to a large extent by the interaction of the senses of taste and smell Hunger and Satiety  Overnight, you have fasted for the longest period of your daily cycle  Many signals and complex interactions between the brain and digestive system that drive your feelings of hunger to consume food and drink and satiety signals which lead you to stop consumption  Glucose and Glycogen Balance o When you are fasting, one of the main reasons you feel hungry is low blood glucose levels o Glucose is important for keeping your body’s functions operating and is the preferred source of energy for the brain o Unlike other organs and tissues, the brain cannot use fat energy stores for fuel, which makes regulating glucose levels a top priority o You are very sensitive to the level of glucose in your blood and this directly relates to your feelings of hunger o 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 o Some glycogen is stored in the muscles, but the main supply is in your liver where it can be readily converted back into glucose when your circulating blood glucose levels are low o This glucose-glycogen balance is mediated to a large degree by the liver and a pancreatic hormone called insulin o After a meal, 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 o As time goes by, your blood glucose levels will correspondingly begin to dip o When these levels get low enough, the liver begins to breakdown its stored glycogen into glucose, releasing it back into circulation o In this way, liver and pancreas help to buffer extreme swings in blood glucose levels o 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 o At some point, the glucose and glycogen levels get too low and you will feel hungry 2 o In the time between a meal and the next morning, your glycogen stores are being depleted o Eating a bowl of cereal increases your blood glucose levels for now and helps to replenish your glycogen stores for later  NPY o Another hunger cue you were likely to experience this morning came from Neuropeptide Y (NPY) o High levels of NPY activity in the hypothalamus are associated with increased appetite and food seeking behaviours (ex. heading to the kitchen) o NPY affects feeding behaviour similarly in fish, reptiles, birds and other non- human mammals  Satiety and the Liver o Just as your liver and send signals to your brain to trigger hunger, it can also send signals to the brain that trigger satiety o Ex. 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 o However, when the same glucose dose is injected into a different vein, such as one that does not connect to the liver, the dog will continue eating o The liver monitors glycogen stores and blood sugar levels o Low blood glucose and low glycogen levels serve as signals of hunger, while high glucose levels and high glycogen stores are signals of satiety  CCK and Meal Duration o The small intestine also has a role to play in feelings of satiety o As your breakfast moves from your stomach to your gut, the small intestine produces Cholecystokinin (CCK), a hormone that is responsible for feelings of satiety or fullness after a meal o Receptors in the brain detect CCK, which serves as a signal to stop eating o Scientists have found that if you inject individuals with CCK, they report feeling satiated sooner o In another study, researchers administered CCK to rats leading to shorter than average meal durations compared to controls o Interestingly, these rats who received CCK ate more total meals per day than the controls and so the total daily food intake was actually the same for both groups o This shows that CCK is a short-term satiety signal o CCK appears to regulate short-term feeding behaviours, but not long-term energy consumption Long-Term Weight Regulation  Animals need to consider more than their current nutritional needs, they also need to store some excess energy for use in times when food is scarce  Whenever possible, long-term energy storage takes place in the form of fat (adipose tissue)  Both short-term and long-term mechanisms interact to regulate overall energy balance and body-weight 3  Adipose Energy Stores o Why do animals store most of their excess energy in the form of fat instead of storing it all as glycogen, which is a quickly transferable source of energy o For one thing, fat has more than twice the energy that carbohydrates like glycogen have o For every 1 gram of fat, there are 9 units of kilocalories, while carbohydrates only contain 4 kilocalories per gram o Unlike glycogen, fat is found in virtually all parts of the body o For the long term, fat is a better choice for storing more energy o But fat or adipose tissue is more than just a passive energy storehouse o It is an active component of your regulatory physiology and was fairly recently classified as an endocrine organ as well  Leptin o Adipose tissue secretes a hormone called leptin, which is involved in long-term energy balance and correlated with fat mass o When leptin levels rise, they act on receptors in the hypothalamus to reduce appetite and consequently, food consumption decreases o Leptin production is controlled by the OB Gene o 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 mice are given regular injections of leptin, causing their eating behaviour and weight to return to normal o These studies suggest that a contributing factor for obesity in humans may involve defective OB genes or receptors o This inference is not supported in clinical findings however o If you were to give an obese animal who has normal leptin levels additional leptin, there is no weight loss to return leptin levels to normal o It appears that humans and other animals are capable of becoming leptin resistant  Beyond a certain point, leptin’s ability to inhibit appetite is reduced o For most of evolutionary history, access to calories was a limited resource for humans o It is more than likely that the primary adaptive function of leptin was to serve as a n indicator of low energy stores, rather than as a signal to directly reduce food intake o Low levels would signal to increase foraging effort or minimize activity in order to conserve energyfv o Rarely would an individual have very high levels of leptin suffer from negative effects associated with excess adipose tissue  NPY o Leptin acts to inhibit the actions of NPY o NPY mediated increase in appetite is prevented by leptin, leading to decreased appetite and energy consumption o Together, leptin and NPY interact to regulate weight to optimal levels 4 o 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 o This revealed interesting results  First, there was an increase in the intake of sucrose  Second, rats will begin to work harder for a cue associated with sucrose  Third, rats also increased the consumption of saccharin (similar taste to sucrose, but without calories)  Finally, these rats will also preferentially choose a diet of carbohydrates over protein or fat o This line of research suggests that NPY action promotes unconditional and conditional behaviours that specifically lead to increased carbohydrate consumption o Rats that showed a higher baseline preference for carbohydrates showed the greatest preference for carbohydrates following the NPY injection o These studies suggest an interesting implication for genetic predisposition toward carbohydrate consumption  Endogenous Opioids o Another hypothesis on overeating o Endogenous opioids have morphine-like actions within the body and also contribute to palatability and reward-driven feeding o Blocking the opioid receptors with a drug called naloxone reduces intake of rewarding foods such as saccharin and sucrose o Consistent with the hypothesis, knock-in mice which have been genetically modified to lack the opioid receptor show lower preference for saccharin than do control mice o Some researchers speculate that overeating in some people may be reflective of a maladaptive opioid-mediated reward-driven feeding  Energy balance and body weight regulation by the hormones and mechanisms seems to be asymmetric  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 5  Summary Molecule/Hormone Source Function Glucose Food, glycogen Primary fuel for brain Glycogen Liver, muscles Stored form of glucose Insulin Pancreas Stimulates glucose metabolism and glycogen synthesis CCK Small intestine Responsible for short-term satiation, terminating meals NPY Hypothalamus Stimulates appetite, food consumption Leptin Adipose High levels inhibit NPY, appetite Low levels promote feeding, energy conservation 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  Special acquired tastes for bitter and sour must be learned through experience  Foods that are sweet, salty or savoury are associated with flavours that are craved because they are more often indicative of foods that are safe, nutritious and rich in energy such as fruits and protein  Individuals who could detect these taste differences had a survival advantage as they were better able to avoid dangerous foods, while accessing reliably sources of energy for good health  Two lines of evidence suggest that certain taste responses are universal and basic to human behaviour o Particular tastes will elicit the same reaction in infants from all over the world o Fully healthy infants as well as those with extensive brain damage, exhibit the same characteristic responses to tastes o Experiment  Infant subjects are given a neutral solution to taste  When given a sweet or salty solution infants show characteristic acceptance responses and smile  When given bitter or sour solutions infants show a characteristic rejection response and are altogether unhappy  Interestingly, these same responses are mirrored by the infant without a cortex and by the infant with hydrocephalus, suggesting that these responses are governed by lower regions of the brain o The perception and response to particular tastes are adaptive mechanisms,
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