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Chapter 12

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McGill University
PSYC 211
Yogita Chudasama

Chapter 12: Ingestive Behaviour Notes taken by: Ashley Brown Contact for mistakes: [email protected] Physiological Regulatory Mechanisms Homeostasis: the process by which the body’s substances and characteristics (such as temperature and glucose level) are maintained at their optimal level Ingestive behaviour: eating or drinking (intake of food, water, and minerals) A physiological regulatory mechanism is one that maintains the constancy of some internal characteristic of the organism in the face of external variability - ex: keeping body temperature constant despite changes in ambient temperature - Contains four essential features: o System variable: a variable that is controlled by a regulatory mechanism, for example, temperature in a heating system. AKA the characteristic to be regulated o Set point: the optimal value of the system variable in a regulatory mechanism o Detector: a mechanism that signals when the system variable deviates from its set point o Correctional mechanism: the mechanism that is capable of changing the value of the system variable - Negative feedback: a process whereby the effect produced by an action serves to diminish or terminate that action; a characteristic of regulatory systems Ingestive behaviours are controlled by satiety mechanisms and by detectors that monitor the system variables - satiety mechanisms are a brain mechanism that causes cessation of hunger or thirst, produced by adequate and available supplies of nutrients or water o they monitor the activity of the correctional mechanism, not the system variable themselves Eating: Some Facts About Metabolism We can achieve water balance by the intake of 2 ingredients: water and sodium chloride Eating needs to obtain adequate amounts of carbohydrates, fats, amino acids, vitamins, and minerals (other than sodium). Control of eating involves: metabolism, regulation of body weight, the environmental and physiological factors that begin and stop a meal, and the neural mechanisms that monitor the nutritional state of our bodies and control our ingestive behaviour. Reasons we eat: to construct and maintain our own organs and to obtain energy for muscular movements and for keeping our bodies warm. Two reservoirs that store nutrients to keep the cells of the body nourished when the gut is empty: a short-term one and a long-term one Short-term reservoir is located in the cells of the liver and the muscles - filled with a complex insoluble carbohydrate called glycogen which is oftern referred to as animal starch - cells in the liver convert glucose into the polysaccharide glycogen and then store it. This process is stimulated by the presence of insulin o insulin is a pancreatic hormone that facilitates the entry of glucose and amino acids into the cell, conversion of glucose into glycogen, and transport of fats into adipose tissue o When glucose and insulin are present the body uses some glucose and fuel and converts the rest to glycogen for use later - This reservoir is used primarily for the CNS o When glucose from the liver reaches the CNS it is absorbed and metabolised by neurons and glia The fall in glucose is detected by cells in the pancreas and in the brain - pancreas responds by stopping its secretion of insulin and starting to secrete glucagon which promotes the conversion of liver glycogen into glucose - this causes the liver to release glucose from its stores Long-term reservoir consist of adipose tissue - filled with triglycerides which are the form of fat storage in adipose cells o consist of a molecule of glycerol (a soluble carbohydrate, also called glycerine. Can be converted to glucose by the liver) combined with three fatty acids (stearic acid, oleic acid, and palmitic acid) - adipose tissue is found under the skin and in various locations in the abdominal cavity o consist of cells that are capable of absorbing nutrients from the blood, converting them to triglycerides, and storing them  these cell can expand enormously (difference in obese and normal weight people is that determined by the amount of triglycerides their fat cells contain) - keeps us alive when we are fasting o as we use the contents of our short term reservoir, fat cells convert triglycerides into a form that we can use o when you wake up with an empty digestive system the cells of the body (not CNS) are living off fatty acids to spare the glucose for the brain o sympathetic nervous system (which is primarily involved in the breakdown and utilization of stored nutrients) increases in activity when digestive system is fasting esp the ones that innervate adipose tissue, the pancreas, and the adrenal medulla o all three effects (direct neural stimulation, secretion of glucagon, and secretion of catecholamines) cause triglycerides in the long-term fat reservoir to be broken down into glycerol and fatty acids o fatty acids can be directly metabolized by cells in all of the body but the brain which needs glucose Insulin not only causes glucose to be converted to glycogen but has other functions like controlling the entry of glucose in cells - glucose is polar, so it can not pass through the nonpolar membranes of cells without glucose transporters o these transporters contain insulin receptors that control its activity: only when insulin is bound to them can glucose come into the cell o cells in the brain don’t need to have insulin bound for these transporters to work so glucose can enter without insulin present Fasting phase: the phase of metabolism during which nutrients are not available from the digestive system; glucose, amino acids, and fatty acids are derived from glycogen, protein, and adipose tissue during this phase - see fig 12.12, page 411 - a fall in blood glucose level causes pancreas to stop secreting insulin and start secreting glucagon - absence of insulin  cells of body can no longer use glucose only CNS - presence of glucagon/absence of insulin  liver starts drawing on the short- term carbohydrate reservoir and converts glycogen into glucose - fat cells start breaking down triglycerides into fatty acids and glycerol o body uses fatty acids o liver converts glycerol to glucose for the brain - if fasting is prolonged, protein, esp that found in muscle, will be broken down into amino acids which can be metabolized by everything but the CNS Absorptive phase: the phase of metabolism during which nutrients are absorbed from the digestive system; glucose and amino acids constitute the principal source of energy for cells during this phase and excess nutrients are stored in adipose tissue in the form of triglycerides - as we start absorbing the nutrients, levels of blood glucose rise  which is detected by cells in the brain  which causes the activity of the sympathetic nervous system to decrease and the activity of the parasympathetic nervous system to increase  change tells the pancreas to stop secreting glucagon and begin secreting insulin  insulin allows all cells of the body to use glucose as fuel  extra glucose is converted to glycogen which fills the short-term carbohydrate reservoir  if glucose still left its converted to fat and absorbed by fat cells - small portion of amino acids received from digestive tract are used as building blocks for proteins and peptide construction  rest are converted to fats and stored in adipose tissue - fats are not used as this time  stored in adipose tissue What Starts a Meal? Regulation of body weight requires a balance between food intake and energy expenditure. If we ingest more calories than we burn we gain weight and vice versa. Signals from the Environment Environment of our ancestors shaped the evolution of these regulatory mechanisms - starvation was a bigger threat than over eating in the past Something has to happen in our body to tell us that we are hungry and need to eat - the factors that motivate us to eat when food is readily available are very different from those that motivate us when food is scarce - when food is plentiful, we tend to eat when the stomach and upper intestine are empty, because the emptiness provides a hunger signal o the time it takes to empty the stomach encourages an establishment of a pattern of eating 3 meals a day - there is also the sight of food, people sitting around eating, the phrase “dinners ready”, the scent of food that stimulate wanting to eat (mainly for like pleasure and such) Signals from the Stomach Ghrelin: a peptide hormone released by the stomach that increases eating; also produced by neurons in the brain - also involved in the realise of growth hormone (GH) - blood levels of ghrelin increase with fasting and are reduced after a meal - ghrelin antibodies or ghrelin receptor antagonist inhibit eating - potent stimulator of food intake - stimulates thoughts about food - injection of nutrients to the stomach or eating causes suppressed ghrelin release but not injection of nutrients to the blood steam  shows release of this hormone is controlled by the contents of the digestive system not by availability of nutrients in the blood - obviously not the only mechanism that can stimulate feeding Duodenum: the first portion of the small intestine, attached directly to the stomach at the pylorus In a study they found that although the stomach secretes ghrelin, its secretion appears to be controlled by receptors present in the upper part of the small intestine. Metabolic Signals A fall in blood glucose level, which is referred to as hypoglycaemia is a potent stimulus for hunger Glucoprivation: a dramatic fall in the level of glucose available to cells; can be caused by a fall in the blood level of glucose or by drugs that inhibit glucose metabolism (like 2- DG) Lipoprivation: a dramatic fall in the level of fatty acids available to cells; usually caused by drugs that inhibit fatty acid metabolism - can also cause hunger There are two sets of detectors that monitor the level of metabolic fuels: one in the brain and the other in the liver - detectors on the brain monitor the nutrients that are available on their side of the blood-brain barrier o only sensitive to glucoprivation - detectors on the liver monitor the nutrients that are available to the rest of the body o sensitive to both glucoprivation and lipoprivation - infusing stuff that causes glucoprivation in the areas these receptors on causes immediate eating hepatic portal vein: the vein that transports blood from the digestive system to the liver Brain receives the hunger signal from the liver through the vagus nerve (connects liver to brain) Even cutting off these receptors doesn’t stop day to day eating  because we need food to function there is a lot of stuff that tells us to eat when we need nutrients What Stops a Meal? Two primary sources of satiety signals (the ones that stop a meal): - short-term satiety signals come from the immediate effects of eating a particular meal and begin long before the food is digested - long-term satiety signals arise in the adipose tissue o do not control the beginning and end of a particular meal but in the long run they control the intake of calories by modulating the sensitivity of the brain mechanisms to the hunger and satiety signals that they receive Because the consequences of starvation are much more serious than overeating natural selection has given us strong mechanisms to start eating and weaker ones to stop eating. Head Factors Head factors refers to several sets of receptors located in the head: the eyes, nose, tongue, and throat - information about the appearance, odour, taste, texture, and temperature of food has some automatic effects on food intake but most of these effects involve learning - important because this information can permit animals to learn about the caloric contents of different foods The act of eating does not produce long-lasting satiety - an animal with a gastric fistula (a tube that drains food out of the stomach before it can be digested) will eat indefinitely Gastric Factors The stomach contains receptors than can detect the presence of nutrients. Studies suggest that animals are able to monitor the amount of food in their stomachs. Intestinal Factors The intestines contain nutrient detectors - afferent axons arising from the duodenum are sensitive to the presence of glucose, amino acids, and fatty acids - some of the chemoreceptors found in the duodenum are also found in the tongue The stomach and intestinal factors can interact. Food reaches stomach  mixed with HCl and pepsin (which breaks down proteins into their amino acids)  food is gradually introduced into the duodenum  in duodenum food is mixed with bile and pancreatic enzymes - duodenum controls the rate of stomach emptying by secreting a peptide hormone called cholecystokinin (CCK) o regulates gastric motility and causes the gallbladder (cholecyst) to contract, releasing bile into the duodenum; appears to provide a satiety signal transmitted to the brain through the vagus nerve The chemical peptide YY 3-36or PYY appears to serve as an additional satiety signal - released after a meal in amounts proportional to the calories that were ingested - only nutrients cause it be release, a large drink of water had no effect Liver Factors Satiety produced by gastric factors and duodenal factors is anticipatory: i.e. these factors predict that the food will eventually restore the system variables that cause hunger The last stage of satiety appears to occur in the liver because it’s the first organ to learn that food is being received from the intestines. This signal continues the satiety that was already started by
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