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Chapter 12 Satiety Hunger I Biology of ingestive behavior A Regulation of Digestion 1 Managed by Hunger and satiety 2 Hunger is still experienced without a stomach suggesting psychological influences 3 Digestion is the gastrointestinal process of breaking down food and drink and absorbing them into the body B Digestive system and steps in Digestion FIG 12 1 1 Chewing mixes food with saliva and initiates digestion 2 Swallowing passes food through esophagus 3 Stomach acts as a reservoir stores unused unprocessed energy HCl hydrochloric acid breaks up food into small particles and Pepsin digestive enzyme secreted by stomach breaks down protein into aminoacids aa 4 Stomach empties content into duodenum where most of the absorption takes place Here digestive enzymes from liver gall bladder and pancreas act on proteins and sugars The products can be absorbed into the blood stream and transported to the liver 5 Bile produced by the liver and stored in the gall bladder emulsifies fat droplets which then passes into the limphatic system 6 The large intestine absorbs most of the remaining water and electrolytes and what is left exits the system through the anus 7 As a consequence of digestion energy is delivered to the body in three main forms 85 by fats stored in adipose 14 5 by protein stored in muscles and 5 by glucose muscle and liver while glucose is the most readily available form of energy it isn t easy to store in that form fat stores twice as much energy more efficient C Phases of energy metabolism Fig 12 3 1 Cephalic Preparatory phase initiated by first sight smell etc of food ends when nutrients enter blood stream High Insulin Low Glucogon 2 Absorptive nutrients in blood are absorbed to meet immediate energy needs High insulin low glucogon 3 Fasting uses stored energy begins when unstored energy depletes and lasts until the next cephalic cycle High glucogon low insulin 4 The flow of energy during these three phases is regulated by two hormones produced by the pancreas insulin and glucagon a High levels of insulin promote the use of glusose by cells the conversion of 1 glucose to fat and glycogen and 2 aminoacids to proteins and the storage of excess energy forms b Low levels of insulin promote gluconeogenesis convertion of proteins to glucose c High levels of glucagon promote release of free fatty acids from adipose and converts them to ketones II Theories of Hunger and Eating Set Points versus Positive Incentives IN PROGRESSIVE ORDER A Set Point Assumption 1 Motivation to eat hunger would come from an energy deficit 2 There would be an energy set point that is maintained at a relatively constant level Fig 12 4 When the energy levels fall below the set point hunger would develop leading to eating behavior Eating brings the level back to set point and the person feels satiated no longer hungry 3 Thermostat metaphor thermostat controls stable temp thermometer detects change heater corrects temp accordingly 4 Set point systems are feed back systems They maintain homeostasis a constant internal environment 5 doesn t explain overeating etc B GLUCOSTATIC THEORY short term 1 It was proposed that there is a glucostat in the VMH ventromedial hypothalamus and a set point for glucose level in blood 2 Glucose would interact with glucoreceptors Low glucose levels stimulated hunger while increases in glucose signaled satiety 3 Later it was proposed that it was not the level of blood glucose which was regulated but the level of glucose utilization led to VMH as Satiety Center a This explain cases of hyperphagia overeating associated with high levels of blood glucose as in patients with diabetes mellitus pancreas does not produce enough insulin which converts food to fat for energy 4 Lateral Hypothalamus LH is the Feeding Center a Lesions of the LH caused aphagia cessation of eating and adipsia cessation of drinking these lesions override VMH lesions b Stimulation of the LH caused eating behavior EXPERIMENT scientists lesioned the VMH in rats rats grossly overate scientist assumed it was because they were not receiving satiety signals 5 Reinterpretation of the Effects of VMH and LH 6 more recent evidence shows that bilateral VMH lesions increase blood insulin levels increasing lipogenesis production of body fat and decreasing lipolysis the breakdown of body fats into molecules that can be utilized for energy production Thus to have calories in the blood that are readily available for immediate energy use the rats must keep eating 7 Some of the effects of VMH lesions can be attributed to lesions of neighboring structures such as the ventral noradrenergic bundle and the paraventricular nucleus 8 In the case of the LH it has been observed that lesions of the LH not only produce aphagia and adipsia but also other effects including motor disturbances general lack of responsiveness to sensory stimuli These observations indicate that the LH is not dedicated solely to feeding regulation 9 DOWNFALL although glucose levels drop just before an expected meal Fig 12 7 this observation does not necessarily support the glucostatic theory The drop in glucose levels is most likely due to the release of insulin that characterizes the cephalic phase of eating behavior rather than to energy deficiency If the expected meal is not served the blood glucose levels return to their previous homeostatic levels C LIPOSTATIC THEORY long term 1 Proposes that there is a set point for body fat so that the level of body fat is maintained at a relatively constant level 2 provides an explanation why short term diets do not work the body regains its normal amount of fat after the diet is over D The Dual Center Set Point model 1 A theory of eating behavior based on the satiety center VMH the hunger center LH and the glucose and body fat set points was very popular combines glucostatic and lipostatic theories 2 Problems with Set Point Theories of Hunger and Eating a Set point theories are rigid and not sufficient to explain all aspects of eating behavior For instance b Early ancestors needed to eat a lot to store energy as fat c Eating behavior is not always motivated by energy deficit d Other factors influence eating behavior such as taste learning and social factors 3 hunger excites L H feeding center eating excites the VMH satiety center inhibiting L H 4 Alternative theories have added significant flexibility E Positive Incentive perspective 1 The positive incentive theory states that eating behavior is driven not so much by

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UW PSYCH 202 - Chapter 12 (Satiety & Hunger)

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