UW PSYCH 202 - Chapter 12 (Satiety & Hunger)

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Chapter 12 (Satiety & Hunger)I. Biology of ingestive behaviorA. Regulation of Digestion1. 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 digestion2. 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 Assumption1. 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 toeating 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) anda set point for glucose level in blood.2.Glucose would interact with glucoreceptors.Low glucose levels stimulated hunger, while increases in glucose signaled satiety3. 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 Centera. 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 Centera. Lesions of the LH caused aphagia (cessation of eating) and adipsia (cessationof 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 LH6. 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 immediateenergy 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 energydeficiency.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 model1. 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 theories2. 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,

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UW PSYCH 202 - Chapter 12 (Satiety & Hunger)

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