| REGULATION OF FOOD INTAKE
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| The nutritional status is determined by a combination of biological, psychological and social factors
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| It depends on the availability of nutrients and on the rate of their utilization. These in turn are influenced by the availability of food, its palatability and variety, and the absence or presence of illness. The food intake is controlled by hunger (a desire to eat) and appetite (a desire for a particular food).
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| The brain is the main regulator in energy homeostasis and it is also the primary regulator of the body weight (Fig. 21.5). According to the lipostatic model of energy homeostasis, signals controlling energy intake originate from the adipose tissue and are sent to the central nervous system; in response, the brain sends efferent signals which are mediated by a complex network of neuropeptides. These signals regulate appetite and hunger. The main signals received by the central nervous system (CNS) are mediated by the adipokine leptin and the pancreatic hormone insulin (see Chapters 15 and 20).
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Leptin and insulin act directly on the central neurones in the regions of the brain, which control appetite and energy expenditure. These neurones are located in the hypothalamic arcuate nucleus and project throughout hypothalamus. They express two neuropeptides: catabolic proopiomelatocortin (POMC), and anabolic neuropeptide Y/agouti-related protein (NPY/AgRP). POMC is cleaved yielding melanocortins (such as alpha-MSH), that decrease food intake. NPY/AgRP links to neurons expressing melanin-concentrating hormone (MCH) and orexins A and B. They in turn, by acting on brain stem neurones, are involved in the control of food intake. These neurones connect with the brain cortex (the satiety center) to promote hunger and to stimulate yet another set of hormones such as thyreoliberin (TRH), corticoliberin (CRH) and oxytocin . Thyreoliberin increases thermogenesis and food intake, whereas corticoliberin decreases food intake and increases energy expenditure through the sympathetic activity.
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| Further signals involved in the control of food intake come from the gastrointestinal tract and are mediated by gastrointestinal peptides such as glucagon, cholecystokinin, glucagon-like peptide, amylin and bombesin-like peptide. Ghrelin, which is secreted by the stomach and stimulates NPY/AgRP-expressing neurons, is the only known appetite-stimulating peptide. Gastric stretch itself also affects the food intake. Finally, hypoglycemia decreases the activity of the satiety centre.
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