By Christopher G. Fairburn
This detailed guide offers and integrates nearly all that's presently recognized approximately consuming issues and weight problems in a single authoritative, available, and eminently functional quantity. From top foreign gurus, 112 concise chapters encapsulate the most recent info on all pertinent themes, from organic, mental, and social approaches linked to probability, to medical equipment for review and intervention. feedback for extra examining on the finish of every bankruptcy exchange prolonged references and improve the sensible price and clarity of the amount.
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Extra info for Eating Disorders and Obesity, Second Edition: A Comprehensive Handbook
2000). Medicinal strategies in the treatment of obesity. — Review of drugs used in the long-term treatment of obesity. Flier, J. , & Maratos-Flier, E. (1998). Obesity and the hypothalamus: Novel peptides for new 10 I. FOUNDATION pathways. —Minireview of hypothalamic peptide systems controlled by the hormone, leptin. Hoebel, B. , Leibowitz, S. , & Hernandez, L. (1992). Neurochemistry of anorexia and bulimia. In G. H. Anderson & S. H. ), The biology of feast and famine (pp. 22–45). —Review of brain neurochemical processes related to eating disorders.
6 Leptin and Body Weight Regulation L. ARTHUR CAMPFIELD Leptin (also known as OB protein) is a protein hormone, encoded by the ob gene, produced primarily by adipocytes and secreted into the circulation, where it binds to a family of binding proteins. Leptin enters the brain through a specific receptor-mediated transport system in brain microvessels and acts on specific brain areas involved in the control of food intake and the regulation of energy balance. It acts through a specific membrane receptor, OB-RL, to alter ongoing brain processes, descending autonomic nervous system activity, and gene expression of neuropeptides involved in the regulation of energy balance.
SMITH JAMES GIBBS The relative importance of the peripheral controls of eating and body weight has increased significantly in the past 5 years. This has been due to the realization that peripheral controls function at every meal, that so-called long-term controls of food intake act by modulating the potency of the peripheral controls, and the discovery of a new genetic obesity in rats that is due to spontaneous mutation of a mechanism of a peripheral control. All of this is the result of using meals as the functional unit of nalysis for investigating the control of eating.