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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Very frequently in acute and chronic pancreatitis, the surgical treatment is indispensable. The disease itself is accompanied by metabolic disturbances, protein deficiency, hepatic lesion, by diabetes and malabsorption syndrome. Following the laboratory parameters we were able to perform partial or total hyperalimentation, correction of acid-base dis-equilibrium and to obtain the positive nitrogen balance, and in this way keep the patients in optimal conditions pre- and postoperatively.
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PMID:[Metabolic disorders and current treatment of the surgical patient with pancreatitis]. 85 52

The cafeteria diet involves feeding experimental animals a choice of palatable human food items to stimulate energy intake, and has been used extensively to study diet-induced thermogenesis. In a recent commentary Moore has argued that this feeding regime is inappropriate for such studies because the nutrient composition cannot be controlled, many of the effects seen are due to protein or nutrient deficiency and accurate measurements of energy intake are difficult to achieve. We argue that all of these criticisms can be overcome by careful use of the feeding regime and well-controlled experiments. Gross nutrient composition of cafeteria diets can be modified over a wide range, and such studies demonstrate that the effects of protein deficiency can be clearly dissociated from those of hyperphagia. There is no experimental evidence for nutritional deficiency in cafeteria-fed animals even over very long periods of time. Furthermore, the alternatives suggested by Moore, i.e., presenting sucrose solutions to drink or high fat diets, suffer the same drawbacks of altered and often uncontrolled nutrient intake and yet produce little or no increase in energy intake. Criticism of the cafeteria diet is not justified simply because of its misuse by nutritionally naive experimenters. The value and validity of this feeding regime is further supported by the enormous impact it has made on our understanding of energy balance regulation and thermogenesis.
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PMID:The cafeteria diet as a tool for studies of thermogenesis. 304 31

The mechanisms by which intake of dietary protein is regulated are poorly understood despite their potential involvement in determining food choice and appetite. In particular, it is unclear whether protein deficiency results in a specific appetite for protein and whether influences on diet are immediate or develop over time. To determine the effects of protein restriction on consumption, preference, and palatability for protein we assessed patterns of intake for casein (protein) and maltodextrin (carbohydrate) solutions in adult rats. To induce a state of protein restriction, rats were maintained on a low protein diet (5% casein) and compared to control rats on non-restricted diet (20% casein). Under these dietary conditions, relative to control rats, protein-restricted rats exhibited hyperphagia without weight gain. After two weeks, on alternate conditioning days, rats were given access to either isocaloric casein or maltodextrin solutions that were saccharin-sweetened and distinctly flavored whilst consumption and licking patterns were recorded. This allowed rats to learn about the post-ingestive nutritional consequences of the two different solutions. Subsequently, during a preference test when rats had access to both solutions, we found that protein-restricted rats exhibited a preference for casein over carbohydrate whereas non-restricted rats did not. Analysis of lick microstructure revealed that this preference was associated with an increase in cluster size and number, reflective of an increase in palatability. In conclusion, protein-restriction induced a conditioned preference for protein, relative to carbohydrate, and this was associated with increased palatability.
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PMID:Restriction of dietary protein leads to conditioned protein preference and elevated palatability of protein-containing food in rats. 2922 95

Proteins are dietary components that contribute to nutritional needs of the body through the provision of nitrogen and amino acids. Protein status is tightly and continuously controlled to prevent or counteract protein deficiency and to maintain or restore an adequate protein status. Animals learn to detect and avoid diets deficient or devoid in protein or in at least one indispensable amino acid and when given a choice reject these diets. Diets restricted marginally in protein or in one or more amino acids more often induce hyperphagia, interpreted as an attempt to increase protein or amino acid intake and to meet the need for protein and amino acids. The increase in energy intake induced by a low protein diet is compensated for by an increased energy expenditure that restrains the gain in adiposity. The status of protein and/or amino acid insufficiency induced by protein or amino acid restricted diets is characterized by a profile of peripheral and central signals that contribute to modulate peripheral metabolic adaptations and central pathways involved in the control of feeding behaviour. These processes impact on the motivation for food and food choice, with an appetite for protein and/or for the limiting amino acid (s) associated with a reward driven sensitivity to protein and amino acid content of food and diets, which leads to restore or maintain an adequate protein status. In contrast to a protein-restricted diet, high-protein diets are usually reported to decrease food intake in both animals and humans, at least for a transient period, in relation to a reported satiating effect of proteins through activation of anorexigenic pathways.
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PMID:Protein status modulates the rewarding value of foods and meals to maintain an adequate protein intake. 3090 31