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

Rats fed a cafeteria diet to produce hyperphagia showed increases in the maximal thermogenic responses (rise in oxygen consumption) to isoprenaline (mixed beta-agonist), prenalterol (beta 1-selective agonist) and clenbuterol (beta 2-agonist), and left-shifts in the dose-response curves to the latter two. The maximal response to phenylephrine (alpha-agonist) was similar for control and cafeteria rats. Ligand binding studies revealed increases in beta-adrenoceptor density of 33-38% in brown fat cells and isolated membranes from cafeteria-fed rats, but a 30% reduction in beta-receptors in heart membranes. Cold-adaptation caused a 22% reduction in beta-receptor density in brown fat membranes, but no change in heart. The ratio of beta 1/beta 2-receptors in brown fat was reduced from 59/45 in control to 47/54 in cafeteria-fed rats, but was not significantly altered in heart (58/44) or in brown fat from cold-adapted animals (64/30). alpha-Adrenoceptor density was increased above control values by 69 and 25% in brown adipose tissue from cafeteria and cold-adapted rats, respectively.
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PMID:Thermogenic responses to adrenoceptor agonists and brown fat adrenoceptors in overfed rats. 301 44

To investigate the involvement of adrenergic mechanisms in the development of obesity, hyperglycaemia and hyperinsulinaemia in Aston ob/ob mice, the sympathomimetic agent ephedrine (12 mg/kg/day) and the predominantly beta 1-adrenergic antagonist atenolol (12 mg/kg/day) were administered alone and in combination to weanling ob/ob mice for 40 days. Excessive weight gain in ob/ob mice was reduced (15-20%) by ephedrine, exacerbated (8-10%) by atenolol, but not significantly altered by a combination of these agents. The effects of ephedrine and atenolol were lost rapidly (within 5 days) when these agents were withdrawn. Ephedrine slightly reduced the hyperphagia in ob/ob mice, and food intake was transiently increased above that of untreated ob/ob mice when this agent was withdrawn. The development of basal hyperglycaemia and hyperinsulinaemia was not significantly altered by any of the treatments studied. None of the treatments significantly altered body weight, food intake, plasma glucose or plasma insulin concentrations in lean (+/+) mice. The results indicate that a defective adrenergic mechanism involving beta 1-adrenergic receptors contributes to the development of obesity in ob/ob mice.
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PMID:Effects of ephedrine and atenolol on the development of obesity and diabetes in ob/ob mice. 351 92

We have attempted to provide a progress report on current research on the role of catecholamines and serotonin receptor subtypes in feeding control. Recent evidence suggests that only some of the several catecholamine receptor subtypes are specifically involved in feeding control. They include the beta 1/2-adrenoceptors, the alpha 1-adrenoceptors and the D1 dopamine receptors: stimulation of these receptors reduces feeding in rats. Stimulation of serotonergic 5-HT1B and 5-HT2C receptors reduces feeding and perhaps enhances the satiating effect of food. Recently, an interesting reciprocal relation between serotonin and cholecystokinin has been discovered in relation to feeding control. The serotonergic 5-HT2A receptors are involved in stress-induced anorexia and regulate the hyperphagia induced by neuropeptide Y in the nucleus paraventricularis of the hypothalamus. Both effects may involve changes in the secretion of corticotropin-releasing factor. These findings may help elaborate neuronal models of feeding control and perhaps facilitate progress in the pharmacotherapy of human obesity and eating disorders.
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PMID:Pharmacology of ingestive behaviour. 876 44

Expression of Na(+)-K(+)-adenosinetriphosphatase (ATPase) in tissues from obese and lean Zucker rats was monitored. The phosphatase activity of the sodium pump was increased in liver and intestinal mucosa from obese animals but was unaltered in skeletal muscle, brown adipose tissue, kidney, and heart. Induction of Na(+)-K(+)-ATPase activity was correlated with increased alpha 1-subunit protein amounts in liver and intestinal mucosa, although alpha 1-subunit mRNA levels were increased only in liver tissue. Neither protein nor mRNA amounts for both subunits were significantly altered in the other tissues analyzed. The only exception was a decrease in the amount of beta 1-protein in kidney from obese rats. alpha 2-Subunit protein and alpha 2- and beta 2-mRNA levels were not altered in brown adipose tissue, heart, and soleus. In summary, this study shows that in obese Zucker rats the expression of the sodium pump is enhanced in tissues that are directly involved in nutrient uptake and processing. This adaptation may be related to the ongoing hyperphagia and to tissue hypertrophia but develops in a different manner in each tissue, suggesting differential regulation of alpha 1-subunit expression.
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PMID:Differential regulation of Na(+)-K(+)-ATPase in the obese Zucker rat. 894 44