Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present studies were undertaken to further assess the role of plasma beta-endorphin (beta-EP) in the hyperphagia induced by the glucose antimetabolite, 2-deoxy-D-glucose (2-DG). Plasma concentrations of immunoreactive beta-EP (ir-beta-EP) were measured at the end of the first hour of feeding in all animals treated with 400 mg/kg 2-DG. Previous studies had shown a consistent, positive association between 2-DG hyperphagia and plasma ir-beta-EP concentrations, but the present data revealed dissociations between hyperphagia and plasma ir-beta-EP. Dexamethasone administration blocked the 2-DG-induced rise in plasma ir-beta-EP, but had no effect on the 2-DG hyperphagia measured at 1 hour. Forced drinking of a 2% NaCl solution decreased 2-DG hyperphagia, but not the 2-DG induced rise in plasma ir-beta-EP. Thus, elevations in plasma ir-beta-EP are not necessary for the full expression of 2-DG-induced hyperphagia in dexamethasone-treated rats. Furthermore, decreased feeding responses to 2-DG could coexist with increased levels of plasma ir-beta-EP in NaCl-treated normal rats. Elevations in plasma ir-beta-EP do not appear to be the critical opiate link in 2-DG induced hyperphagia.
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PMID:Experimental dissociation of food intake and plasma beta-endorphin following 2-deoxy-D-glucose in rats. 293 39

Concentrations of the potent hypothalamic appetite stimulating peptide neuropeptide Y (NPY), and its mRNA, are increased in rats with experimental diabetes, suggesting a role in the hyperphagia of this disorder. The 2-h feeding responses to intracerebroventricular (i.c.v.) injection of neuropeptide Y (NPY) (5, 10, and 15 mu g doses) were measured in male Wistar rats treated with streptozotocin (55 mg/kg) to induce diabetes. Streptozotocin-diabetic rats given i.c.v. NPY exhibited reduced feeding responses compared to controls (P < 0.05). Dexamethasone treated rats exhibit similar changes in NPY content and mRNA in the hypothalamus to those seen in diabetes, but are not hyperphagic. Feeding responses were also measured in this model, to assess whether high levels of endogenous NPY might account for the reduced response in diabetes. In contrast, the feeding response to NPY in comparison to controls was unaltered in dexamethasone treated rats. To investigate whether altered NPY receptor number or affinity, was the underlying mechanism for these divergent responses, receptor binding experiments were performed using (125)I-PYY and membranes prepared from rat hypothalamus. No significant difference was found in receptor number or affinity between the 2 groups (B(max): 114.7 +/- 18.9 vs 127.4 +/- 27.1 fmol/mg protein, K(d): 99.6 +/- 28.2 vs 135.1 +/- 32.4 pM). Similarly no difference was found between hypothalamic membranes prepared from dexamethasone-treated and control animals. NPY receptor subtypes in the hypothalamus were compared with that of cortex (predominantly Y1) and hippocampus (predominantly Y2) using the Y1-specific ligand [Leu(31)Pro(34)] NPY. These studies showed that the binding profile in the hypothalamus most closely matched that in the hippocampus, suggesting that the majority of hypothalamic receptors were of the Y2 subtype. Receptor autoradiography revealed low binding in the hypothalamus, and particularly in the paraventricular nucleus of the hypothalamus. Competition with [Leu(31)Pro(34)] NPY confirmed that only a low density of binding to Y1 like receptors was present in the hypothalamus. No difference was observed between control and streptozotocin treated animals. The feeding response to exogenous NPY is reduced in experimental diabetes, but not in dexamethasone treated rats. These differing responses do not appear to be due to altered NPY receptor number or affinity in the hypothalamus.
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PMID:Reduced NPY induced feeding in diabetic but not steroid-treated rats: lack of evidence for changes in receptor number or affinity. 886 Dec 84

The functional role of corticosterone (CORT) in regulating migratory hyperphagia and lipogenesis was investigated in an annual migrant, the dark-eyed junco (Junco hyemalis). Intraperitoneal injections of either dexamethasone (9 microg DXM/500 microL of 5% EtOH in saline, n=10) to inhibit an increase in baseline CORT or saline (5% EtOH, n=9) were given every 48 h for 15 d after transfer from short (10.5L:13.5D) to long (15.5L:8.5D) days. Food intake, body mass, furcular fat deposition scores, and nocturnal migratory activity were recorded for 29 d after photostimulation. Both groups showed the same increase in daily food intake over the study period (DXM=52%, control=41%). Controls began to increase baseline CORT and mass about 2 wk after photostimulation. DXM-treated birds maintained low CORT and did not increase mass or CORT until injections ceased, at which time they gained mass at the same rate shown earlier by controls. DXM-treated birds did not show greater levels of migratory activity despite experiencing an increase in energy intake during the CORT-inhibited period. Collectively, the results support the migration modulation hypothesis, illustrating how an increase in baseline CORT is needed to support the development of migratory condition. We address the apparent conflict with earlier studies on CORT and migratory food intake and propose a model in which migratory hyperphagia is supported by changes in centrally regulated responses to CORT that can occur even if CORT remains low and lipogenesis is regulated predominantly by peripheral mechanisms that require an increase in baseline CORT.
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PMID:The role of corticosterone in supporting migratory lipogenesis in the dark-eyed Junco, Junco hyemalis: a model for central and peripheral regulation. 1716 Aug 85