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)

Galanin (GAL), a 29 aminoacid peptide, is widely distributed in the central nervous system and especially in the hypothalamus. It strongly stimulates food intake when it is injected in the paraventricular nucleus (PVN) of normal rats. The obese Zucker rat with a well-established hyperphagia is characterized by a general dysregulation of some important neuropeptides involved in the regulation of feeding behavior e.g. neurotensin, NPY or CCK and the aim of this study was to measure GAL in different microdissected brain areas in lean (Fa/Fa) and obese (fa/fa) male Zucker rats. As feeding status may modulate the central peptide concentrations, it was measured in ad libitum fed rats and in 48-h fasted rats of both genotypes. GAL was measured by a specific radioimmunoassay in the arcuate nuclei (ARC) and parvocellular (PVNp) and magnocellular (PVNm) parts of the PVN as well as in the median eminence (ME), median preoptic area (MPOA), supraoptic (SON) and dorsomedian (DMN) nuclei. Two-way analysis of variance revealed a very significant effect of genotype in the PVNp (P < 0.001), SON (P < 0.001) and in the ME (P < 0.02). No significant variations at all were noted in the ARC, PVNm, MPOA and DMN. GAL concentrations were more than doubled in the PVNp and SON of ad lib obese rats when compared to the ad lib lean rats (P < 0.005). On the other hand, in the ME where GAL concentration was about 4-fold greater than in the other areas, there was a 20 to 30% decrease in GAL concentrations in the obese rat (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Galanin in the hypothalamus of fed and fasted lean and obese Zucker rats. 769 1

The glucostatic theory supports the role of central and peripheral substrate "sensors" in monitoring cellular glucose metabolism. Induction of hyperphagia and hyperglycemia by intracerebroventricular (i.c.v.) delivery of drugs inhibiting glucose uptake or oxidation suggests that glucose "sensors" are accessible from the cerebroventricular system. Although glucopenia elevates neurohypophyseal vasopressin (VP) and oxytocin (OXY) secretion and induces c-fos expression by hypothalamic paraventricular (PVN) and supraoptic (SON) neurons, the origin of glucoprivic regulatory signals impinging upon these cell populations is unclear. The following study evaluated immunolabeling of hypothalamic VP and OXY neurons for the nuclear transcription factor, Fos, following systemic vs. i.c.v. delivery of the glucose antimetabolite, 2-deoxy-D-glucose (2DG). Intraperitoneal drug treatment resulted in Fos expression by a high proportion of AVP- and OXY-ir neurons in the PVN and SON, whereas i.c.v. antimetabolite administration resulted in immunostaining of a smaller proportion of AVP neurons and a lack of colabeling of OXY neurons in both sites. These results suggest that decreased glucose metabolism within the periventricular CNS is a stimulus for central mechanisms that activate the Fos stimulus-transcription cascade in a discrete subpopulation of VP neurons in the PVN and SON. Alternatively, the absence of demonstrable Fos expression by OXY neurons in the same structures suggests that the functional status of these cells is regulated by glucoprivic stimuli of peripheral and/or nonperiventricular central origin.
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PMID:Intraventricular 2-deoxy-D-glucose induces Fos expression by hypothalamic vasopressin, but not oxytocin neurons. 1071 20