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)

Ileal prostaglandin (PGs) biosynthesis was compared in female rats in normal mild hemorrhage (exposed to mild hypotension, reperfusion, and maintenance on hyperalimentation for 5 days) and control groups (instrumentation and hyperalimentation without hemorrhage). Tissue PG levels were analyzed by radiochromatographic analysis of microsomal membrane fractions prepared from the ileum in each group. Total cyclooxygenase activity in the normal and control groups was modest, with low levels of 6-keto-PGF1 alpha, PGE2, PGF2 alpha, thromboxane B2, PGA2, and PGD2 being produced. Hemorrhage, reperfusion, and maintenance on hyperalimentation for 5 days markedly induced total cyclooxygenase activity in the female rat ileum. Ileal microsomal membrane fractions obtained from the mild hemorrhage group synthesized levels of individual PGs three- to seven-fold higher than the normal or control groups, with 6-keto- PGF1 alpha (breakdown product of prostacyclin), PGE2, and PGA2 demonstrating the highest levels of biosynthesis. These data suggest that the gastrointestinal tract could serve as a source for the elevated PGs known to occur in various shock models.
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PMID:Elevated PGI2 and PGE2 production in the rat ileum following mild hypotension. 313 63

Obesity is a complex syndrome that involves defective signaling by a number of different factors that regulate appetite and energy homeostasis. Treatment with exogenous leptin reverses hyperphagia and obesity in ob/ob mice, which have a mutation that causes leptin deficiency, proving the importance of this factor and its receptors in the obesity syndrome. Cells with leptin receptors have been identified outside of the appetite regulatory centers in the brain. Thus leptin has peripheral targets. Because macrophages express signaling-competent leptin receptors, these cells may be altered during chronic leptin deficiency. Consistent with this concept, the present study identifies several phenotypic abnormalities in macrophages from ob/ob mice, including decreased steady-state levels of uncoupling protein-2 mRNA, increased mitochondrial production of superoxide and hydrogen peroxide, constitutive activation of CCAAT enhancer binding protein (C/EBP)-beta, an oxidant-sensitive transcription factor, increased expression of interleukin-6 and cyclooxygenase (COX)-2, two C/EBP-beta target genes, and increased COX-2-dependent production of PGE2. Given the importance of macrophages in the general regulation of inflammation and immunity, these alterations in macrophage function may contribute to obesity-related pathophysiology.
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PMID:Phenotypic abnormalities in macrophages from leptin-deficient, obese mice. 995 Jul 66