Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone is an important regulator of metabolism; both acromegaly and GH therapy in GH-deficiency are associated with a tendency towards insulin-resistance and loss of adiposity. A possible mediator of these effects is the recently identified white adipose tissue (WAT)-derived factor resistin that has been shown to impair glucose tolerance and inhibit adipocyte differentiation. We found that WAT resistin gene expression was significantly suppressed in GH-deficient (SDR) rats compared with their Sprague-Dawley background strain. However, within 4 h of treatment of SDRs with a bolus of rhGH (1.5 mg/kg) there was a significant 150-170% increase in WAT resistin mRNA. Moreover, 24 h continuous infusion of recombinant human GH (1 mg/kg/day) caused marked increases in epididymal and subcutaneous WAT resistin of 720% and 950%, respectively, compared to controls. By 48 h of infusion these values had fallen to 510% and 330%. Infusion of porcine GH (1 mg/kg/day) had a similar inductive effect on WAT resistin mRNA. Our data demonstrate an unexpected marked, rapid and sustained up-regulation of resistin by GH. This may indicate a role for resistin in GH-dependent metabolic and differentiative effects in WAT.
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PMID:Growth hormone rapidly induces resistin gene expression in white adipose tissue of spontaneous dwarf (SDR) rats. 1202 Dec 11

In order to identify the mutual interaction between GH and leptin, we studied the effect of GH on fatty Zucker rats. GH administration at a high dose (5.0 IU/kg) reduced % body fat after 7 days. The leptin mRNA level in subcutaneous fat tissue was not changed but that in epididymal fat tissue was decreased by an even lower dose of GH (1.5 IU/kg). IGF-I treatment (200 microg/kg/day) did not change the % body fat or leptin mRNA level. These observations suggest that GH directly interacts with visceral fat and reduces fat mass and leptin expression. We also measured serum leptin levels in patients. The levels in patients with acromegaly were significantly lower than those in normal subjects with the same amount of body fat, but serum IGF-I and urinary C peptide excretion rates were higher in the acromegalic. These observations also suggests that GH directly interacts with adipose tissue and reduces leptin expression. Next we investigated the direct action of leptin on GH release from the pituitary. Leptin pretreatment of pituitary cells in culture or rats in a fasted or fed condition did not change GRH induced GH secretion. As indicated also by other recent studies, leptin may increase GRH or decrease somatostatin secretion by the hypothalamus. Thus GH interacts with fat tissues and leptin may be a good marker of the interaction.
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PMID:Interaction between leptin and growth hormone (GH)/IGF-I axis. 1205 13

Bovine growth hormone (bGH) transgenic mice mimic the clinical condition of acromegaly, having high circulating growth hormone (GH) levels. These mice are giant, have decreased adipose tissue (AT) mass, impaired glucose metabolism and a shortened lifespan. The detrimental effects of excess GH have been suggested, in part, to be a result of its depot-specific actions on AT. To investigate this relationship, we evaluated gene expression, biological mechanisms, cellular pathways and predicted microRNA (miRNA) in two AT depots (subcutaneous [Subq] and epididymal [Epi]) from bGH and littermate controls using RNA sequencing analysis. Two analyses on the differentially expressed genes (DEG) were performed: (i) comparison of the same AT depot between bGH and wild-type (WT) mice (genotype comparison) and (ii) comparison of Subq and Epi AT depots within the same genotype (depot comparison). For the genotype comparison, we found a higher number of significant DEG in the Subq AT depot of bGH mice compared to WT controls, corroborating previous reports that GH has a greater impact on the Subq depot. Furthermore, most of the DEG in bGH mice were not shared by WT mice, suggesting that excess GH induces the expression of genes not commonly present in AT. Through gene ontology and pathway analysis, the genotype comparison revealed that the DEG of the Subq depot of bGH mice relate to fatty acid oxidation, branched-chain amino acid degradation and the immune system. Additionally, the AT depot comparison showed that the immune cell activation and T-cell response appear up-regulated in the Subq compared to the Epi AT depot. The miRNA prediction also suggested a modulation of T-cell-related biological process in Subq. In summary, the present study provides a unique resource for understanding the specific differences in gene expression that are driven by both excess GH action and AT depot location.
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PMID:Differential gene signature in adipose tissue depots of growth hormone transgenic mice. 3304 5