Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.9 (glucose-6-phosphatase)
 3,081 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early obesity and late onset of insulin resistance associated with hormonal imbalances occur in FSH receptor-deficient follitropin receptor knockout female mice. This study tests the hypothesis that chronic high-fat diet aggravates obesogenic changes in a depot-specific manner and explores some molecular links of hormone imbalances with insulin resistance. In SV 129 mice, hormonal imbalances seem obligatory for exacerbation of diet-induced obesity. Visceral adiposity, glucose intolerance, and lipid disturbances in 9-month follitropin receptor knockout females were associated with decrease in adiponectin signaling. High-molecular-weight plasma adiponectin and adipose tissue adiponectin mRNA were decreased. Adiponectin receptors R1 and R2 mRNA was selectively altered in mesenteric fat but not periuterine fat. R2 decreased in the liver and R1 was higher in muscle. Whereas hepatic adenosine monophosphate T-activated protein kinase activity was down-regulated, both phosphoenolpyruvate carboxykinase and glucose-6-phosphatase enzymes were up-regulated. Longitudinally, diminishing sex hormone signaling in adipose tissue was associated with progressive down-regulation of adiponectin activity and gradual impaired glucose tolerance. Chronic high-fat diet in SV129 wild-type mice did not produce overt obesity but induced visceral fat depot changes accompanied by liver lipid accumulation, high cholesterol, and up-regulation of inflammation gene mRNAs. Thus, TNF-alpha, C-C motif chemokine receptor-2, and C-C motif chemokine ligand-2 were selectively elevated in mesenteric fat without altering glucose tolerance and adiponectin signaling. Our study highlights adiponectin signaling and regulation to be involved in hormone imbalance-induced insulin resistance and demonstrates selective visceral adipose depot alterations by chronic high-fat diet and induction of inflammatory genes.
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PMID:Changes in adiponectin and inflammatory genes in response to hormonal imbalances in female mice and exacerbation of depot selective visceral adiposity by high-fat diet: implications for insulin resistance. 1771 50

Type 2 diabetes mellitus (T2DM) is a chronic progressive disease, which manifests as an endocrine disorder. Among the different methods of surgery available to treat patients with T2DM, Roux-en-Y gastric bypass (RYGBP) and ileal transposition (IT) are the most commonly performed. The aim of the present study was to investigate the effects of RYGBP combined with IT on rats with T2DM. A total of 8 healthy male rats were used as a control group and 40 GK rats were randomly divided into 5 groups: A diabetes mellitus (DM) group, a sham operative group (SO), a RYGBP group, an IT group and a RYGBP+IT group. The results demonstrated that fasting blood glucose, triglyceride, total cholesterol and gastric inhibitory polypeptide levels in all treatment groups were significantly lower than those of the SO and DM groups. Furthermore, levels TC and TG in the RYGBP+IT group were significantly lower than in the RYGBP and IT groups. Levels of phosphoenolpyruvate carboxykinase and glucose-6-phosphatase mRNA and IRS-2 protein in all treatment groups were also significantly lower than those of the SO group; and they were significantly lower in the RYGBP+IT group compared with the RYGBP and IT groups. The expression of phosphorylated Akt in the treatment groups was significantly higher than the SO group and was significantly higher in the RYGBP+IT group compared with the RYGBP and IT groups. These results indicate that RYGBP and IT surgical treatment can induce T2DM remission by mediating the expression of insulin-related factors to reverse insulin resistance. The current study also indicated that the effect of RYGBP combined with IT may be developed as a novel first-line method of treating T2DM.
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PMID:Effect of gastric bypass combined with ileal transportation on type 2 diabetes mellitus. 2972 90