Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin resistance is the physiopathologic foundation of metabolic syndrome. TRB3 has been revealed to be involved in insulin resistance in the liver by interacting directly with Akt and blocking its activation. Our investigation aims at exploring the relationship between metabolic syndrome and TRB3 mRNA expression in adipose tissue of rats. Two groups were studied as follows: the control group (CONTROL, n = 12) was fed a standard rodent chow, and the experimental group (Fructose n = 9) was fed a high-fructose diet. Body weight and systolic blood pressure were measured per 4 weeks. At the end of 38 weeks, levels of tribbles mRNAs in adipose tissue were determined by quantitative real-time polymerase chain reaction (PCR), and Akt/phospho-Akt expression was assessed by Western blot. Results show that levels of TRB1-3 mRNAs were expressed in adipose tissue of rats of both groups, and tribbles mRNAs were TRB1 (CONTROL: 0.00515, Fructose: 0.00497), TRB2 (CONTROL: 0.02104, Fructose: 0.01988), and TRB3 (CONTROL: 0.00457, Fructose: 0.00822), respectively. Of the three, TRB3 mRNA alone significantly increased by 94% in adipose tissue of fructose-fed rats compared with those in adipose tissue of the controls (P<0.05), and there was significant positive correlation between TRB3 mRNA levels and HOMA-R in fructose group (r = 0.68, P<0.05). Western blot analysis showed that phospho-Akt (Ser-473) expression was significantly decreased in adipose tissue of fructose-fed rats compared with controls (P<0.001). The present study suggests that TRB3 may be involved in metabolic syndrome by inhibiting activation of Akt in adipose tissue.
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PMID:Overexpression of TRB3 gene in adipose tissue of rats with high fructose-induced metabolic syndrome. 1849 49