Abstract
Cardiac TGR5 expression enhanced by hyperglycaemia in diabetic rats: A preclinical warning for disorders with excess bile acids
Highlights
Diabetes mellitus (DM) is a metabolic disease caused by the complex interactions of genetic, immunological and environmental factors
The increased levels of TGR5 and the ratio of p-signal transducer and activator of transcription 3 (STAT3) to STAT3 in cardiac tissues exposed to hyperglycaemic conditions were reversed by treating the hyperglycaemia
TGR5 expression increased in parallel with the increased ratio of phosphorylated STAT3 (p-STAT3) and STAT3 in H9c2 cells exposed to HG, and these effects were reversed by treatment with stattic at a dose sufficient to inhibit STAT3
Summary
Diabetes mellitus (DM) is a metabolic disease caused by the complex interactions of genetic, immunological and environmental factors. DM is a prime risk factor for aberrant cardiovascular function, including diabetic cardiomyopathy [1]. The hallmark of diabetic cardiomyopathy is a subclinical phase associated with cellular structural abnormalities including cardiac hypertrophy, cardiac inflammation, fibrosis and increased apoptosis that initially leads to diastolic dysfunction and later to systolic dysfunction, eventually causing heart failure [3]. The occurrence of hyperglycaemia, hyperlipidaemia, and oxidative stress in diabetes has been extensively documented and is implicated in the pathogenesis of various cardiovascular complications including cardiomyopathy [5]. Diabetes is a risk factor for cardiovascular disorders. The objective of this study was to investigate the potential mechanism(s) for the increase in TGR5 levels in the hearts of diabetic rats
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
