It also attenuated tubulointerstitial fibrosis and glomerulosclerosis induced by HFD feeding in kidney. Metformin was effective in lowering elevated basal blood pressure and acute change in mean arterial pressure in response to angiotensin II (Ang II). In kidney, metformin increased the activation of AMP-activated protein kinase (AMPK) and decreased inflammatory markers (COX-2 and IL-1β) and apoptotic markers (poly(ADP-ribose) polymerase (PARP) and caspase 3). Interestingly, metformin along with diet reversal restored the levels of blood glucose, triglycerides, cholesterol, blood urea nitrogen, and creatinine.
Diet reversal could improve lipid profile but could not prevent renal complications induced by HFD. Blood pressure and in vivo vascular reactivity to angiotensin II (200 ng kg −1) were also checked. Biochemical and histological markers of insulin resistance and kidney function were measured. Then the rats were subjected to diet reversal alone and along with metformin for 8 weeks. Male adult Sprague-Dawley rats were rendered insulin-resistant by feeding high fat diet for 16 weeks. Here we checked the hypothesis whether concomitant diet reversal and metformin could overcome HFD-induced metabolic memory and renal damage. Recently, we have shown that high fat diet (HFD) in vivo and in vitro generates metabolic memory by altering H3K36me2 and H3K27me3 on the promoter of FOXO1 (transcription factor of gluconeogenic genes) (Kumar, S., Pamulapati, H., and Tikoo, K. Glycobiology and Extracellular Matrices.
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