While reducing obesity is effective in reducing inflammation and delaying disease onset and progression, including diabetes, CKD and metabolic syndrome, the metabolic effects of hyperglycemia also lead to production of AGE, TGF-β and protein kinase C. These toxic products have some role in nephropathy and clinical albuminuria with histological changes of thickening of glomerular basement membrane, mesangial matrix expansion and arteriolar hyalinosis. Here, TGFB1 is linked to obesity due to melanocortin 4 receptor deficiency.