In contrast, administration of an anti-CD25 antibody to deplete Tregs in db/db mice leads to worsening IR, increased visceral AT inflammation, and worsening of diabetic nephropathy; whereas repletion of Tregs in db/db mice improves insulin sensitivity and diabetic nephropathy, suggesting a role for AT Tregs in diabetic complications [18]. This evidence concerns the gene INS and diabetic kidney disease.