In mice with obesity and insulin issues, turning off insulin signals in the kidney led to about half as much of a certain protein (SGLT2) that helps control sugar reabsorption — especially when they were given a hormone that affects salt balance. This suggests insulin helps keep this protein working in the kidneys.

In fat mice that don't respond well to insulin, giving a hormone-like drug called fludrocortisone reveals that insulin receptors in the kidney play a role in controlling blood pressure and blood sugar — but only when that hormone signal is turned up.

In mice with obesity and high blood pressure caused by a hormone called fludrocortisone, turning off the insulin receptor in the kidney's tubules only slightly lowers blood pressure—by about 2.3 points—suggesting insulin in the kidneys plays a small role in raising blood pressure here.

When scientists turned off insulin's signal in the kidneys of obese, insulin-resistant mice on a certain hormone, the mice started spilling a lot of sugar in their urine—way more than normal—showing that insulin in the kidneys helps control how much sugar gets reabsorbed.

Mice that had their insulin receptors turned off in kidney tubes didn’t get as high blood pressure when given a hormone that usually raises it — suggesting insulin in the kidneys might play a role in blood pressure control when the body has trouble using insulin properly.

In mice on a high-fat diet, turning off insulin's signal in the kidney doesn't change blood pressure or salt balance — meaning insulin in the kidney might not be needed to hold onto salt when obesity is caused just by diet.