Elevated arginine vasopressin (AVP) signaling through V1a receptors increases hepatic glucose production and lipogenesis, leading to insulin resistance and fatty liver disease, while activation of V1b receptors increases glucagon and cortisol secretion, further impairing glucose homeostasis.

When the body is dehydrated, it releases a hormone called AVP, which binds to receptors in the liver, pancreas, and adrenal glands. In the liver, this triggers the production of more sugar and fat. In the pancreas, it causes the release of glucagon, which further increases sugar production and indirectly boosts insulin. In the adrenal glands, it prompts the release of cortisol and epinephrine, which block insulin action and increase sugar output. At the same time, AVP stops fat breakdown in fat tissue, causing fat to build up in the liver. Together, these actions raise blood sugar, reduce insulin effectiveness, and cause fat to accumulate in the liver.