Impact Of Initiation Of Insulin Therapy On Serum Prolactin And Cortisol Levels In Type 2 Diabetic Male Patients

Abstract

Type 2 Diabetes Mellitus is a common metabolic disease characterized by a decline in insulin sensitivity and relative insulin insufficiency-induced hyperglycemia. In type 2 diabetic patients who have failed to achieve target glycemic control goals on oral anti-diabetic drug therapy, Initiating insulin therapy significantly improved overall glycemic control. Insulin, the primary regulator of glucose balance, lowers postprandial plasma glucose by increasing glucose uptake and usage from peripheral tissues and decreasing gluconeogenesis and glycogenolysis. In contrast, counter regulatory hormones against insulin action, such as glucagon, growth hormone, epinephrine and cortisol, prevent hypoglycaemia by increasing gluconeogenesis and glycogenolysis and decreasing glucose uptake and consumption from peripheral tissues during fasting. Cortisol shows its effect as an insulin antagonist. It suppresses insulin secretion from pancreatic beta cells. On the other hand, glucocorticoids increase the vagal stimulus regarding insulin secretion with their central effect. The balance between these effects can cause insulin resistance together with compensatory hyperinsulinemia and hyperglycaemia in the blood. As a result, the blood glucose level elevates, and glycogen formation increases in the liver.