High Incomplete Skeletal Muscle Fatty Acid Oxidation Explains Low Muscle Insulin Sensitivity in Poorly Controlled T2D.

Context: Almost 50% of type 2 diabetic (T2D) patients are poorly controlled [glycated hemoglobin (HbA1c) ≥ 7%]; however, the mechanisms responsible for progressively worsening glycemic control are poorly understood. Lower skeletal muscle mitochondrial respiratory capacity is associated with low insulin sensitivity and the development of T2D.

Objective: We investigated if skeletal muscle insulin sensitivity (SI) was different between well-controlled T2D (WCD) and poorly controlled T2D (PCD) and if the difference was associated with differences resulting from mitochondrial respiratory function.

Insulin sensitivity is related to glycemic control in type 2 diabetes and diabetes remission after Roux-en Y gastric bypass.

Background: After initial onset, adequate glycemic control in patients with type 2 diabetes (T2DM) presents a continuing challenge even with aggressive pharmacologic treatment, and longer disease duration is associated with poorer resolution in response to Roux-en Y gastric bypass (RYGB). Skeletal muscle insulin sensitivity is an important determinant of glycemic control. We investigated whether skeletal muscle insulin sensitivity is predictive of T2DM resolution with RYGB and is in general lower in patients with longer-duration T2DM.