What is the mechanism of action of Thiazolidinediones?

Thiazolidinediones (TZDs) primarily work by enhancing the sensitivity of peripheral tissues to insulin, particularly in muscle and adipose tissue. This mechanism involves the activation of peroxisome proliferator-activated receptor-gamma (PPAR-γ), which is a type of nuclear receptor that regulates gene expression involved in glucose and lipid metabolism. By activating PPAR-γ, TZDs improve insulin sensitivity, leading to better glucose uptake and utilization by these tissues, which helps to lower blood sugar levels in patients with insulin resistance.

The actions of TZDs contrast with the other options provided. While inhibiting hepatic glucose production or enhancing insulin secretion are mechanisms seen in other classes of diabetes medications (like metformin or sulfonylureas), they do not accurately describe the primary action of TZDs. Similarly, while some medications can delay carbohydrate absorption, this is not a function of TZDs. Hence, the action of sensitizing peripheral tissues to insulin is the hallmark of Thiazolidinediones' mechanism and is central to their role in managing type 2 diabetes.