Purpose of review: Insulin resistance is closely linked to accumulation of lipid outside adipose tissue (ectopic fat storage). VLDL particles transport lipids from the liver to peripheral tissues. However, whether abnormalities in VLDL-triglyceride storage in muscle and adipose tissue exist in type 2 diabetes has previously been unknown, primarily because of methodological difficulties. Here, we review recent research on VLDL-triglyceride storage.
Recent findings: In a recent study, men with type 2 diabetes had increased skeletal muscle VLDL-triglyceride storage compared to weight-matched nondiabetic men, potentially leading to intramyocellular triglyceride accumulation. In contrast, studies of adipose tissue VLDL-triglyceride storage have shown similar storage capacity in men with and without diabetes, both in the postabsorptive and the postprandial period. In the initial submission, studies have failed to show associations between lipoprotein lipase activity, considered the rate-limiting step in storage of lipids from lipoproteins, and VLDL-TG storage in both muscle and adipose tissue.
Summary: Differences in muscle VLDL-triglyceride storage may lead to ectopic fat storage and contribute to the development of type 2 diabetes, whereas the ability to store VLDL-triglyceride in adipose tissue is preserved in type 2 diabetes.