Vol 2, No 4 (2001): Practical Diabetology
Other materials agreed with the Editors
Published online: 2001-11-19
Skeletal muscle triglyceride. An aspect of regional adiposity and insulin resistance
Diabetologia Praktyczna 2001;2(4):255-266.
Abstract
Recent evidence derived from four independent methods
indicates that an excess triglyceride storage
within skeletal muscle is linked to insulin resistance.
Potential mechanisms for this association include
apparent defects in fatty acid metabolism that are
centered at the mitochondria in obesity and in type
2 diabetes. Specifically, defects in the pathways for
fatty acid oxidation during postabsorptive conditions
are prominent, leading to diminished use of
fatty acids and increased esterification and storage
of lipid within skeletal muscle. These impairments
in fatty acid metabolism during fasting conditions
may be related to a metabolic inflexibility in insulin
resistance that is not limited to defects in glucose
metabolism during insulin-stimulated conditions.
Thus, there is substantial evidence implicating perturbations
in fatty acid metabolism during accumulation
of skeletal muscle triglyceride and in the pathogenesis
of insulin resistance. Weight loss by caloric
restriction improves insulin sensitivity, but the
effects on fatty acid metabolism are less conspicuous.
Nevertheless, weight loss decreases the content
of triglyceride within skeletal muscle, perhaps contributing to the improvement in insulin action
with weight loss. Alterations in skeletal muscle substrate
metabolism provide insight into the link between
skeletal muscle triglyceride accumulation and
insulin resistance, and they may lead to more appropriate
therapies to improve glucose and fatty acid
metabolism in obesity and in type 2 diabetes.
Keywords: triglyceride storageinsulin resistanceregional obesity