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Fatty acids and insulin resistance

¹Division of Endocrinology/Metabolism and Diabetes, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.

|April 1, 1996

Summary

High free fatty acid levels impair glucose uptake in both healthy individuals and those with type 2 diabetes. This finding highlights the role of fatty acids in causing insulin resistance, a key factor in obesity and NIDDM.

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Area of Science:

Metabolism
Endocrinology
Physiology

Background:

Insulin resistance is a hallmark of obesity and type 2 diabetes (NIDDM).
The precise mechanisms by which elevated free fatty acids (FFAs) contribute to insulin resistance require further elucidation.

Purpose of the Study:

To investigate the impact of physiological elevations in plasma free fatty acid concentrations on insulin-stimulated glucose uptake.
To identify the underlying mechanisms responsible for FFA-induced insulin resistance.

Main Methods:

Infusion of fat to elevate plasma free fatty acid concentrations in normal subjects and patients with NIDDM.
Measurement of insulin-stimulated glucose uptake.
Assessment of glucose transport/phosphorylation and muscle glycogen synthase activity.

Main Results:

Plasma free fatty acid elevations inhibited insulin-stimulated glucose uptake in a dose-dependent manner.
A fat-related inhibition of glucose transport/phosphorylation was observed after 3-4 hours of fat infusion.
Decreased muscle glycogen synthase activity was noted after 4-6 hours of fat infusion.

Conclusions:

Physiological elevations in plasma FFAs induce insulin resistance.
FFA-induced insulin resistance involves impaired glucose transport/phosphorylation and reduced glycogen synthase activity.
Elevated plasma FFAs may play a significant role in the pathogenesis of insulin resistance in obesity and NIDDM.

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