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Acute hyperinsulinemia and very-low-density and low-density lipoprotein subfractions in obese subjects^1,2,3

¹ From the Clinical Diabetes Unit, Division of Endocrinology and Diabetology, and the Division for Treatment of Chronic Diseases, University Hospital, Geneva, and the Institute of Physiology, University Hospital, Lausanne, Switzerland.

Background: The influence of hyperinsulinemia on concentrations of lipoprotein subfractions in obese, nondiabetic persons has not been clarified.

Objective: We analyzed VLDL and LDL subfractions before and after a euglycemic, hyperinsulinemic clamp.

Design: Lipoprotein subfractions were isolated from plasma samples obtained in the basal state and after a 4-h clamp from obese patients, obese patients with type 2 diabetes, and nonobese control subjects.

Results: Hyperinsulinemia tended to reduce concentrations (: 20%) of large, triacylglycerol-rich VLDL₁ in obese patients but had a minor effect on VLDL₂ and VLDL₃. Placing obese patients into insulin-sensitive and insulin-resistant subgroups revealed distinct effects of the degree of insulin sensitivity on VLDL. VLDL₁ concentrations decreased by a mean of 38% (P < 0.05) in insulin-sensitive patients after the clamp, similar to but less marked than the decrease observed in control subjects (: 62%; P < 0.01). VLDL₁ concentrations did not change significantly after the clamp in insulin-resistant patients (and patients with type 2 diabetes), whereas VLDL₃ concentrations decreased in both groups, in contrast with the changes seen in the insulin-sensitive patients and control subjects. Acute hyperinsulinemia modified the LDL subfraction profile toward a greater prevalence of small, dense LDLs in insulin-resistant patients and patients with type 2 diabetes.

Conclusions: Insulin resistance appears to be the primary determinant of the modifications to VLDL subfraction concentrations. Our results suggest a continuum of impaired insulin action on VLDL, ranging from that in healthy persons to that in patients with type 2 diabetes, in which obese patients occupy a transition state. Insulin resistance may also play a role in detrimental modifications to the LDL profile by allowing the development of hypertriglyceridemia.

Key Words: Obesity • NIDDM • type 2 diabetes • VLDL • LDL • atherosclerosis • glucose disposal • hyperinsulinemic clamp • insulin resistance

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