Literature DB >> 10648256

Acute hyperinsulinemia and very-low-density and low-density lipoprotein subfractions in obese subjects.

S Bioletto1, A Golay, R Munger, B Kalix, R W James.   

Abstract

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 (&amp;xmacr;: 20%) of large, triacylglycerol-rich VLDL(1) in obese patients but had a minor effect on VLDL(2) and VLDL(3). Placing obese patients into insulin-sensitive and insulin-resistant subgroups revealed distinct effects of the degree of insulin sensitivity on VLDL. VLDL(1) 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 (&amp;xmacr;: 62%; P < 0.01). VLDL(1) concentrations did not change significantly after the clamp in insulin-resistant patients (and patients with type 2 diabetes), whereas VLDL(3) 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.

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Year:  2000        PMID: 10648256     DOI: 10.1093/ajcn/71.2.443

Source DB:  PubMed          Journal:  Am J Clin Nutr        ISSN: 0002-9165            Impact factor:   7.045


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