Abstract
Insulin resistance of glucose utilization is fully restored following BMI normalization after bariatric surgery. We investigated if this also pertains to insulin-induced effects on fatty acid handling. Forty-three women with obesity (OB) were investigated before and 2 years after Roux-en-Y gastric by-pass when BMI was <30 kg/m2 (PO) and compared with 26 never obese women (NO). The Adipo-IR index was used as measure of insulin antilipolytic sensitivity. Changes (delta) in circulating glycerol and fatty acid levels during hyperinsulinemic euglycemic clamp represented the insulin maximum antilipolytic effect. Overall fatty acid utilization was reflected by delta fatty acids minus 3 × delta glycerol. Adipo-IR was higher in OB than in NO and PO (p < 0.0001), the latter two groups having similar values. Insulin lowered glycerol levels by about 70% in all groups, but delta glycerol was 30% larger in PO than in NO (p = 0.04). Delta adds and adds utilization were similar in all groups. We conclude that women with obesity, whose BMI is normalized after bariatric surgery, have improved maximum in vivo antilipolytic effect of insulin above expected in absolute but not relative terms as regards glycerol changes, while the handling of circulating fatty acids is changed to the normal state.
Highlights
Insulin inhibits lipolysis in fat cells through spare receptors [1]
Whether the same pertains to antilipolysis and/or fatty acid utilization is unknown reduction of BMI from about 43 to 32 kg/m2 normalized the antilipolytic effect of insulin in vitro [5]
Adipose insulin resistance may develop before other metabolic alterations and directly contribute to impaired insulin action in state during the last hour of clamp as for glucose disposal rate
Summary
Insulin inhibits lipolysis in fat cells through spare receptors [1]. Adipose insulin resistance at early signal steps is mirrored by the half maximum effective concentration (insulin sensitivity), while resistance at distal steps at very high hormone concentrations reflects maximum action (responsiveness). Subjects with obesity or overweight display decreased sensitivity but normal responsiveness for the antilipolytic effect in fat cells [2]. Insulin resistance may involve additional fatty acid metabolic events [3]. In post-obesity, in vivo insulin-induced glucose metabolism is completely normalized [4]. Whether the same pertains to antilipolysis and/or fatty acid utilization is unknown reduction of BMI from about 43 to 32 kg/m2 normalized the antilipolytic effect of insulin in vitro [5]
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