Long-term Outcome of Body Composition, Ectopic Lipid, and Insulin Resistance Changes With Surgical Treatment of Acromegaly
Open Access
- 21 February 2023
- journal article
- research article
- Published by The Endocrine Society in Journal of the Endocrine Society
- Vol. 7 (5), bvad028
- https://doi.org/10.1210/jendso/bvad028
Abstract
Context Acromegaly presents a unique pattern of lower adiposity and insulin resistance in active disease but reduction in insulin resistance despite a rise in adiposity after surgery. Depot specific adipose tissue masses and ectopic lipid are important predictors of insulin resistance in other populations, but whether they are in acromegaly is unknown. Long-term persistence of body composition changes after surgery is unknown. Objectives To determine how depot-specific body composition and ectopic lipid relate to insulin resistance in active acromegaly and whether their changes with surgery are sustained long-term. Design Cross-sectional study in patients with active acromegaly and longitudinal study in in newly diagnosed patients studied before and in long-term follow up, 3(1-8) years (median, range), after surgery. Patients 71 with active acromegaly studied cross-sectionally and 28 with newly diagnosed acromegaly studied longitudinally. Main Outcome Measures Visceral (VAT), subcutaneous (SAT) and inter-muscular (IMAT) adipose tissue masses by whole-body magnetic resonance imaging (MRI); intrahepatic lipid (IHL) by proton magnetic resonance spectroscopy (1H-MRS), insulin resistance measures derived from fasting and OGTT insulin and glucose levels. Results SAT and IGF-1 level, but not VAT or IHL, were independent predictor of insulin resistance in active acromegaly. VAT, SAT and IHL gains were sustained long-term after surgery. VAT mass rise with surgery correlated inversely with rise in QUICKI while SAT rise correlated with fall in HOMA score. Conclusions SAT and disease activity are important predictors of insulin resistance in active acromegaly. Adiposity gains are sustained long-term after surgical treatment and impact on the accompanying improvement in insulin resistance.Funding Information
- NIH (R01 DK110770, DK064720, UL1 RR024156, UL1 TR000040)
- NCATS
- NIH (P30-DK026687)
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