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A history of previous gestational diabetes mellitus is associated with adverse changes in insulin secretion and VLDL metabolism independently of increased intrahepatocellular lipid

Author(s): S. Forbes, I. F. Godsland, S. D. Taylor-Robinson, J. D. Bell, E. L. Thomas, N. Patel, G. Hamilton, K. H. Parker, I. Marshall, C. D. Gray, D. Bedford, M. Caslake, B. R. Walker, D. G. Johnston

Abstract:
We have previously reported a high prevalence of non-alcoholic fatty liver disease (NAFLD) among women with previous gestational diabetes mellitus (pGDM). We wanted to confirm that intrahepatocellular lipid (IHCL) is associated with pGDM independently of adiposity and determine: (1) if VLDL metabolism is dysregulated; and (2) the extent to which NAFLD and IHCL account for the dysmetabolic phenotype in pGDM. We analysed data from a cohort of 234 women (114 with pGDM) and identified effects of pGDM on lipid and glucoregulation that were independent of ultrasound-diagnosed NAFLD. We then measured IHCL by MR spectroscopy in a representative subgroup (n = 36) and conducted detailed metabolic studies (IVGTT, VLDL apolipoprotein B [apoB] kinetics and palmitate turnover) and measurement of regional body fat by MRI to demonstrate effects of IHCL that were independent of a history of pGDM. pGDM was associated with increased IHCL (p = 0.04) after adjustment for adiposity. Independently of IHCL, pGDM was associated with a lower IVGTT disposition index (p = 0.02) and acute insulin response to glucose (pGDM+/NAFLD-, 50% lower; pGDM+/NAFLD+, 36% lower; effect of pGDM, p = 0.03), increased VLDL apoB pool size (pGDM+/NAFLD-, 3.1-fold higher; pGDM+/NAFLD+, 1.2-fold higher; effect of pGDM, p = 0.02) and, at borderline significance (p = 0.05), increased rate of VLDL apoB synthesis. pGDM is associated with increased IHCL independently of adiposity. The increased liver fat contributes to the phenotype, but pGDM status is independently associated with diminished insulin secretion and (shown for the first time) augmented VLDL metabolism. IHCL with pGDM may compound a dysmetabolic phenotype.

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ISBN: 0012-186X
Publication Year: 2013
Periodical: Diabetologia
Periodical Number: 9
Volume: 56
Pages: 2021-2033
Author Address: Forbes, S Univ Edinburgh, Queens Med Res Inst, Univ BHF Ctr Cardiovasc Sci, Endocrinol Unit, 47 Little France Crescent, Edinburgh EH16 4TJ, Midlothian, Scotland Univ Edinburgh, Queens Med Res Inst, Univ BHF Ctr Cardiovasc Sci, Endocrinol Unit, Edinburgh EH16 4TJ, Midlothian, Scotland Univ London Imperial Coll Sci Technol & Med, Dept Med, Div Diabet Endocrinol & Metab, London, England Univ London Imperial Coll Sci Technol & Med, MRC Clin Sci Inst, Imaging Sci Dept, London, England Univ London Imperial Coll Sci Technol & Med, Dept Bioengn, London, England Univ Edinburgh, Ctr Clin Brain Sci, Edinburgh EH16 4TJ, Midlothian, Scotland Univ Edinburgh, Queens Med Res Inst, Clin Res Imaging Ctr, Edinburgh EH16 4TJ, Midlothian, Scotland Univ Glasgow, Inst Cardiovasc & Med Sci, Glasgow, Lanark, Scotland