title: Increased intramyocellular lipid concentration identifies impaired glucose metabolism in women with previous gestational diabetes.
abstract: Women with previous gestational diabetes (pGDM) are frequently insulin-resistant, which could relate to intramyocellular lipid content (IMCL). IMCL were measured with (1)H nuclear magnetic resonance spectroscopy in soleus (IMCL-S) and tibialis-anterior muscles (IMCL-T) of 39 pGDM (32 +/- 2 years, waist-to-hip ratio 0.81 +/- 0.01) and 22 women with normal glucose tolerance (NGT; 31 +/- 1 years, 0.76 +/- 0.02) at 4-6 months after delivery. Body fat mass (BFM) was assessed from bioimpedance analysis, insulin sensitivity index (S(I)), and glucose effectiveness (S(G)) from insulin-modified frequently sampled glucose tolerance tests. pGDM exhibited 45% increased BFM, 35% reduced S(I) and S(G) (P < 0.05), and 40% (P < 0.05) and 55% (P < 0.005) higher IMCL-S and IMCL-T, respectively. IMCL related to body fat (BFM P < 0.005, leptin P < 0.03), but only IMCL-T correlated (P < 0.03) with S(I) and glucose tolerance index independent of BMI. Insulin-resistant pGDM (n = 17) had higher IMCL-S (+66%) and IMCL-T (+86%) than NGT and insulin-sensitive pGDM (+28%). IMCL were also higher (P < 0.005, P = 0.05) in insulin-sensitive pGDM requiring insulin treatment during pregnancy and inversely related to the gestational week of GDM diagnosis. Thus, IMCL-T reflects insulin sensitivity, whereas IMCL-S relates to obesity. IMCL could serve as an additional parameter of increased diabetes risk because it identifies insulin-resistant pGDM and those who were diagnosed earlier and/or required insulin during pregnancy.
authors.affiliation: Department of Internal Medicine III, Division of Endocrinology and Metabolism, University of Vienna, Austria.
authors.forename: Alexandra
authors.initials: A
authors.lastname: Kautzky-Willer
authors.forename: Martin
authors.initials: M
authors.lastname: Krssak
authors.forename: Christine
authors.initials: C
authors.lastname: Winzer
authors.forename: Giovanni
authors.initials: G
authors.lastname: Pacini
authors.forename: Andrea
authors.initials: A
authors.lastname: Tura
authors.forename: Serdar
authors.initials: S
authors.lastname: Farhan
authors.forename: Oswald
authors.initials: O
authors.lastname: Wagner
authors.forename: Georg
authors.initials: G
authors.lastname: Brabant
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Horn
authors.forename: Harald
authors.initials: H
authors.lastname: Stingl
authors.forename: Barbara
authors.initials: B
authors.lastname: Schneider
authors.forename: Werner
authors.initials: W
authors.lastname: Waldhäusl
authors.forename: Michael
authors.initials: M
authors.lastname: Roden
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000378:metabolism*; D001824:Body Constitution; D015992:Body Mass Index; D016640:Diabetes, Gestational / Q000097:blood* / Q000503:physiopathology; D005260:Female; D018149:Glucose Intolerance / Q000097:blood*; D005951:Glucose Tolerance Test; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology*; D020738:Leptin / Q000097:blood; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008279:Magnetic Resonance Imaging; D018482:Muscle, Skeletal / Q000378:metabolism*; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000378:metabolism; D054411:Receptors, Leptin; D012044:Regression Analysis
chemical_list: D001786:Blood Glucose; D020738:Leptin; D008055:Lipids; D011956:Receptors, Cell Surface; D054411:Receptors, Leptin