OBJECTIVE: Women with prior gestational diabetes mellitus (pGDM) are at increased risk of developing type 2 diabetes and associated vasculopathy. Because increased fat mass and inflammatory processes are angiopathic risk factors, the relationship between insulin sensitivity, parameters of subclinical inflammation, and plasma concentrations of adipocytokines was investigated in pGDM both at 3 months and 12 months after delivery. RESEARCH DESIGN AND METHODS: Insulin sensitivity (through a frequently sampled intravenous glucose tolerance test) and plasma concentrations of ultrasensitive C-reactive protein (CRP), adiponectin, plasminogen activator inhibitor (PAI)-1, tumor necrosis factor-alpha, leptin, and interleukin-6 were measured in 89 pGDM (BMI 26.9 +/- 0.5 kg/m(2), age 32 +/- 0.5 years) and in 19 women with normal glucose tolerance during pregnancy (NGT) (23.7 +/- 0.9 kg/m(2), 31 +/- 1.3 years). RESULTS: pGDM showed lower (P < 0.0001) plasma adiponectin (6.7 +/- 0.2 microg/ml) than NGT (9.8 +/- 0.6 microg/ml) and a decreased (P < 0.003) insulin sensitivity index (S(i)) and disposition index (P < 0.03), but increased plasma leptin (P < 0.003), PAI-1 (P < 0.002), and CRP (P < 0.03). After adjustment for body fat mass, plasma adiponectin remained lower in pGDM (P < 0.004) and correlated positively with S(i) (P < 0.003) and HDL cholesterol (P < 0.0001) but negatively with plasma glucose (2-h oral glucose tolerance test [OGTT]) (P < 0.0001), leptin (P < 0.01), CRP (P < 0.007), and PAI-1 (P < 0.0001). On regression analysis, only HDL cholesterol, postload (2-h OGTT) plasma glucose, and S(i) remained significant predictors of plasma adiponectin, explaining 42% of its variability. Of note, adiponectin further decreased (P < 0.05) only in insulin-resistant pGDM despite unchanged body fat content and distribution after a 1-year follow-up. CONCLUSIONS: Lower plasma adiponectin concentrations characterize women with previous GDM independently of the prevailing insulin sensitivity or the degree of obesity and are associated with subclinical inflammation and atherogenic parameters.
OBJECTIVE:Women with prior gestational diabetes mellitus (pGDM) are at increased risk of developing type 2 diabetes and associated vasculopathy. Because increased fat mass and inflammatory processes are angiopathic risk factors, the relationship between insulin sensitivity, parameters of subclinical inflammation, and plasma concentrations of adipocytokines was investigated in pGDM both at 3 months and 12 months after delivery. RESEARCH DESIGN AND METHODS: Insulin sensitivity (through a frequently sampled intravenous glucose tolerance test) and plasma concentrations of ultrasensitive C-reactive protein (CRP), adiponectin, plasminogen activator inhibitor (PAI)-1, tumor necrosis factor-alpha, leptin, and interleukin-6 were measured in 89 pGDM (BMI 26.9 +/- 0.5 kg/m(2), age 32 +/- 0.5 years) and in 19 women with normal glucose tolerance during pregnancy (NGT) (23.7 +/- 0.9 kg/m(2), 31 +/- 1.3 years). RESULTS: pGDM showed lower (P < 0.0001) plasma adiponectin (6.7 +/- 0.2 microg/ml) than NGT (9.8 +/- 0.6 microg/ml) and a decreased (P < 0.003) insulin sensitivity index (S(i)) and disposition index (P < 0.03), but increased plasma leptin (P < 0.003), PAI-1 (P < 0.002), and CRP (P < 0.03). After adjustment for body fat mass, plasma adiponectin remained lower in pGDM (P < 0.004) and correlated positively with S(i) (P < 0.003) and HDL cholesterol (P < 0.0001) but negatively with plasma glucose (2-h oral glucose tolerance test [OGTT]) (P < 0.0001), leptin (P < 0.01), CRP (P < 0.007), and PAI-1 (P < 0.0001). On regression analysis, only HDL cholesterol, postload (2-h OGTT) plasma glucose, and S(i) remained significant predictors of plasma adiponectin, explaining 42% of its variability. Of note, adiponectin further decreased (P < 0.05) only in insulin-resistant pGDM despite unchanged body fat content and distribution after a 1-year follow-up. CONCLUSIONS: Lower plasma adiponectin concentrations characterize women with previous GDM independently of the prevailing insulin sensitivity or the degree of obesity and are associated with subclinical inflammation and atherogenic parameters.
Authors: S Bo; A Signorile; G Menato; R Gambino; C Bardelli; M L Gallo; M Cassader; M Massobrio; G F Pagano Journal: J Endocrinol Invest Date: 2005-10 Impact factor: 4.256
Authors: Vasilis Z Marmarelis; Dae C Shin; Yaping Zhang; Alexandra Kautzky-Willer; Giovanni Pacini; David Z D'Argenio Journal: J Diabetes Sci Technol Date: 2013-07-01
Authors: C Kim; C A Christophi; R B Goldberg; L Perreault; D Dabelea; S M Marcovina; X Pi-Sunyer; E Barrett-Connor Journal: Diabet Med Date: 2015-05-29 Impact factor: 4.359
Authors: A Tranidou; T Dagklis; I Tsakiridis; A Siargkas; A Apostolopoulou; A Mamopoulos; D G Goulis; M Chourdakis Journal: J Endocrinol Invest Date: 2020-11-23 Impact factor: 4.256
Authors: Erica P Gunderson; Catherine Kim; Charles P Quesenberry; Santica Marcovina; David Walton; Robert A Azevedo; Gary Fox; Cathie Elmasian; Stephen Young; Nora Salvador; Michael Lum; Yvonne Crites; Joan C Lo; Xian Ning; Kathryn G Dewey Journal: Metabolism Date: 2014-04-13 Impact factor: 8.694
Authors: Andrew S Bomback; Yelena Rekhtman; Adam T Whaley-Connell; Abhijit V Kshirsagar; James R Sowers; Shu-Cheng Chen; Suying Li; Kavitha M Chinnaiyan; George L Bakris; Peter A McCullough Journal: Diabetes Care Date: 2010-08-31 Impact factor: 19.112
Authors: Zhong Q Wang; Xian H Zhang; Yongmei Yu; Russell C Tipton; Ilya Raskin; David Ribnicky; William Johnson; William T Cefalu Journal: Metabolism Date: 2013-05-21 Impact factor: 8.694