Document Detail

Pregnancy induces molecular alterations reflecting impaired insulin control over glucose oxidative pathways that only in women with a family history of Type 2 diabetes last beyond pregnancy.
MedLine Citation:
PMID:  19337007     Owner:  NLM     Status:  MEDLINE    
In circulating lymphomonocytes (CLM) of patients with Type 2 diabetes (DM2) pyruvate dehydrogenase (PDH), the major determinant of glucose oxidative breakdown, is affected by a cohort of alterations reflecting impaired insulin stimulated glucose utilization. The cohort is also expressed, although incompletely, in 40% of healthy young subjects with a DM2-family history (FH). Pregnancy restrains glucose utilization in maternal peripheral tissues to satisfy fetal requirements. Here we explore whether pregnant women develop the PDH alterations and, if so, whether there are differences between women with and without FH (FH+, FH-). Ten FH+ and 10 FH- were evaluated during pregnancy (12-14, 24-26, and 37-39 weeks) and 1 yr after (follow-up) for fasting plasma glucose and insulin as well as body mass index (BMI), and for the PDH alterations. Twenty FH- and 20 FH+ non-pregnant women served as controls. All FH+ and FH- controls exhibited normal clinical parameters and 8 FH+ had an incomplete cohort of PDH alterations. In FH- and FH+ pregnant women at 12-14 weeks clinical parameters were normal; from 24-26 weeks, with unvaried glucose, insulin and BMI rose more in FH- and only in the latter recovered the 12-14 weeks values at follow-up. In all FH-, the cohort of PDH alterations was incomplete at 24-26 weeks, complete at 37-39 weeks, and absent at follow-up but complete from 12-14 weeks including follow-up in all FH+. In FH-, the cohort is an acquired trait restricted to pregnancy signaling transiently reduced insulin-stimulated glucose utilization; in FH+, instead, it unveils the existence of an inherited DM2-related background these women all have, that is awakened by pregnancy and as such lastingly impairs insulin-stimulated glucose utilization.
M Piccinini; M Mostert; M A Seardo; S Bussolino; G Alberto; E Lupino; C Ramondetti; B Buccinnà; M T Rinaudo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of endocrinological investigation     Volume:  32     ISSN:  1720-8386     ISO Abbreviation:  J. Endocrinol. Invest.     Publication Date:  2009 Jan 
Date Detail:
Created Date:  2009-04-01     Completed Date:  2009-07-17     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7806594     Medline TA:  J Endocrinol Invest     Country:  Italy    
Other Details:
Languages:  eng     Pagination:  6-12     Citation Subset:  IM    
Department of Medicine and Experimental Oncology-Section of Biochemistry, University of Turin, 10126 Turin, Italy.
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MeSH Terms
Blood Glucose / metabolism*
Diabetes Mellitus, Type 2 / blood*,  genetics
Insulin / blood*
Insulin Resistance / physiology
Monocytes / metabolism
Pregnancy in Diabetics / genetics,  metabolism*
Pyruvate Dehydrogenase Complex / metabolism*
Reg. No./Substance:
0/Blood Glucose; 0/Pyruvate Dehydrogenase Complex; 11061-68-0/Insulin

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