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Decreased variation of inflammatory markers in gestational diabetes
Author(s) -
PöyhönenAlho Maritta,
Ebeling P.,
Saarinen A.,
Kaaja R.
Publication year - 2011
Publication title -
diabetes/metabolism research and reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.307
H-Index - 110
eISSN - 1520-7560
pISSN - 1520-7552
DOI - 10.1002/dmrr.1170
Subject(s) - endocrinology , medicine , gestational diabetes , diabetes mellitus , type 2 diabetes , serum amyloid a , insulin resistance , insulin , gestation , inflammation , pregnancy , biology , genetics
Background Gestational diabetes is a prediabetic state. Sub‐clinical inflammation may play a role in the transition from gestational diabetes to type 2 diabetes; the role of the autonomic nervous system as a mediating system has been raised. We aimed to study the association of the sympathetic nervous system and sub‐clinical inflammation in women with gestational diabetes. Methods We studied 41 Caucasian women with gestational diabetes and 22 healthy pregnant and 14 non‐pregnant controls. We assayed plasma noradrenaline, insulin, C‐reactive protein, interleukin‐6, insulin growth factor‐1, serum amyloid A, steroid hormone‐binding globulin, α‐1 acid glycoprotein and cortisol at 2400, 0400 and 0700 h. Results No differences existed in the concentrations of inflammatory markers between gestational diabetes and normal pregnancy but women with gestational diabetes showed loss of variation in C‐reactive protein and serum amyloid A. Levels of hormone‐binding globulin were lower in hypertensive compared with normotensive women with gestational diabetes at all time points and lowest at midnight when α‐1 acid glycoprotein levels were higher in hypertensive women. Conclusions Gestational diabetes is associated with loss of natural variation of C‐reactive protein and serum amyloid A, suggesting altered modulation of inflammation. Hypertension in gestational diabetes seems not to be associated with higher levels of inflammatory markers other than α‐1 acid glycoprotein. Copyright © 2011 John Wiley & Sons, Ltd.