Implication de l'adiponectine dans la physiopathologie du diabete gestationnel

Pregnancy is characterized by a gradual physiologic increase in insulin resistance and a compensatory insulin secretion by pancreatic β cells. Gestational diabetes mellitus (GDM) is an imbalance between insulin resistance and insulin secretion capacity, resulting in maternal hyperglycemia. Several mechanisms for the increased insulin resistance in pregnancy have been proposed to date, including decrease in adiponectin. Adiponectin is an adipokine suspected to have insulin sensitizing and anti-inflammatory properties. In many studies, lower adiponectin levels were strongly associated with higher insulin resistance and increased risk of developing type 2 diabetes. Since GDM and type 2 diabetes share similar etiologic pathways, adiponectin may also be involved in the pathophysiology of GDM. However, studies on the association between adiponectin levels in pregnant women and the risk of GDM are few and contradictory. Thus, the objectives of the study I conducted over the course of my graduate studies were 1) to determine the association between 1 st trimester adiponectin levels and the risk of developing GDM during pregnancy; and 2) to determine the association between 1st and 2nd trimesters plasma adiponectin levels and indices of insulin resistance / sensitivity, as well as β cell function and β cell compensation at 2nd trimester.;Thus, the results of our study suggest that 1) low adiponectin levels at 1st trimester is a reliable marker of increased risk of developing GDM; 2) low adiponectin levels reflect the level of insulin resistance that predispose women to develop GDM, and 3) pregnancy-related increase in insulin resistance is not caused by a change in adiponectin levels, given the negligible change in adiponectin levels between 1st and 2nd trimesters.;Key words: gestational diabetes mellitus, insulin resistance, adiponectin, observational prospective cohort, pregnancy.;We demonstrated that adiponectin levels were lower in women with GDM (n = 38) than in normoglycemic (NG; n = 407) women at 1st and 2nd trimesters of pregnancy. Our analyses also showed that lower 1st trimester adiponectin levels were associated with an increased risk of developing GDM during the 2nd trimester, independently of age, adiposity and glycemic measurements at 1st trimester. In addition, our results showed that 1st and 2 nd trimesters adiponectin levels were inversely associated with insulin resistance at 2nd trimester, regardless of age, adiposity and insulin secretion. Adiponectin levels were not associated with insulin secretion or β cell function at 2nd trimester after adjustment for confounders, but were associated with β cell compensation in face of insulin resistance. Finally, unlike trends suggested by previous reports, our results showed that the change in adiponectin levels between 1 st and 2nd trimesters was not significant, neither in NG nor in GDM women.