Abstract
Background Defects in incretin have been shown to be related to the pathogenesis of type 2 diabetes. Whether such a deficiency happens in gestational diabetes mellitus (GDM) remains to be confirmed. We assessed the association of fasting glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) with GDM. We also studied the longitudinal circulation of these peptides during pregnancy and afterwards. Methods 53 women with GDM (30 managed with diet only (GDM-diet) and 23 treated with insulin (GDM-insulin)) and 43 pregnant women with normal glucose tolerance (NGDM) were studied, with GIP and GLP-1 levels measured at 24–28 weeks (E1), prior (E2) and after (E3) delivery, and postpuerperium (E4). Results Basal GIP was shown to be low in GDM groups compared to NGDM in E1, and in E4 for GDM-diet. GLP-1 was low in GDM groups during pregnancy and afterwards. At E1, serum GIP and GLP-1 were inversely associated with GDM and participants with lower levels of GIP (<0.23 ng/mL) and GLP-1 (<0.38 ng/mL) had a 6 (95% CI 2.5-14.5)- and 7.6 (95% CI 3.0-19.1)-fold higher risk of developing GDM compared with the higher level, respectively. In the postpuerperium, when there is a drop in β-cell function, participants with previous GDM (pGDM) presented lower GLP-1 (in both GDM subgroups) and lower GIP in GDM-diet subgroup compared to controls. Conclusion There is an independent, inverse association between fasting incretins and higher risk of GDM. Furthermore, lowered levels of these peptides may play an important role in the abnormality of glucose regulation following pregnancy.
Highlights
The gastrointestinal tract is the largest endocrine organ in the body, generating hormones that have significant signalling and sensing important roles in regulating body weight and energy expenditure [1]
We evaluated alterations in the basal level of serum glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) levels in women with and without gestational diabetes mellitus (GDM), in an attempt to investigate the role of these peptides in glucose homeostasis during pregnancy and afterwards
Low basal circulating level of incretins is due to rapid degradation by dipeptidyl peptidase-4 (DPP-4) [17]; lower amounts of these peptides are essential for glucoregulation and their consequent inhibitory effect on pancreatic α-cells [17]
Summary
The gastrointestinal tract is the largest endocrine organ in the body, generating hormones that have significant signalling and sensing important roles in regulating body weight and energy expenditure [1]. The physiological importance of islet-derived GLP-1 and GIP in insulin secretion has been previously studied [4], where their contribution to the regulation of β-cell mass is debated in the pathophysiology of type 1 and type 2 diabetes (T1&T2DM) [5, 6]. A study by Amato et al [8] has suggested that fasting incretins play an important role in the pathophysiology of T2DM. Defects in incretin have been shown to be related to the pathogenesis of type 2 diabetes Whether such a deficiency happens in gestational diabetes mellitus (GDM) remains to be confirmed. We assessed the association of fasting glucosedependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) with GDM. Lowered levels of these peptides may play an important role in the abnormality of glucose regulation following pregnancy
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