Insulin Secretion and Incretin Hormone Concentration in Women with Previous Gestational Diabetes Mellitus

Abstract

BackgroundWe examined the change in the levels of incretin hormone and effects of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) on insulin secretion in women with previous gestational diabetes (pGDM).MethodsA 75-g oral glucose tolerance test (OGTT) was conducted on 34 women with pGDM. In addition, 11 women with normal glucose tolerance, matched for age, height and weight, were also tested. The insulin, GIP, GLP-1, and glucagon concentrations were measured, and their anthropometric and biochemical markers were also measured.ResultsAmong 34 women with pGDM, 18 had normal glucose tolerance, 13 had impaired glucose tolerance (IGT) and 1 had diabetes. No significant differences were found in GLP-1 concentration between the pGDM and control group. However, a significantly high level of glucagon was present in the pGDM group at 30 minutes into the OGTT. The GIP concentration was elevated at 30 minutes and 60 minutes in the pGDM group. With the exception of the 30-minute timepoint, women with IGT had significantly high blood glucose from 0 to 120 minutes. However, there was no significant difference in insulin or GLP-1 concentration. The GIP level was significantly high from 0 to 90 minutes in patients diagnosed with IGT.ConclusionGLP-1 secretion does not differ between pGDM patients and normal women. GIP was elevated, but that does not seem to induce in increase in insulin secretion. Therefore, we conclude that other factors such as heredity and environment play important roles in the development of type 2 diabetes.

Reduced postprandial GLP‐1 responses in women with gestational diabetes mellitus

“…The elevated postprandial GIP responses observed in the patients with GDM volunteering in the present study (during TT as well as during PP), is consistent with previous findings of higher GIP levels in women with previous GDM [33], and could represent an early consequence of disturbed glucose homeostasis. Thus, increased postprandial response of GIP (by some perceived as a 'diabetogenic' hormone -perhaps acting via glucagonotropic signalling [9][10][11]) could, perhaps, contribute to the increased susceptibility to development of type 2 diabetes among GDM patients.…”

Association of GLP-1 secretion with parameters of glycemic control in women after gestational diabetes mellitus

“…In line with our findings, decreased GLP-1 secretion during OGTT and lower second-phase GLP-1/glucose ratios were observed in post-GDM normoglycemic women9 and in post-GDM women who had developed pre-diabetes 15. In a smaller study, a preserved GLP-1 response to oral glucose was described in normoglycemic women after GDM 13. These discrepancies may be explained by differences in the phenotype of study participants, for example, the degree of obesity and insulin resistance, the average time after the index pregnancy (2–3 months to several years), and the assays used to measure total or intact GLP-1 plasma concentration.…”

“…Controversial results were also reported postpartum. A slightly reduced GLP-1 response to oral glucose load was observed in normoglycemic post-GDM women,9 12 whereas other studies showed no difference13 14 or detected decreased GLP-1 secretion in post-GDM women having developed a pre-diabetic metabolic state 15…”

Increased Pro-Inflammatory T Cells, Senescent T Cells, and Immune-Check Point Molecules in the Placentas of Patients With Gestational Diabetes Mellitus

“… 1 2 GDM can cause various perinatal and fetal complications, such as preeclampsia, macrosomia, and fetal distress, and affects the short- or long-term risk of type 2 diabetes and cardiovascular disease of the mother even after delivery. 2 3 4 5 In normal pregnancy conditions, insulin resistance increases according to fetal growth, and the beta cells of the pancreas promote cell proliferation and secrete more insulin in response to the insulin requirement. GDM is characterized by the inability of pancreatic beta cells to respond adequately to increased insulin resistance, resulting in hyperglycemia of various degrees.…”