Progesterone in gestational diabetes mellitus: guilty or not guilty?

  title={Progesterone in gestational diabetes mellitus: guilty or not guilty?},
  author={Dumitru D. Branisteanu and Chantal Mathieu},
  journal={Trends in Endocrinology \& Metabolism},
Steroids and insulin resistance in pregnancy
The role of oestrogens in the adaptation of islets to insulin resistance
It has been demonstrated that E2 acts directly on β–cells to increase insulin biosynthesis and to enhance GSIS through different molecular mechanisms, which suggests E2 may act as a messenger between adipocytes and islets in obesity.
The impact of insulin resistance on proinsulin secretion in pregnancy: hyperproinsulinemia is not a feature of gestational diabetes.
GDM is not independently associated with hyperproinsulinemia as measured by the proinsulin-to-C-peptide ratio, and in pregnant women, increased insulin resistance is associated with decreased pro insulin- to-C -peptid ratio, independently of glucose tolerance status.
Basal insulin requirements after progesterone treatment in a type 1 diabetic pregnant woman.
The present case is the first report to evaluate deterioration of glycemic control induced by progesterone treatment and to determine the dose of insulin required in a type 1 diabetic pregnant woman whose insulin secretion was completely depleted.
Steroids, steroid associated substances and gestational diabetes mellitus.
These substances involve the sulfated Δ5 steroids primarily acting via modulating different ion channels and influencing the development of GDM in different directions, mostly diabetogenic progesterone and predominantly anti-diabetic estradiol acting both in genomic and non-genomic way.
Placental Endocrine Activity: Adaptation and Disruption of Maternal Glucose Metabolism in Pregnancy and the Influence of Fetal Sex
An overview on the adaptation and maladaptation of maternal glucose metabolism by placenta-derived factors is provided, and sex differences in this regulatory network are highlighted.
Vitamins Modulate the Expression of Antioxidant Genes in Progesterone-Treated Pancreatic β Cells: Perspectives for Gestational Diabetes Management
The results suggest that the protein encoded by these genes might protect cells against progesterone induced-oxidative damage, opening perspectives to elucidate the molecular mechanism involved in progester one action in GD, as well as for the development of antioxidant strategies for the prevention and treatment of this disease.
Insulin sensitivity during late gestation in ewes affected by pregnancy toxemia and in ewes with high and low susceptibility to this disorder.
There is reduced pancreatic first-phase insulin response and impaired insulin-dependent inhibition of the ketone body formation during late pregnancy in the HR and PT ewes, which might represent 1 causative factor in the pathogenesis of ovine pregnancy toxemia.
Pathogenesis of Gestational Diabetes Mellitus
Hormonal, inflammatory, and immunologic factors contribute to GDM pathogenesis; suboptimal lifestyle, such as hypercaloric diet, unhealthy nutritional habits, and reduced physical activity, contributes to central obesity, a triggering factor for GDM.
Sulfated Progesterone Metabolites That Enhance Insulin Secretion via TRPM3 Are Reduced in Serum From Women With Gestational Diabetes Mellitus
Epiallopregnanolone sulfate (PM5S) concentrations were reduced in GDM, in women with higher fasting plasma glucose, and in early pregnancy samples from women who subsequently developed GDM with BMI ≥35 kg/m2 (P < 0.05).


Carbohydrate and lipid metabolism in pregnancy: normal compared with gestational diabetes mellitus.
  • N. Butte
  • Medicine, Biology
    The American journal of clinical nutrition
  • 2000
Recent advances in carbohydrate metabolism during pregnancy suggest that preventive measures should be aimed at improving insulin sensitivity in women predisposed to GDM, and further research is needed to elucidate the mechanisms and consequences of alterations in lipid metabolism duringregnancy.
Progesterone receptor knockout mice have an improved glucose homeostasis secondary to β-cell proliferation
An important role of progesterone signaling in insulin release and pancreatic function is demonstrated and it is suggested that it affects the susceptibility to diabetes.
Etiology and pathogenesis of gestational diabetes.
  • C. Kühl
  • Medicine, Biology
    Diabetes care
  • 1998
Hormones that circulate in high concentrations in pregnancy have all been shown, in animal models, to be able to influence beta-cell function and/or the peripheral tissue sensitivity to insulin, but whether they play similar roles in human pregnancy remains to be investigated.
The effects of pregnancy steroids on adaptation of beta cells to pregnancy involve the pancreatic glucose sensor glucokinase.
The results indicate that estradiol and progesterone do not influence significantly glucokinase mRNA expression, while they induce a dose-dependent and time-dependent increase of glucokin enzyme activity in RIN 1046-38 cells.
Regulation of energy balance by leptin.
  • A. Hamann, S. Matthaei
  • Biology
    Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
  • 1996
The current status of the rapidly growing evidence that leptin plays an important role in the regulation of body weight and fat deposition is summarized.
Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats.
The results suggest that, in the last third of pregnancy, B-cell proliferation is no longer stimulated by lactogenic hormones in contrast to the insulin secretory response which is sustained.
Progesterone Inhibits Insulin Secretion by a Membrane Delimited, Non-genomic Action
Progesterone covalently linked to albumin had a similar inhibitory effect as progesterone itself, and it is concluded that the steroid acts at the outer surface of the β-cell plasma membrane.
Gestational diabetes and the incidence of type 2 diabetes: a systematic review.
Differences in rates of progression between ethnic groups was reduced by adjustment for various lengths of follow-up and testing rates, so that women appeared to progress to type 2 diabetes at similar rates after a diagnosis of GDM.
Progesterone stimulates pancreatic cell proliferation in vivo.
It is concluded that progesterone stimulates pancreatic cell proliferation indirectly; gonadal factor(s), not identical to oestradiol, is (are) probably involved.