Gestational diabetes mellitus (GDM) is a serious pregnancy complication, in which women without previously diagnosed diabetes develop chronic hyperglycemia during gestation. In most cases, this hyperglycemia is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of chronic insulin resistance. Risk factors for GDM include overweight and obesity, advanced maternal age, and a family history or any form of diabetes. Consequences of GDM include increased risk of maternal cardiovascular disease and type 2 diabetes and macrosomia and birth complications in the infant. There is also a longer-term risk of obesity, type 2 diabetes, and cardiovascular disease in the child. GDM affects approximately 16.5% of pregnancies worldwide, and this number is set to increase with the escalating obesity epidemic. While several management strategies exist—including insulin and lifestyle interventions—there is not yet a cure or an efficacious prevention strategy. One reason for this is that the molecular mechanisms underlying GDM are poorly defined. This review discusses what is known about the pathophysiology of GDM, and where there are gaps in the literature that warrant further exploration.

Pancreatic β-cell mass adapts to changing insulin demands in the body. One of the most amazing reversible β-cell adaptations occurs during pregnancy and postpartum conditions. During pregnancy, the increase in maternal insulin resistance is compensated by maternal β-cell hyperplasia and hyperfunctionality to maintain normal blood glucose. Although the cellular mechanisms involved in maternal β-cell expansion have been studied in detail in rodents, human studies are very sparse. A summary of these studies in rodents and humans is described below. Since β-cell mass expands during pregnancy, unraveling the endocrine/paracrine/autocrine molecular mechanisms responsible for these effects can be of great importance for predicting and treating gestational diabetes and for finding new cues that induce β-cell regeneration in diabetes. In addition to the well known implication of lactogens during maternal β-cell expansion, additional participants are being discovered such as serotonin and HGF. Transcription factors, such as hepatocyte nuclear factor-4α and the forkhead box protein-M1, and cell cycle regulators, such as menin, p27 and p18, are important intracellular signals responsible for these effects. In this article, we summarize and discuss novel studies uncovering molecular mechanisms involved in the maternal β-cell adaptive expansion during pregnancy.

Rates of gestational diabetes mellitus (GDM) are on the rise worldwide, and the number of pregnancies impacted by GDM and resulting complications are also increasing. Pregnancy is a period of unique metabolic plasticity, during which mild insulin resistance is a physiological adaptation to prioritize fetal growth. To compensate for this, the pancreatic β-cell utilizes a variety of adaptive mechanisms, including increasing mass, number and insulin-secretory capacity to maintain glucose homeostasis. When insufficient insulin production does not overcome insulin resistance, hyperglycemia can occur. Changes in the maternal system that occur in GDM such as lipotoxicity, inflammation and oxidative stress, as well as impairments in adipokine and placental signalling, are associated with impaired β-cell adaptation. Understanding these pathways, as well as mechanisms of β-cell dysfunction in pregnancy, can identify novel therapeutic targets beyond diet and lifestyle interventions, insulin and antihyperglycemic agents currently used for treating GDM.

Maternal diabetes and overweight or obesity are known to be associated with increased risk of congenital heart defects (CHDs) in offspring, but there are no large studies analyzing outcomes associated with these factors in 1 model.

妊娠期糖尿病与妊娠期甲状腺疾病的发病率均呈上升趋势，且二者均会引起流产、早产、胎盘早剥、子痫、死胎等不良妊娠结局。二者的发病机制尚未明确，研究发现胰岛素抵抗、某些炎性因子、脂肪细胞因子、甲状腺相关抗体参与其发病。近年来二者的关系备受瞩目，若能明确两者间是否存在关联、甲状腺自身抗体是否与妊娠期糖尿病的风险增加有关、早期干预对妊娠结局的影响等，将会对妊娠期糖尿病的早期防治及改善妊娠结局产生重大意义。本文旨在探讨妊娠期糖尿病与妊娠期甲状腺疾病的关系，从而在妊娠早期加强孕妇甲状腺功能及甲状腺自身抗体的检查，及时给予甲状腺激素补充治疗，减少不良妊娠结局。糖尿病，妊娠；甲状腺疾病；胰岛素；胰岛素抵抗；甲状腺自身抗体10.12114/j.issn.1007-9572.2018.00.217

Gestation is accompanied by alterations in the microbial repertoire; however, the mechanisms driving these changes are unknown. Here, we demonstrate a dramatic shift in the gut microbial composition of women and mice during late pregnancy, including an increase in the relative abundance of Bifidobacterium. Using in-vivo-transplanted pellets, we found that progesterone, the principal gestation hormone, affects the microbial community. The effect of progesterone on the richness of several bacteria species, including Bifidobacterium, was also demonstrated in vitro, indicating a direct effect. Altogether, our results delineate a model in which progesterone promotes Bifidobacterium growth during late pregnancy.Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.

Prior studies have shown that Helicobacter pylori (H. Pylori) has the important role in the development of gastrointestinal diseases and diabetes in patients with diabetes. Due to the contradictory results on the prevalence of H. pylori in patients, we carried out a systematic review and meta-analysis to discover the pooled prevalence of H. Pylori in patients with diabetes.A systematic literature search was performed utilizing international databases including Medline (PubMed), Web of sciences, Scopus, EMBASE, Cochrane, Ovid and CINHAL to retrieve all cross-sectional studies which had reported H. pylori prevalence in patients with diabetes between January 1990 and March 2019. The random effects models were applied to calculate the pooled prevalence with 95% confidence interval.A total of 13 articles were selected for meta-analysis according to PRISMA guideline. The pooled prevalence of H. Pylori was obtained 54% (95% CI: 44%-64%) in patients with diabetes. The highest and least prevalence of H. pylori were associated to Africa (66%; 95%CI: 49%-73%) and USA (15%; 95%CI: 8%-26%). In addition, the rapid urease test and biopsy/histology had the most strength in detecting of the H. pylori infection. The meta-regression analysis demonstrated that H. pylori prevalence is not affected by patients' age, publication year, study duration, and HbA1C.Given that the high prevalence of H. pylori in patients with diabetes and its important role in the development of gastrointestinal diseases and diabetes, treatment and eradication of this bacterium should be considered in patients with diabetes.Copyright © 2020 Diabetes India. Published by Elsevier Ltd. All rights reserved.