Vitronectin promotes insulin resistance in trophoblast cells by activating JNK in gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) is a common disorder in the clinic, which may lead to severe detrimental outcomes both for mothers and infants. However, the underlying mechanisms for GDM are still not clear. In the present study, we performed label-free proteomics using placentas from GDM patients and normal controls.

Recent advances of long non-coding RNAs in control of hepatic gluconeogenesis.

Gluconeogenesis is the main process for endogenous glucose production during prolonged fasting, or certain pathological conditions, which occurs primarily in the liver. Hepatic gluconeogenesis is a biochemical process that is finely controlled by hormones such as insulin and glucagon, and it is of great importance for maintaining normal physiological blood glucose levels. Dysregulated gluconeogenesis induced by obesity is often associated with hyperglycemia, hyperinsulinemia, and type 2 diabetes (T2D).

Identification of methylation-driven genes, circulating miRNAs and their potential regulatory mechanisms in gestational diabetes mellitus.

Objective: Gestational diabetes mellitus (GDM) is a major pregnancy complication. The purpose of this study is to investigate the molecular regulatory mechanisms of GDM.

Methods: RNA-seq and methylation data of GDM were retrieved from the Gene Expression Omnibus database.

Decreased expression of programmed death-1 on CD8 effector memory T lymphocytes correlates with the pathogenesis of type 1 diabetes.

Aims: Chronic inflammation of autoimmune diseases, including type 1 diabetes (T1D), is mainly mediated by memory T(Tm) cells, predominantly effector memory T (Tem) cells. The roles of the programmed death-1 (PD-1) receptor on lymphocytes have been well studied in tumor and other infection models. However, little is known about the relationship between the expression of PD-1 on CD8 Tem cells and the pathogenesis of T1D.

The expression of Tim-1 and Tim-4 molecules in regulatory T cells in type 1 diabetes.

Purpose: The TIM family comprises of eight genes in the mouse, three of which are conserved in humans (TIM-1, TIM-3, and TIM-4). Previous studies have revealed the relationships between Tim3 Tregs and autoimmune disease. There was little study about the expression of Tim1 and Tim4 surface molecules on Tregs.