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Introduction Glucose intolerance during pregnancy, known as gestational diabetes mellitus (GDM), is one of the most common pregnancy complications and affects nearly 17% of all pregnancies globally and ~7% in the United States ( Newbern

( Zhu et al . 2004 ). Both mitochondrial fission-to-fusion imbalance and a reduced overall level of mitochondrial dynamics have been linked with decreased glucose-stimulated insulin secretion in pancreatic beta cells ( Deng et al . 2004 , Anello et

Introduction Glucokinase (GK) is a type IV isoenzyme that belongs to the family of hexokinases (ATP: d -hexose 6-phosphotransferase; EC 2.7.1.1) and catalyzes the formation of glucose 6 phosphate in eukaryotic cells. This

respiration, gluconeogenesis and glucose transport, glycogenolysis, fatty acid oxidation, peroxisomal remodeling, muscle fiber-type switching, and oxidative phosphorylation ( Corona & Duchen 2015 ). As such, PGC-1α is a very attractive target for antidiabetic

Introduction It has been postulated that an increased glucose load in vivo on islet β-cells may participate in disease progression in type 1 and type 2 diabetes ( Weir et al . 1986 , 2009 , Rossetti et al . 1990 , Wilkin 2001 , Chang

Introduction The pancreatic β-cell rapidly releases insulin in response to nutrients, such as amino acids or glucose ( Campbell et al. 1982 ). To ensure the immediate replenishment of insulin within the β-cell, there is a rapid

, they were reported to be slightly glucose intolerant ( Harding et al . 2001 ); however, Wang and coworkers found that Perk +/− mice exhibited enhanced insulin secretion during neonatal and juvenile development, resulting in a transient reduction in

been tested in normal sheep fetuses to evaluate adrenergic inhibition of insulin secretion and insulin action on glucose clearance ( Bassett & Hanson 1998 , Bassett & Hanson 2000 , Chen et al. 2014 , Davis et al. 2020 ). In these experimental

mouse is one of, if not the most commonly used model of metabolic disease and prediabetes as it rapidly and robustly develops obesity, insulin resistance and glucose intolerance ( Surwit et al . 1988 , 1991 , Winzell & Ahren 2004 , Turner et al

-mediated hypothesis posits that nutrient-stimulated insulin release depends on the capacity of nutrients to be metabolized by the β-cell as an energy source. In the adult islet, leucine increases its own oxidative metabolism. Leucine also stimulates glucose metabolism