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impairments such as T2D after a GDM-complicated pregnancy ( Dickens & Thomas 2019 ). Maternal obesity and GDM are closely intertwined, with both characterised by metabolic derangements such as hyperglycaemia, inflammation, hyperinsulinaemia, hyperleptinaemia

sheep, hypoinsulinaemia induced either by pancreas removal or streptozocin treatment is associated with hyperglycaemia and decreases in umbilical glucose uptake (both absolute and relative to fetal body weight), fetal glucose utilization and the fraction

Introduction It has been well established that abnormal elevation in circulating glucagon leads to an increase in hepatic glucose production and glycogen metabolism that contribute to hyperglycaemia in diabetes ( Unger 1978 ). For this reason

hyperglycaemia or glucose intolerance. Furthermore, differences concerning disease severity and therapy response can be observed ( Fajans & Bell 2011 , Bansal et al. 2017 , Hattersley & Patel 2017 , Owen 2018 ). Interestingly, phenotypic heterogeneity is

adults with tissue-specific alterations to Gr mRNA expression, including t is associated in adults with tissue-specific alterations he liver, leading to hepatic expression of the gluconeogenic enzyme pepck and hyperglycaemia. Although blood glucose

is affected by hyperglycaemia in pregnancy, most of those due to GDM ( International Diabetes Federation 2017 ). GDM is associated with neonatal adverse outcomes such as large for gestational age infants and increased risk of obesity and

steatosis was more marked in the ob/ob mice, whereas the activity of 5β-reductase was increased to a greater extent in db/db mice. The db/db mice demonstrated partial insulin deficiency, and progression towards hyperglycaemia, whereas the ob/ob mice

Introduction Type 2 diabetes, characterised by hyperglycaemia in the context of insulin resistance, is one of the most common metabolic diseases in the world. Insulin production from pancreatic β-cells plays a vital role in maintaining the

. 2001 ). Although programmed increases in the expression of key hepatic gluconeogenic enzymes may later underpin hyperglycaemia ( Nyirenda et al . 1998 , 2001 ), little is known of the mechanisms by which glucocorticoids ‘programme’ higher blood

Holmes MC Burchell A Houston PM Scholl D Jamieson PM Best R Brown RW Edwards CRW Seckl JR 1997 11β-Hydroxysteroid dehydrogenase type 1 knockout mice show attenuated glucocorticoid inducible responses and resist hyperglycaemia on