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Mari van de Vyver

leading to insulin resistance. In response to hyperglycaemia, a metabolic shift causes the excess glucose to enter the polyol pathway in which glucose is reduced to the intermediate product, sorbitol, by aldose reductase in a nicotinamide adenine

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MJ Nyirenda, LA Welberg, and Seckl JR

In a previous study, we showed that exposure of rats to dexamethasone (Dex) selectively in late pregnancy produces permanent induction of hepatic phosphoenolpyruvate carboxykinase (PEPCK) expression and hyperglycaemia in the adult offspring. The mechanisms by which glucocorticoids cause this programming are unclear but may involve direct actions on the fetus/neonate, or glucocorticoids may act indirectly by affecting maternal postnatal nursing behaviour. Using a cross-fostering paradigm, the present data demonstrate that switching the offspring at birth from Dex-treated dams to control dams does not prevent induction of PEPCK or hyperglycaemia. Similarly, offspring born to control dams but reared by Dex-treated dams from birth maintain normal glycaemic control. During the neonatal period, injection of saline per se was sufficient to cause exaggeration in adult offspring responses to an oral glucose load, with no additional effect from Dex. However, postnatal treatment with either saline or Dex did not alter hepatic PEPCK activity. Prenatal Dex permanently raised basal plasma corticosterone levels, but under stress conditions there were no differences in circulating corticosterone levels. Likewise, Dex-exposed rats had similar plasma catecholamine concentrations to control animals. These findings show that glucocorticoids programme hyperglycaemia through mechanisms that operate on the fetus or directly on the neonate, rather than via effects that alter maternal postnatal behaviour during the suckling period. The hyperglycaemic response does not appear to result from abnormal sympathoadrenal activity or hypothalamic-pituitary-adrenal response during stress.

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Anna Krook

). Development of insulin resistance in the context of hypoinsulinaemia and type 1 diabetes has been attributed in part to the hyperglycaemia per se ( Yki-Järvinen et al . 1987 , Rossetti et al . 1990 ), although the molecular mechanisms mediating this

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Hongbin Liu, Anthony E Dear, Lotte B Knudsen, and Richard W Simpson

Introduction Type 2 diabetes is characterized by accelerated atherosclerosis ( Hobb 2006 ). Elevated tumour necrosis factor α (TNF) levels and hyperglycaemia are implicated in diabetes-associated endothelial cell dysfunction and may be causal in

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Antonia Hufnagel, Laura Dearden, Denise S Fernandez-Twinn, and Susan E Ozanne

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

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G Üçkaya, P Delagrange, A Chavanieu, G Grassy, M-F Berthault, A Ktorza, E Cerasi, G Leibowitz, and N Kaiser

diabetes with moderate obesity, insulin resistance, marked hyperglycaemia and hyperlipidaemia ( Kalderon et al. 1986 ). Hyperglycaemia in P. obesus is associated with marked depletion of islet insulin content and increased β-cell apoptosis ( Donath et

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Alex Rafacho, Henrik Ortsäter, Angel Nadal, and Ivan Quesada

effects, including peripheral insulin resistance (IR) and glucose intolerance as well as overt hyperglycaemia and diabetes. These side effects are observed particularly in susceptible individuals such as pregnant women, obese subjects, IR individuals or

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Paul W Caton, Nanda K Nayuni, Julius Kieswich, Noorafza Q Khan, Muhammed M Yaqoob, and Roger Corder

Introduction Prevalence of type 2 diabetes mellitus (T2DM) has increased dramatically over the past four decades. T2DM is characterised by insulin resistance, hyperinsulinaemia and hyperglycaemia. Increased glucose production through abnormally

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Yasushi Kirino, Youichi Sato, Takayuki Kamimoto, Kazuyoshi Kawazoe, Kazuo Minakuchi, and Yutaka Nakahori

4 activity in vivo . Considering these clinical findings, it may be complicated to define the correlation of DPP4 activity to the severity of hyperglycaemia because of the diverse clinical background; therefore, experimental diabetic models with

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Salvatore P Mangiafico, Shueh H Lim, Sandra Neoh, Helene Massinet, Christos N Joannides, Joseph Proietto, Sofianos Andrikopoulos, and Barbara C Fam

) resulting in inappropriately elevated endogenous glucose production (EGP; Lamont et al . 2003 ), will cause glucose intolerance and fasting hyperglycaemia, as observed in T2D ( Consoli et al . 1989 , Nurjhan et al . 1992 , Perriello et al . 1997