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The stress of starvation: glucocorticoid restraint of beta cell development

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  • Biology
  • Ecology
  • Geography
  • Medicine


COMMENTARY The stress of starvation: glucocorticoid restraint of beta cell development L. C. Matthews & N. A. Hanley Received: 27 September 2010 /Accepted: 6 October 2010 /Published online: 12 November 2010 # The Author(s) 2010. This article is published with open access at Abstract Developmental insults during gestation, such as under-nutrition, are known to restrict the number of beta cells that form in the fetal pancreas and are maintained in adulthood, leading to increased risk of type 2 diabetes. There are now substantial data indicating that glucocorticoids mediate this effect of under-nutrition on beta cell mass and that even at physiological levels they restrain fetal beta cell development in utero. There are emerging clues that this occurs downstream of endocrine commitment by neurogenin 3 but prior to terminal beta cell differentiation. Deciphering the precise mechanism will be important as it might unveil new pathways by which to manipulate beta cell mass that could be exploited as novel therapies for patients with diabetes. Keywords Beta cell . Corticosterone . Cortisol . Development . Glucocorticoid . Glucocorticoid receptor . Human . Insulin . Mouse . Neurogenin 3 . Pancreas . Under-nutrition Abbreviations E Embryonic day GC Glucocorticoid GR Glucocorticoid receptor NGN3 Neurogenin 3 The last 20 years have seen marked interest in the hypothesis that environmental insults to the fetus can programme future cardiovascular and metabolic disorders in the offspring [1, 2]. The ‘fetal origins of adult disease’ hypothesis was borne of epidemiological data associating gestational under-nutrition and low birthweight with future conditions, including type 2 diabetes. As adult euglycaemia is dependent on gaining an adequate number of insulin- secreting beta cells (‘beta cell mass’) as well as their subsequent maintenance, mechanistic studies have since queried how such insults might compromise beta cell development within the fetal pancreas [3]. Major

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