Literature DB >> 12586777

Programming of rat muscle and fat metabolism by in utero overexposure to glucocorticoids.

Mark E Cleasby1, Paul A T Kelly, Brian R Walker, Jonathan R Seckl.   

Abstract

In utero overexposure to glucocorticoids may explain the association between low birth weight and subsequent development of the metabolic syndrome. We previously showed that prenatal dexamethasone (dex) exposure in the rat lowers birth weight and programs adult fasting and postprandial hyperglycemia, associated with increased hepatic gluconeogenesis driven by elevated liver glucocorticoid receptor (GR) expression. This study aimed to determine whether prenatal dex (100 microg/kg per day from embryonic d 15 to embryonic d 21) programs adult GR expression in skeletal muscle and/or adipose tissue and whether this contributes to altered peripheral glucose uptake or metabolism. In utero dex-exposed rats remained lighter until 6 months of age, despite some early catch-up growth. Adults had smaller epididymal fat pads, with a relative increase in muscle size. Although glycogen storage was reduced in quadriceps, 2-deoxyglucose uptake into extensor digitorum longus muscle was increased by 32% (P < 0.05), whereas uptake in other muscles and adipose beds was unaffected by prenatal dex. GR mRNA was not different in most muscles but selectively reduced in soleus (by 23%, P < 0.05). However, GR mRNA was markedly increased specifically in retroperitoneal fat (by 50%, P < 0.02). This was accompanied by a shift from peroxisomal proliferator-activated receptor gamma 1 to gamma 2 expression and a reduction in lipoprotein lipase mRNA (by 28%, P < 0.02). Adipose leptin, uncoupling protein-3 and resistin mRNAs, muscle GLUT-4, and circulating lipids were not affected by prenatal dex. These data suggest that hyperglycemia in 6-month-old rats exposed to dexamethasone in utero is not due to attenuated peripheral glucose disposal. However, increased GR and attenuated fatty acid uptake specifically in visceral adipose are consistent with insulin resistance in this crucial metabolic depot and could indirectly contribute to increased hepatic glucose output.

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Year:  2003        PMID: 12586777     DOI: 10.1210/en.2002-220559

Source DB:  PubMed          Journal:  Endocrinology        ISSN: 0013-7227            Impact factor:   4.736


  29 in total

1.  Novel diagnostics of metabolic dysfunction detected in breath and plasma by selective isotope-assisted labeling.

Authors:  Julia A Haviland; Marco Tonelli; Dermot T Haughey; Warren P Porter; Fariba M Assadi-Porter
Journal:  Metabolism       Date:  2012-02-02       Impact factor: 8.694

2.  Prenatal dexamethasone exposure potentiates diet-induced hepatosteatosis and decreases plasma IGF-I in a sex-specific fashion.

Authors:  David L Carbone; Damian G Zuloaga; Ryoko Hiroi; Chad D Foradori; Marie E Legare; Robert J Handa
Journal:  Endocrinology       Date:  2011-11-08       Impact factor: 4.736

Review 3.  Fetal stress and programming of hypoxic/ischemic-sensitive phenotype in the neonatal brain: mechanisms and possible interventions.

Authors:  Yong Li; Pablo Gonzalez; Lubo Zhang
Journal:  Prog Neurobiol       Date:  2012-05-22       Impact factor: 11.685

4.  Growth and insulin dynamics in two generations of female offspring of mothers receiving a single course of synthetic glucocorticoids.

Authors:  Nathan M Long; Desiree R Shasa; Stephen P Ford; Peter W Nathanielsz
Journal:  Am J Obstet Gynecol       Date:  2012-06-19       Impact factor: 8.661

5.  Exposure to dexamethasone during late gestation causes female-specific decreases in core body temperature and prepro-thyrotropin-releasing hormone expression in the paraventricular nucleus of the hypothalamus in rats.

Authors:  David L Carbone; Damian G Zuloaga; Anthony F Lacagnina; Robert F McGivern; Robert J Handa
Journal:  Physiol Behav       Date:  2012-08-02

6.  Foetal exposure to Panax ginseng extract reverts the effects of prenatal dexamethasone in the synthesis of testosterone by Leydig cells of the adult rat.

Authors:  Maria I Wanderley; Karina L A Saraiva; Juliany S B César Vieira; Christina A Peixoto; Daniel P Udrisar
Journal:  Int J Exp Pathol       Date:  2013-06       Impact factor: 1.925

7.  Glucocorticoids suppress beta-cell development and induce hepatic metaplasia in embryonic pancreas.

Authors:  Chia-Ning Shen; Jonathan R Seckl; Jonathan M W Slack; David Tosh
Journal:  Biochem J       Date:  2003-10-01       Impact factor: 3.857

Review 8.  Role of the hypothalamic-pituitary-adrenal axis in developmental programming of health and disease.

Authors:  Fuxia Xiong; Lubo Zhang
Journal:  Front Neuroendocrinol       Date:  2012-11-27       Impact factor: 8.606

9.  Genetic predisposition to hypertension sensitizes borderline hypertensive rats to the hypertensive effects of prenatal glucocorticoid exposure.

Authors:  Andrea G Bechtold; Kathy Vernon; Tina Hines; Deborah A Scheuer
Journal:  J Physiol       Date:  2007-11-15       Impact factor: 5.182

10.  Prenatal programming of metabolic syndrome in the common marmoset is associated with increased expression of 11beta-hydroxysteroid dehydrogenase type 1.

Authors:  Moffat J Nyirenda; Roderick Carter; Justin I Tang; Annick de Vries; Christina Schlumbohm; Stephen G Hillier; Frank Streit; Michael Oellerich; Victor W Armstrong; Eberhard Fuchs; Jonathan R Seckl
Journal:  Diabetes       Date:  2009-08-31       Impact factor: 9.461

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