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PMID: 12586777 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

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

Endocrinology ·Vol. 144 ·No. 3 ·2003-03-00 ·Pages 999-1007

Cleasby ME, Kelly PA, Walker BR, Seckl JR

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.

MeSH Terms
Adipose Tissue/anatomy & histology,chemistry,metabolism Animals Birth Weight/drug effects Blood Glucose/analysis Body Weight Deoxyglucose/metabolism Dexamethasone/adverse effects Epididymis Fatty Acids/metabolism Female Glucocorticoids/adverse effects Glucose Transporter Type 4 Glycogen/analysis Hyperglycemia/etiology Insulin Resistance Male Monosaccharide Transport Proteins/analysis Muscle Proteins Muscle, Skeletal/anatomy & histology,chemistry,metabolism Organ Size Pregnancy Prenatal Exposure Delayed Effects RNA, Messenger/analysis Rats Rats, Wistar Receptors, Cytoplasmic and Nuclear/genetics Receptors, Glucocorticoid/genetics Transcription Factors/genetics
Chemicals
Blood Glucose Fatty Acids Glucocorticoids Glucose Transporter Type 4 Monosaccharide Transport Proteins Muscle Proteins RNA, Messenger Receptors, Cytoplasmic and Nuclear Receptors, Glucocorticoid Slc2a4 protein, rat Transcription Factors Dexamethasone Glycogen Deoxyglucose
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Cleasby Mark E
Endocrinology Unit, Department of Medical Sciences, University of Edinburgh, Western General Hospital, Crewe Road South, Edinburgh EH4 2XU, United Kingdom.
Kelly Paul A T
Walker Brian R
Seckl Jonathan R
Article Info
Journal
Endocrinology
Abbr.
Endocrinology
ISSN
0013-7227
Published
2003-03-00
Pages
999-1007
Language
English
Region
United States
NLM ID
0375040
Subset
IM
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