Faculty Collaboration Database

Metabolomic analysis of adrenal lipids during hypoxia in the neonatal rat: implications in steroidogenesis. Am J Physiol Endocrinol Metab 2004 May;286(5):E697-703

Date

01/08/2004

Pubmed ID

14709419

DOI

10.1152/ajpendo.00502.2003

Scopus ID

2-s2.0-1942422633 (requires institutional sign-in at Scopus site)   15 Citations

Abstract

The nursing rat pup exposed to hypoxia from birth exhibits ACTH-independent increases in corticosterone and renin/ANG II-independent increases in aldosterone. These increases are accompanied by significant elevation of plasma lipid concentrations in the hypoxic neonates. The purpose of the present study was to compare changes in the concentrations of specific fatty acid metabolites and lipid classes in serum and adrenal tissue from normoxic and hypoxic rat pups. We hypothesized that lipid alterations resulting from hypoxia may partly explain increases in steroidogenesis. Rats were exposed to normoxia or hypoxia from birth, and pooled serum and adrenal tissue from 7-day-old pups were subjected to metabolomic analyses. Hypoxia resulted in specific and significant changes in a number of fatty acid metabolites in both serum and the adrenal. Hypoxia increased the concentrations of oleic (18:1 n-9), eicosapentaenoic (EPA; 20:5 n-3), and arachidonic (20:4 n-6) acids in the triacylglyceride fraction of serum and decreased oleic and EPA concentrations in the cholesterol ester fraction. In the adrenal, hypoxia caused an increase in several n-6 fatty acids in the triacylglyceride fraction, including linoleic (18:2 n-6) and arachidonic acid. There was also an increase in the concentration of alpha-linolenic acid (18:3 n-3) in the triacylglyceride fraction of the hypoxic adrenal, along with an increase in linoleic acid concentration in the diacylglyceride fraction. We propose that specific changes in lipid metabolism in the adrenal, as a result of hypoxia, may partly explain the increased steroidogenesis previously observed. The mechanism responsible may involve alterations in cellular signaling and/or mitochondrial function. These cellular changes may be a mechanism by which the neonate can increase circulating adrenal steroids necessary for survival, therefore bypassing a relative insensitivity to normal stimuli.

Author List

Bruder ED, Lee PC, Raff H

Author

Hershel Raff PhD Professor in the Academic Affairs department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Adrenal Glands
Animals
Animals, Newborn
Animals, Suckling
Arachidonic Acid
Eicosapentaenoic Acid
Fatty Acids, Unsaturated
Female
Hypoxia
Linoleic Acids
Male
Oleic Acid
Rats
Rats, Sprague-Dawley
Serum
Steroids