Exp Clin Endocrinol Diabetes 2004; 112(1): 2-9
DOI: 10.1055/s-2004-815719
Review

J. A. Barth Verlag in Georg Thieme Verlag Stuttgart · New York

Hormonal and Nutritional Regulation of Adipose Tissue Mitochondrial Development and Function in the Newborn

A. Mostyn 1 , 2 , S. Pearce 1 , T. Stephenson 1 , M. E. Symonds 1
  • 1Centre for Reproduction and Early Life, Institute of Clinical Research, University Hospital, Nottingham, United Kingdom
  • 2Department of Agricultural Science, Imperial College London (Wye Campus), Wye, Ashford, Kent, United Kingdom
Further Information

Publication History

Received: January 16, 2003 First decision: August 20, 2003

Accepted: October 6, 2003

Publication Date:
03 February 2004 (online)

Abstract

Growth, development, and maturation of adipose tissue in the fetus can determine both survival at birth as well as having longer term consequences for adult disease. The mitochondrial proteins uncoupling protein (UCP) 1, voltage dependent anion channel (VDAC), and cytochrome c have an important role in cellular energy regulation. Activity of these proteins is particularly important during the transition from fetal to neonatal life when cellular energy requirements are at near maximal rates. The regulation of these proteins by endocrine factors is highly complex and may be dependent on both fetal number and maternal nutrition. The cytokine hormones leptin and prolactin have well established functions in energy regulation and lactation respectively. However, recent data proposes a role in regulation of mitochondrial proteins, particularly UCP1, and thermogenesis. Cortisol is an adrenal hormone with a critical role in fetal tissue maturation, especially the lung. It has now been shown to influence the abundance of UCP1 in the fetus, a role that may in part be regulated by the metabolically active thyroid hormone triiodothyronine. A greater understanding of the regulation of mitochondrial proteins within adipose tissue by endocrine and nutritional factors is likely to be important in preventing neonatal morbidity and mortality. It could also add substantially to our understanding of pathological conditions such as obesity and non-insulin dependent diabetes.

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Dr Michael E. Symonds

Academic Division of Child Health, School of Human Development, Queen's Medical Centre, University Hospital

Nottingham, NG7 2UH

United Kingdom

Phone: 441159709257

Fax: 44 11 59 70 93 82

Email: Michael.Symonds@nottingham.ac.uk

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