Mitochondrial dysfunction in obesity : Current Opinion in Endocrinology, Diabetes and Obesity (original) (raw)
Obesity and nutrition: Edited by Caroline M. Apovian and Jeffrey I. Mechanick
aDepartments of Molecular and Human Genetics
bPediatrics, Baylor College of Medicine
cTexas Children's Hospital, Houston, Texas, USA
Correspondence to Chester W. Brown, MD, PhD, Associate Professor, Departments of Molecular and Human Genetics and Pediatrics, Baylor College of Medicine, BCM 225, Room R717, One Baylor Plaza, Houston, TX 77030, USA Tel: +1 713 798 3994; fax: +1 713 798 7418;.e-mail: [email protected]
Current Opinion in Endocrinology, Diabetes and Obesity 17(5):p 446-452, October 2010. | DOI: 10.1097/MED.0b013e32833c3026
Abstract
Purpose of review
The review highlights recent findings regarding the functions of mitochondria in adipocytes, providing an understanding of their central roles in regulating substrate metabolism, energy expenditure, disposal of reactive oxygen species (ROS), and in the pathophysiology of obesity and insulin resistance, as well as roles in the mechanisms that affect adipogenesis and mature adipocyte function.
Recent findings
Nutrient excess leads to mitochondrial dysfunction, which in turn leads to obesity-related pathologies, in part due to the harmful effects of ROS. The recent recognition of ‘ectopic’ brown adipose in humans suggests that this tissue may play an underappreciated role in the control of energy expenditure. Transcription factors, PGC-1α and PRDM16, which regulate brown adipogenesis, and members of the TGF-β superfamily that modulate this process may be important new targets for antiobesity drugs.
Summary
Mitochondria play central roles in ATP production, energy expenditure, and disposal of ROS. Excessive energy substrates lead to mitochondrial dysfunction with consequential effects on lipid and glucose metabolism. Adipocytes help to maintain the appropriate balance between energy storage and expenditure and maintaining this balance requires normal mitochondrial function. Many adipokines, including members of the TGF-β superfamily, and transcriptional coactivators, PGC-1α and PRDM16, are important regulators of this process.
© 2010 Lippincott Williams & Wilkins, Inc.