obesity pandemic: Where have we been and where are we going?

Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheri...

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Bibliographic Details
Published in:	Obesity (Silver Spring, Md.) Vol. 12; no. 90002; pp. 88S - 101S
Main Authors:	Roth, J, Qiang, X, Marban, S.L, Redelt, H, Lowell, B.C
Format:	Journal Article
Language:	English
Published:	Oxford, UK Blackwell Publishing Ltd 01-11-2004
Subjects:	Adipose Tissue - pathology Adipose Tissue - secretion adiposity Aging Body Composition Humans Hydrocortisone - biosynthesis Insulin Resistance Islets of Langerhans Liver Macrophages - pathology Metabolic Syndrome Muscles Obesity - epidemiology Obesity - genetics Obesity - physiopathology Obesity - therapy pandemic Signal Transduction Weight Loss
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Summary:	Obesity, a new pandemic, is associated with an increased risk of death, morbidity, and accelerated aging. The multiple therapeutic modalities used to promote weight loss are outlined with caution, especially for patients who are very young or old. Except for very rare single gene defects, the inheritance of obesity is complex and still poorly understood, despite active investigations. Recent advances that have shed light on the pathophysiology of obesity are the recognition that 1) excess fat is deposited in liver, muscle, and pancreatic islets; 2) fat tissue secretes a large number of active signaling molecules including leptin, adiponectin, and resistin, as well as free fatty acids; and 3) activated macrophages colonize the adipose tissue. Other candidates for key roles in the causes and consequences of obesity include 1) metabolic programming, where food acts as a developmental regulator; 2) the constellation of defects known as the “metabolic syndrome;” 3) cortisol overproduction in the adipose tissue; and especially, 4) insulin resistance. The possible etiologies of insulin resistance include cytokine excess, elevated free fatty acids, and hyperinsulinemia itself, as with transgenic overproduction of insulin in mice.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Feature-3 ObjectType-Review-1
ISSN:	1071-7323 1930-7381 1550-8528 1930-739X
DOI:	10.1038/oby.2004.273