Obesity is characterized by an increase in adipose tissue mass. Contrary to the previous view of adipose tissue as simply an inert tissue devoted to energy storage, studies over the past decade have shown that adipose tissue is actively involved in regulating physiological processes and participates in disease. Adipose tissue secretes factors that exert local and systemic effects. Leptin, pro-inflammatory cytokines, resistin and proteins involved in haemodynamic regulation and coagulation are increased in obesity while adiponectin is reduced. The production of active corticosteroids is also increased in obesity. There is now growing evidence that adipocyte secretory factors regulate energy homoeostasis, as well as cardiovascular and immune systems. Some adipocyte hormones, most notably leptin, act in the brain to influence the neuroendocrine axis and energy balance, whereas adiponectin and resistin exert opposing effects on glucose and lipids. Understanding the actions of adipocyte hormones will provide novel insights into the pathophysiology and treatment of obesity.
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February 2006
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Review Article|
January 17 2006
Neuroendocrine and metabolic effects of adipocyte-derived hormones
Malaka B. Jackson;
Malaka B. Jackson
*Division of Endocrinology, University of Pennsylvania School of Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, U.S.A.
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Rexford S. Ahima
†Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, U.S.A.
Correspondence: Dr Rexford S. Ahima (email [email protected]).
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Publisher: Portland Press Ltd
Received:
August 03 2005
Revision Received:
August 18 2005
Accepted:
September 19 2005
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society
2006
Clin Sci (Lond) (2006) 110 (2): 143–152.
Article history
Received:
August 03 2005
Revision Received:
August 18 2005
Accepted:
September 19 2005
Citation
Malaka B. Jackson, Rexford S. Ahima; Neuroendocrine and metabolic effects of adipocyte-derived hormones. Clin Sci (Lond) 1 February 2006; 110 (2): 143–152. doi: https://doi.org/10.1042/CS20050243
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