Purpose of review: In addition to storing energy, adipose tissue secretes various proteins including leptin, adiponectin, resistin, cytokines, coagulation and vasoactive peptides. The levels of these 'adipokines' are related to adiposity; hence, they could provide molecular mechanisms for diabetes, dyslipidemia, atherosclerosis and other complications of obesity. Recent findings: Leptin inhibits feeding by binding to the long leptin receptor (LRb) in the brain, leading to activation of the JAK-STAT pathway. The leptin signal is terminated through induction of SOCS3 and FTP1B activity. The importance of these molecules has been confirmed in knockout mice. Ablation of LRb or STAT3 in neurons causes hyperphagia, obesity and neuroendoerine deficits, while the loss of SOCS3 or PTP1B prevents obesity. Adiponectin has also attracted attention because it is reduced in obesity and diabetic humans and animals. Treatment with adiponectin improves insulin sensitivity, decreases lipids by enhancing oxidation, and protects against vascular inflammation and atherosclerosis, Adiponectin is increased by thiazolidinediones and likely mediates the antidiabetics effects of these drugs. Resistin exerts an opposite effect to adiponectin by inhibiting insulin action in rodents; however, its role in humans is less certain. Summary: Identification of the key molecular pathways underlying the actions of adipocyte hormones provides new insights into their roles in health and disease. Specific targets of adipocyte hormones could potentially benefit the diagnosis and treatment of obesity and other metabolic diseases.
|Original language||English (US)|
|Number of pages||8|
|Journal||Current Opinion in Endocrinology and Diabetes|
|State||Published - Apr 1 2005|
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism