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Submitted on August 24, 2005
Accepted on December 30, 2005
and Glucocorticoid Synergistically Increase Leptin Production in Human Adipose Tissue - Role for p38 MAPK
Dept. of Nutritional Sciences, Rutgers University, Division of Endocrinology, Univ. of Medicine and Dentistry of New Jersey, New Brunswick, NJ; JM-USDA HNRCA, Tufts University, Boston, MA; and Division of Endocrinology, Diabetes and Nutrition, Dept. of Medicine, Univ. of Maryland School of Medicine and Baltimore Veterans Administration Medical Center, Baltimore, MD
* To whom correspondence should be addressed. E-mail: sfried{at}medicine.umaryland.edu.
Context: TNF increases plasma leptin in humans in vivo, but previous studies showed it decreases leptin in vitro.
Objective and participants: To determine the effect of TNF on leptin release from human adipose tissue from healthy subjects undergoing elective surgery or needle aspirations of adipose tissue at a university hospital.
Design: Human omental (Om) and abdominal sc adipose tissue fragments from non-obese and obese subjects were placed in organ culture without or with TNF added in the presence or absence of insulin and/or dexamethasone (dex, a synthetic glucocorticoid) for up to 2 d.
Results: In the absence of hormones, culture with TNF decreased leptin release. In contrast, when added in the presence of dex, TNF increased secreted leptin and leptin mRNA abundance in adipose tissue from non-obese and obese subjects. The TNF+dex stimulated increase in leptin was associated with an increase in p38 MAPK activity, and was totally blocked by p38 MAPK inhibitors. In contrast, inhibition of p38 MAPK only partially blocked the effect of TNF on interleukin-6 production. Culture of obese adipose tissue with either p38 or p44/42 MAPK inhibitors also blunted the spontaneous increase in media leptin that occurred from day 1 to day 2 of culture in Om adipose tissue of obese subjects.
Conclusion: Synergistic effects of increased local or systemic TNF in combination with glucocorticoids may contribute to increased leptin expression in response to stress, including infection and obesity.
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