Regulation of tumour necrosis factor-alpha release from human adipose tissue in vitro

Sewter, CP, Digby, JE, Blows, F, Prins, J and O'Rahilly, S (1999) Regulation of tumour necrosis factor-alpha release from human adipose tissue in vitro. Journal of Endocrinology, 163 1: 33-38. doi:10.1677/joe.0.1630033


Author Sewter, CP
Digby, JE
Blows, F
Prins, J
O'Rahilly, S
Title Regulation of tumour necrosis factor-alpha release from human adipose tissue in vitro
Journal name Journal of Endocrinology   Check publisher's open access policy
ISSN 0022-0795
Publication date 1999-10-01
Year available 1999
Sub-type Article (original research)
DOI 10.1677/joe.0.1630033
Open Access Status
Volume 163
Issue 1
Start page 33
End page 38
Total pages 6
Place of publication BRISTOL
Publisher SOC ENDOCRINOLOGY
Language eng
Abstract Tumour necrosis factor-alpha (TNF-alpha), secreted by cells of the macrophage-monocyte lineage, has a well established role in inflammation and host-defence. The more recent discovery that adipocytes also secrete TNF-alpha has led to a substantial body of research implicating this molecule in the insulin resistance of obesity. However, Little is known about the normal regulation of TNF-alpha release from human adipose tissue. In particular, it is not known whether adipocyte production of TNF-alpha is responsive to similar or different molecular regulators than those relevant to macrophages. TNF-alpha release from cultured human adipose tissue and isolated adipocytes was examined using an ELISA. Insulin, cortisol or the thiazolidinedione, BRL 49653, did not have a significant effect on TNF-alpha release from adipose tissue or isolated adipocytes. In contrast, lipoycalysaccaride (LPS), a major stimulus of TNF-alpha protein production in monocytes and macrophages, resulted in a fivefold stimulation of TNF-alpha release from human adipose tissue. Significant stimulation of TNF-alpha release was also seen from isolated adipocytes, indicating that the increase in TNF-alpha release from adipose tissue in the presence of LPS is unlikely to be entirely attributable to contaminating monocytes or macrophages. Consistent with this observation was the finding that mRNA for CD14, a known cellular receptor for LPS, is expressed in human adipocytes. The increase in TNF-alpha protein release in response to LPS was blocked by an inhibitor of the matrix metalloproteinase responsible for the cleavage of the membrane-bound proform of TNF-alpha, indicating that this release represented regulated secretion and was not due to cell lysis.
Keyword Activated Receptor-Gamma
Insulin-Resistance
Gene-Expression
Lipoprotein-Lipase
3T3-L1 Adipocytes
Thiazolidinediones
Differentiation
Obesity
Cells
Metabolism
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: ResearcherID Downloads - Archived
 
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