Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity.

Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Research Abstract Details 

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Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Abstract Text:

Bart M De Taeye,Tatiana Novitskaya,Owen P McGuinness,Linda Gleaves,Mousumi Medda,Joseph W Covington,Douglas E Vaughan,

Obesity is commonly associated with development of insulin resistance and systemic evidence of inflammation. Macrophages contribute to inflammatory amplification in obesity and may contribute directly to insulin resistance and the development of nonalcoholic fatty liver disease through the production of inflammatory cytokines, including tumor necrosis factor (TNF)-alpha. To test this hypothesis, we transplanted male wild-type (WT) and TNF-alpha deficient (KO) mice with either TNF-alpha-sufficient (TNF-alpha(+/+)) or TNF-alpha-deficient (TNF-alpha(-/-)) bone marrow. After consuming a high-fat diet for 26 wk, metabolic and morphometric characteristics of the animals were analyzed. While there were no differences in terms of relative weight gain, body composition analysis yielded a lower relative adipose and higher relative lean mass in mice lacking TNF-alpha, which was partially explained by reduced epididymal fat pad and liver weight. TNF-alpha(-/-) -->KO mice exhibited enhanced insulin sensitivity compared with that observed in TNF-alpha(+/+)-->KO mice; remarkably, no protection against insulin resistance was provided by transplanting TNF-alpha(-/-) bone marrow in WT mice compared with TNF-alpha(+/+)-->WT. The preserved insulin sensitivity seen in TNF-alpha(-/-)-->KO mice provided protection against the development of hepatic steatosis. Taken together, these data indicate that macrophage-derived TNF-alpha contributes to the pattern and extent of fat accumulation and insulin resistance in diet-induced obesity; however, this contribution is negligible in the presence of host-derived TNF-alpha.

Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Publishing Authors By Initials

BM De Taeye,T Novitskaya,OP McGuinness,L Gleaves,M Medda,JW Covington,DE Vaughan,

For similar peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research abstracts see: peptides: intercellular signaling peptides and proteins: cytokines: monokines: tumor necrosis factor-alpha research

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Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Endocrinology and

VOLUME: 293

Page Numbers: E713-25

Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

ISSN: 0193-1849

DAY: 19

MONTH: 06

YEAR: 2007

Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901226

Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Keywords Mesh Terms:

KEYWORDS: Tumor Necrosis Factor-alpha

MESH TERMS: metabolism

Chemical & Substance for Abstract: Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity. Information

Substance Name: Tumor Necrosis Factor-alpha

Registry Number: 0

Grant and Affiliation Information for Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity.

AFFILIATION: Departments of Medicine, Vanderbilt University, Nashville, Tennessee 37232, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: U24 DK-59637

ACRONYM: DK

MEDLINETA: Am J Physiol Endocrinol Metab

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