Nitric oxide mediates down regulation of lipoprotein lipase activity induced by tumor necrosis factor-α in brown adipocytes

Uchida, Yuzo; Tsukahara, Fujiko; Ohba, Ken‐ichi; Irie, Koichiro; Fujii, Emiko; Yoshimoto, Takanobu; Yoshioka, Toshimasa; Muraki, Takamura

doi:10.1016/s0014-2999(97)01181-3

Cited by 31 publications

(23 citation statements)

References 47 publications

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“…From the literature, it seemed possible that the response of LPL to TNF-␣ might involve nitric oxide (38) or a prostaglandin (9). To test this, rats were pretreated with L-NAME (an inhibitor of nitric oxide synthetase) or with indomethacin (an inhibitor of cyclooxygenase).…”

Section: Resultsmentioning

confidence: 99%

Rapid downregulation of adipose tissue lipoprotein lipase activity on food deprivation: evidence that TNF-α is involved

Brouckaert²,

Olivecrona³

2004

American Journal of Physiology-Endocrinology and Metabolism

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When food was removed from young rats in the early morning, adipose tissue tumor necrosis factor (TNF)-␣ activity increased 50% and lipoprotein lipase (LPL) activity decreased 70% in 6 h. There was a strong negative correlation between the TNF-␣ and LPL activities. Exogenous TNF-␣ further decreased LPL activity. Pentoxifylline, known to decrease production of TNF-␣, had no effect on LPL activity in fed rats but almost abolished the rise of TNF-␣ and the decrease of LPL activity in rats deprived of food. The specific activity of LPL decreased from 0.92 mU/ng in fed rats to 0.35 and 0.24 mU/ng in rats deprived of food given saline or TNF-␣, indicating a shift in the LPL molecules toward an inactive state. Lipopolysaccharide increased adipose tissue TNF-␣ and decreased LPL activity. Both of these effects were strongly impeded by pretreatment of the rats with pentoxifylline, or dexamethasone. Pretreatment of the rats with actinomycin D virtually abolished the response of LPL activity to food deprivation or exogenous TNF-␣. We conclude that food deprivation, like lipopolysaccharide, signals via TNF-␣ to a gene whose product causes a rapid shift of newly synthesized LPL molecules toward an inactive form and thereby shuts down extraction of lipoprotein triglycerides by the adipose tissue.

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Section: Resultsmentioning

confidence: 99%

Rapid downregulation of adipose tissue lipoprotein lipase activity on food deprivation: evidence that TNF-α is involved

Brouckaert²,

Olivecrona³

2004

American Journal of Physiology-Endocrinology and Metabolism

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“…59 In brown adipocytes, the down-regulation of LPL activity induced by TNF-a was mediated by nitric oxide (NO). 60 In addition, TNF-a could suppress LPL expression in J774.2 macrophages at the transcriptional level, 61 which might be through tyrosine kinase and the phosphatidylinositol-3 0 -kinase (PI3K) signaling pathways. 62 HSL is an ''old'' enzyme expressed in multiple tissues and plays a number of roles in lipid metabolism.…”

Section: Effects Of Tnf-a On Lipid-metabolism-related Enzymesmentioning

confidence: 99%

TNF‐α, a potent lipid metabolism regulator

Chen

Xun

Chen³

et al. 2009

Cell Biochemistry & Function

190

120

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As a multifunctional cytokine, tumor necrosis factor alpha (TNF-a) exerts a series of biological actions in different cells, tissues, organs, and species and has been demonstrated to regulate and interfere with energy metabolism, especially lipid homeostasis. A large body of researches suggested that the effects of TNF-a on lipid metabolism mainly include five aspects: (1) suppresses free fatty acid (FFA) uptake and promotes lipogenesis; (2) induces lipolysis; (3) inhibits lipid-metabolism-related enzymes activity; (4) regulates cholesterol metabolism; (5) regulates other adipocyte-derived adipokines. The molecular mechanisms underlying these actions are complex and several signal transduction pathways might be involved. Regulation of metabolism-related gene expression at transcriptional and protein levels and impact on enzymes activity might be of importance. Identification and verification of these pathways might provide novel potential strategies and drug targets for dyslipidemia therapy. However, the inconsistent and even conflict conclusions on lipid profile drawn from human subjects after infliximab therapy poses the possibility that the effect of TNF-a on lipid metabolism might be more complicated than it appeared to be.

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“…Whereas increased NO formation may contribute to cold-associated vasodilation in brown adipose tissue in rats (2,9), microdialysis measurements revealed that inhibition of NO synthesis does not influence adipose tissue blood flow in humans (4,10,11). Blocking NO synthesis abolished the cGMP-dependent suppressive effect of tumor necrosis factor-␣ on lipoprotein lipase activity in mouse brown adipocytes (12). In vivo, insulin-stimulated glucose uptake in rat white adipose tissue was dependent on intact NO synthesis (13).…”

mentioning

confidence: 99%

Regulation of the nitric oxide system in human adipose tissue

Engeli

Janke

Gorzelniak

et al. 2004

Journal of Lipid Research

107

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Nitric oxide (NO) is involved in adipose tissuebiology by influencing adipogenesis, insulin-stimulated glucose uptake, and lipolysis. The enzymes responsible for NO formation in adipose cells are endothelial NO synthase (eNOS) and inducible NO synthase (iNOS), whereas neuronal NO synthase (bNOS) is not expressed in adipocytes. We characterized the expression pattern and the influence of adipogenesis, obesity, and weight loss on genes belonging to the NO system in human subcutaneous adipose cells by combining in vivo and in vitro studies. Expression of most of the genes known to belong to the NO system (eNOS, iNOS, subunits of the soluble guanylate cyclase, and both genes encoding cGMP-dependent protein kinases) in human adipose tissue and isolated human adipocytes was detected. In vitro adipogenic differentiation increased the expression level of iNOS significantly, whereas eNOS expression levels were not influenced. The genes encoding eNOS, iNOS, and cGMP-dependent protein kinase 1 were expressed at higher levels in obese women. Expression of these genes, however, was not influenced by 5% weight loss. Insulin and angiotensin II (Ang II) increased NO production by human preadipocytes in vitro.Increased eNOS and iNOS expression in adipocytes and local effects of insulin and Ang II may increase adipose tissue production of NO in obesity. -Engeli, S., J.

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Nitric oxide mediates down regulation of lipoprotein lipase activity induced by tumor necrosis factor-α in brown adipocytes

Cited by 31 publications

References 47 publications

Rapid downregulation of adipose tissue lipoprotein lipase activity on food deprivation: evidence that TNF-α is involved

Rapid downregulation of adipose tissue lipoprotein lipase activity on food deprivation: evidence that TNF-α is involved

TNF‐α, a potent lipid metabolism regulator

Regulation of the nitric oxide system in human adipose tissue

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