Involvement of nitric oxide in noradrenaline-induced increase in blood flow through brown adipose tissue

Nagashima, Takahide; Ohinata, Hiroshi; Kuroshima, Akihiro

doi:10.1016/0024-3205(94)00573-7

Cited by 95 publications

(76 citation statements)

References 14 publications

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“…Regarding another major organ of glucose metabolism, previous studies have shown that norepinephrine stimulates iNOS activity and NO release from brown adipose tissue (BAT) (13,14). Recent studies have also corroborated the expression and function of both eNOS and iNOS in BAT (15).…”

Section: Introductionmentioning

confidence: 88%

Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes

Tanaka

Nakatani

Morioka³

et al. 2003

European Journal of Endocrinology

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Objective: It is well known that nitric oxide synthase (NOS) is expressed and that it modulates glucose transport in skeletal muscles. Recent studies have shown that adipose tissues also express inducible and endothelial nitric oxide synthase (eNOS). In the present study, we investigated whether nitric oxide (NO) induces glucose uptake in adipocytes, and the signaling pathway involved in the NOstimulated glucose uptake in 3T3-L1 adipocytes. Methods: First, we determined the expression of eNOS in 3T3-L1 adipocytes, and then these cells were treated with the NO donor sodium nitroprusside (SNP) and/or insulin, and glucose uptake and phosphorylation of insulin receptor substrate (IRS)-1 and Akt were evaluated. Moreover, we examined the effects of a NO scavenger, a guanylate cyclase inhibitor or dexamethasone on SNP-stimulated glucose uptake and GLUT4 translocation.Results: SNP at a concentration of 50 mmol/l increased 2-deoxyglucose uptake (1.8-fold) without phosphorylation of IRS-1 and Akt. Treatment with the NO scavenger or guanylate cyclase inhibitor decreased SNP-stimulated glucose uptake to the basal level. Dexamethasone reduced both insulinand SNP-stimulated glucose uptake with impairment of GLUT4 translocation. Conclusion: NO is capable of stimulating glucose transport through GLUT4 translocation in 3T3-L1 adipocytes, via a mechanism different from the insulin signaling pathway.

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Section: Introductionmentioning

confidence: 88%

Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes

Tanaka

Nakatani

Morioka³

et al. 2003

European Journal of Endocrinology

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“…As depolarization leads to a decrease in the driving force for calcium and thus to a decrease in the cytosolic Ca2+ level (Lee, Nuccitelli & Pappone, 1993), a blockade of the non-selective cation channels by nitric oxide would enable the cell to maintain a high Ca2+ level during adrenergic stimulation. In brown adipose tissue, nitric oxide is apparently released during adrenergic stimulation, although it is not known from which cells in the tissue the nitric oxide is released (Nagashima, Ohinata & Kuroshima, 1994); the brown fat cell itself would, of course, be a candidate. In the intact brown fat cells, the degree of channel blockade would depend on the balance between the amount of nitric oxide present and the redox potential of the cytosol.…”

Section: Mode Of Action Of Nitric Oxidementioning

confidence: 99%

Modulation of calcium‐activated non‐selective cation channel activity by nitric oxide in rat brown adipose tissue.

Koivisto

Nedergaard

1995

The Journal of Physiology

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1. Single-channel calcium-activated non-selective cation currents from isolated rat brown fat cells were measured using the inside-out patch configuration of the patch-clamp technique.The existence of a possible modulatory effect of nitric oxide on the putative redoxmodulatory site located on the intracellular side of the non-selective cation channel was investigated. 2. The nitric oxide-releasing substances nitroglycerin, sodium nitroprusside, S-nitrosocysteine and S-nitroso-N-acetyl-D,L-penicillamine (all at 100 /M) were able to block channel activity almost completely. 3. In each case the blockade was persistent and could not be washed away. Dithiothreitol (DTT, 2 mM) was able to reverse the blockade to a large extent, whereas oxidized DTT (2 mM) was without effect. 4. It was concluded that nitric oxide can modulate non-selective cation channel activity by oxidizing sulfhydryl groups and that this effect can be reversed by reduction.

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“…Lipid accumulation and lipogenic enzymes are also induced by NO in rat white preadipocytes (8). 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).…”

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confidence: 99%

Regulation of the nitric oxide system in human adipose tissue

Engeli

Janke

Gorzelniak

et al. 2004

Journal of Lipid Research

108

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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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Involvement of nitric oxide in noradrenaline-induced increase in blood flow through brown adipose tissue

Cited by 95 publications

References 14 publications

Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes

Nitric oxide stimulates glucose transport through insulin-independent GLUT4 translocation in 3T3-L1 adipocytes

Modulation of calcium‐activated non‐selective cation channel activity by nitric oxide in rat brown adipose tissue.

Regulation of the nitric oxide system in human adipose tissue

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