A nitric oxide‐mediated mechanism regulates lipolysis in human adipose tissue <i>in vivo</i>

Andersson, Kurt; Gaudiot, Nicolas; Ribière, Catherine; Elizalde, Montserrat; Giudicelli, Yves; Arner, Peter

doi:10.1038/sj.bjp.0702430

Cited by 106 publications

(103 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…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).…”

mentioning

confidence: 99%

“…Enzymes responsible for NO formation by rat and human adipose cells are the membrane-bound endothelial NO synthase (eNOS) and the cytoplasmically localized inducible NO synthase (iNOS) (2)(3)(4)(5)(6). In vitro, NO inhibits proliferation and stimulates the expression of two adipogenic marker genes, peroxisome proliferator-activated receptor ␥ and uncoupling protein 1, in rat brown preadipocytes (7).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Regulation of the nitric oxide system in human adipose tissue

Engeli

Janke

Gorzelniak

et al. 2004

Journal of Lipid Research

108

View full text Add to dashboard Cite

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.

show abstract

mentioning

confidence: 99%

mentioning

confidence: 99%

Regulation of the nitric oxide system in human adipose tissue

Engeli

Janke

Gorzelniak

et al. 2004

Journal of Lipid Research

108

View full text Add to dashboard Cite

show abstract

“…12 In concert with the blood flow regulation in many other tissues, nitric oxide (NO) could be a major vasodilator in adipose tissue, or possibly a direct or indirect mediator of insulin vasodilatation. 14 However, N G -monomethyl-Larginine (L-NMMA), an NO synthase inhibitor, did not seem to alter local ATBF 15 and attenuated the isoproterenolinduced vasodilatation 16 only during adipose tissue microdi-alysis. These measurements were made by use of the ethanol outflow/inflow ratio, which has an inherently low sensitivity.…”

mentioning

confidence: 99%

Nitric Oxide and β-Adrenergic Stimulation Are Major Regulators of Preprandial and Postprandial Subcutaneous Adipose Tissue Blood Flow in Humans

et al. 2004

View full text Add to dashboard Cite

Background-Blood flow mediates the metabolic and endocrine roles of adipose tissue. We have previously shown that the postprandial adipose tissue blood flow (ATBF) increase is dependent on insulin sensitivity. However, subcutaneous local insulin delivery had no demonstrable effect on either preprandial or postprandial ATBF. We hypothesized that insulin may act indirectly via sympathetic activation, mainly in the postprandial period, and that nitric oxide may be an overall major regulator of subcutaneous ATBF. Methods and Results-We investigated the endogenous preprandial and postprandial regulation of ATBF by applying local tissue blockade of ␤-adrenergic (propranolol), ␣-adrenergic (phentolamine and yohimbine), and nitric oxide (N G -monomethyl-L-arginine, L-NMMA) regulation of blood flow. Healthy subjects (body mass index, 18 to 31 kg/m 2 ) were challenged with 75 g glucose for endogenous stimulation of ATBF. We used the novel "microinfusion" technique, which allows for simultaneous local delivery of pharmacological agents (or contralateral saline) and measurement of ATBF with the 133 Xe washout method. Compared with control, the preprandial ATBF was not affected by propranolol but was increased by 21% (PϽ0.013) and 15% (Pϭ0.004) with phentolamine and yohimbine, respectively. A decrease of 42% (2.97Ϯ0.33 versus 4.75Ϯ0.47 mL · min Ϫ1 · 100 g tissue

show abstract

“…Therefore, the primary goals of this study were to 1) determine the basic mechanism of FID in human visceral fat arterioles and 2) determine whether the mechanism of FID in the adipose circulation is altered by the presence of CAD. 1 …”

mentioning

confidence: 99%

The mechanism of flow-induced dilation in human adipose arterioles involves hydrogen peroxide during CAD

Phillips

Hatoum

Gutterman

2007

American Journal of Physiology-Heart and Circulatory Physiology

106

116

View full text Add to dashboard Cite

Phillips SA, Hatoum OA, Gutterman DD. The mechanism of flowinduced dilation in human adipose arterioles involves hydrogen peroxide during CAD. Am J Physiol Heart Circ Physiol 292: H93-H100, 2007. First published October 13, 2006; doi:10.1152/ajpheart.00819.2006 is an important physiological stimulus that regulates tissue blood flow and is mediated by endotheliumderived factors that play a role in vascular integrity and the development of atherosclerosis. In coronary artery disease (CAD), conduit artery FID is impaired. The purpose of this study was to determine the mechanism of FID in human visceral adipose and examine whether the presence of conduit coronary atherosclerosis is associated with altered endothelial function in visceral fat. FID was determined in isolated visceral fat arterioles from patients with and without CAD. After constriction with endothelin-1, increases in flow produced an endothelium-dependent vasodilation that was sensitive to N -nitro-Larginine methyl ester (L-NAME) in visceral fat arterioles from patients without CAD. In contrast, L-NAME alone or in combination with indomethacin had no effect on FID in similarly located arterioles from patients with CAD. Flow increased dichlorofluorescein (DCF) and dihydroethidium fluorescence accumulation in arterioles from patients with CAD versus without, indicative of the production of oxidative metabolites and superoxide, respectively. Both the dilation and DCF fluorescence to flow were reduced in the presence of the H 2O2 scavenger polyethylene glycol-catalase. Exogenous H2O2 elicited similar relaxations of arterioles from patients in both groups. These data indicate that FID in visceral fat arterioles is nitric oxide dependent in the absence of known CAD. However, in the presence of CAD, H 2O2 replaces nitric oxide as the mediator of endotheliumdependent FID. This study provides evidence that adverse microvascular changes during CAD are evident in human visceral adipose, a tissue associated with CAD. coronary artery disease; blood flow; vasodilation; microcirculation FLOW-INDUCED DILATION (FID) is a physiologically important stimulus regulating vascular tone and homeostasis of the peripheral circulation. This important endothelial mechanism of vasodilation occurs in virtually every vascular bed and, in large arteries, may be critical for preventing atherosclerosis through release of the endothelium-derived antiproliferative compounds nitric oxide (NO) and prostacyclin (PGI 2 ) (21,25,39,51). Many of the studies implicating the role of NO (24) and PGI 2 (26) in FID have been performed in animal models in the absence of coronary artery disease (CAD). However, no studies have evaluated the mechanism of FID in isolated human microvessels from human visceral adipose with or without CAD. Human adipose has been proposed as a source for endocrine and paracrine modulation of vascular function during the establishment of atherosclerosis, and therefore vessels in this region could serve as sentinels for endothelial alterations produced by the proatheroscler...

show abstract

A nitric oxide‐mediated mechanism regulates lipolysis in human adipose tissue in vivo

Cited by 106 publications

References 31 publications

Regulation of the nitric oxide system in human adipose tissue

Regulation of the nitric oxide system in human adipose tissue

Nitric Oxide and β-Adrenergic Stimulation Are Major Regulators of Preprandial and Postprandial Subcutaneous Adipose Tissue Blood Flow in Humans

The mechanism of flow-induced dilation in human adipose arterioles involves hydrogen peroxide during CAD

Contact Info

Product

Resources

About