Involvement of Nitric Oxide in Endothelium-Dependent Arterial Relaxation by Leptin

Kimura, Keizo; Tsuda, Kazushi; Baba, Akira; Kawabe, Takao; Boh-Oka, Shin-Ichi; Ibata, Masayo; Moriwaki, Chizu; Hano, Takuzo; Nishio, Ichiro

doi:10.1006/bbrc.2000.3005

Cited by 143 publications

(118 citation statements)

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“…[33][34][35] Several mechanisms have been suggested to be behind these associations, including mediation of platelet aggregation, increased sympathetic activity and stimulation of inflammation. 36,37 The regulatory effects of leptin on vascular endothelial cells in rodents are also well established, 2,11,38 but less is known about putative effects on human endothelial function and blood flow regulation in vivo. The non-significant results after adjustments for BMI in this study should be interpreted with caution, because leptin and measures of obesity are strongly correlated and it is debatable whether models exploring the effect of leptin should be adjusted for obesity.…”

Section: Discussionmentioning

confidence: 99%

“…10 Putative modulators of a link between obesity, ATBF, nitric oxide activity and autonomic activity include the adipokines leptin and adiponectin, which are secreted into the peripheral circulation from AT. 2,[11][12][13] These adipokines predict risk for type 2 diabetes and cardiovascular disease, [14][15][16] and in vitro studies have demonstrated the nitric oxide-mediated vasorelaxation effects of both leptin and adiponectin. 2,[11][12][13] With menopause, women change their fat distribution to a more central (android) location.…”

Section: Introductionmentioning

confidence: 99%

“…2,[11][12][13] These adipokines predict risk for type 2 diabetes and cardiovascular disease, [14][15][16] and in vitro studies have demonstrated the nitric oxide-mediated vasorelaxation effects of both leptin and adiponectin. 2,[11][12][13] With menopause, women change their fat distribution to a more central (android) location. 17 On the basis of the metabolic differences between subcutaneous and visceral fat, and our recent demonstration of dysregulation of ABTF in post-menopausal overweight women, 10 we hypothesised that ATBF is closely related to the size of the abdominal fat depot.…”

Section: Introductionmentioning

confidence: 99%

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Association of adipose tissue blood flow with fat depot sizes and adipokines in women

et al. 2011

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Objective: To explore possible associations between adipose tissue (AT) blood flow (ATBF), AT depot sizes and adipocytederived hormones (adipokines) in women. Subjects: In all, 43 healthy women were divided into four groups: normal-weight (n ¼ 11) and obese (n ¼ 11) pre-menopausal women and normal-weight (n ¼ 10) and obese (n ¼ 11) post-menopausal women. Methods: Fasting levels of adipokines were obtained, and a single-slice computed tomography scan at the level of L4-L5 was used to estimate fat depot sizes. ATBF was assessed by xenon washout while in a fasting state and after oral glucose load. We also measured glucose, insulin and non-esterified fatty acids. Results: Total, subcutaneous and visceral AT areas strongly correlated with ATBF (all Po0.001). Circulating leptin levels strongly and inversely correlated with ATBF (P ¼ 0.001), but this association did not remain after adjustment for body mass index. Adiponectin was not associated with blood flow. Conclusion: ATBF is closely linked to subcutaneous and visceral AT size. Further analyses are needed to determine possible mediators of this association, including mechanistic studies to assess a putative role for leptin as a significant modulator of blood flow.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Association of adipose tissue blood flow with fat depot sizes and adipokines in women

et al. 2011

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“…A higher plasma concentration of leptin is associated with the development and progression of microvascular complications in patients with T2DM (17)(18)(19). At the molecular level the effectof leptinonendothelial functionis unclear as leptin both stimulates the activity ofeNOS andreducesthe bioavailability ofLargininerequiredfor NO synthesis (20)(21)(22). In addition, the results of studies exploring the relationship between leptin and microvascularcomplications in patients with T1DM…”

Section: Evaluation Of the Hypothesismentioning

confidence: 99%

The role of endothelial dysfunction driven by adipocitokines in the development and progression of microvascular complications in patients with type 1 and type 2 diabetes

2015

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“…In relation to this role, the author's group was the first to identify NO as the key molecule responsible for the depressor response induced by leptin (Frühbeck, 1999). Subsequent studies have further shown that leptin acts on the endothelium, inducing the synthesis of NO via the activation of endothelial NO synthase, which induces an endothelium-dependent vasodilation (Kimura et al 2000;Lembo et al 2000;Winters et al 2000;Beltowski et al 2002;Vecchione et al 2002;Beltowski, 2006a). Since OB-R are also expressed in the underlying smooth muscle layer, it is considered that VSMC also represent an important target for the vascular actions of leptin (Fortuño et al 2002;Rodríguez et al 2006).…”

Section: Leptinmentioning

confidence: 99%

The Sir David Cuthbertson Medal Lecture Hunting for new pieces to the complex puzzle of obesity

Frühbeck

2006

Proc. Nutr. Soc.

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Disentangling the neuroendocrine systems that regulate energy homeostasis and adiposity has been a long-standing challenge in pathophysiology, with obesity being an increasingly important public health problem. Adipose tissue is no longer considered a passive bystander in bodyweight regulation. It actively secretes a large number of hormones, growth factors, enzymes, cytokines, complement factors and matrix proteins, at the same time as expressing receptors for most of these elements, which influence fuel storage, mobilisation and utilisation at both central and peripheral sites. Thus, an extensive cross talk at a local and systemic level in response to specific external stimuli or metabolic changes underpins the multifunctional characteristics of adipose tissue. In addition to the already-known adipokines, such as IL, TNFa, leptin, resistin and adiponectin, more recently attention has been devoted to 'newcomers' to the 'adipose tissue arena', which include aquaporin, caveolin, visfatin, serum amyloid A and vascular endothelial growth factor. While in vitro and in vivo experiments have provided extremely valuable information, the advances in genomics, proteomics and metabolomics are offering a level of information not previously attainable to help unlock the molecular basis of obesity. The potential and power of combining pathophysiological observations with the wealth of information provided by the human genome, knock-out models, transgenesis, DNA microarrays, RNA silencing and other emerging technologies offer a new and unprecedented view of a complex disease, conferring novel insights into old questions by identifying new pieces to the unfinished jigsaw puzzle of obesity.

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Involvement of Nitric Oxide in Endothelium-Dependent Arterial Relaxation by Leptin

Cited by 143 publications

References 21 publications

Association of adipose tissue blood flow with fat depot sizes and adipokines in women

Association of adipose tissue blood flow with fat depot sizes and adipokines in women

The role of endothelial dysfunction driven by adipocitokines in the development and progression of microvascular complications in patients with type 1 and type 2 diabetes

The Sir David Cuthbertson Medal Lecture Hunting for new pieces to the complex puzzle of obesity

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