4.P.121 Leptin stimulates rat aortic smooth muscle cell proliferation and migration

Oda, A.; Taniguchi, Toru; Takahash, A.; Shimizu, Hidehisa; Yoshida, Hiroaki; Kawasaki, Susumu; Okimura, Yasuhiko; Chihara, Kazuhisa; Ishikawa, Yasuko; Yokoyama, Masahiro

doi:10.1016/s0021-9150(97)89646-3

Cited by 150 publications

(211 citation statements)

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“…Our study in healthy adolescents suggests a marked influence of leptin on arterial distensibility. This observation, together with evidence from experimental models [15][16][17][18][19][20] and from prospective studies that show an influence of leptin on clinical outcomes, 32,33 strongly suggests that leptin is one mechanism by which body fatness is linked to the early stages of atherosclerosis.…”

Section: Discussionmentioning

confidence: 92%

“…13,14 However, the widespread distribution of functioning leptin receptors on vascular cells suggests that leptin also plays an important role in vascular physiology. [15][16][17][18][19][20] In experimental models, leptin has been shown to have angiogenic activity, 15,16 increase oxidative stress in endothelial cells, 17 and to promote vascular cell calcification 19 and smooth muscle cell proliferation and migration. 20 Leptin's role linking fat mass and atherogenesis is supported by findings in the ob/ob mouse, which lacks a functioning leptin gene.…”

Section: See P 1904mentioning

confidence: 99%

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Influence of Leptin on Arterial Distensibility

et al. 2002

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Background-The mechanisms by which obesity increases the risk of atherosclerotic cardiovascular disease (CVD) are poorly understood. In experimental models, leptin, a hormone produced by adipose tissue, has been shown adversely to affect vascular health. Therefore, we tested the hypothesis that high leptin concentrations are associated with lower arterial distensibility, an index of circulatory function relevant to the atherosclerotic process. Methods and Results-Noninvasive, high-resolution, vascular ultrasound was used to measure brachial artery distensibility in 294 healthy adolescents (aged 13 to 16 years) who had a broad range of body mass indexes. Fat mass was measured by bioelectric impedance analysis; fasting serum leptin concentration by radioimmunoassay; and lipid profile, fasting insulin, glucose, and C-reactive protein concentrations by standard laboratory techniques. Higher leptin concentrations were associated with impaired arterial distensibility (regression coefficient, Ϫ1.3% change in arterial distension per 10% increase in leptin; 95% CI, Ϫ1.9% to Ϫ0.8%; PϽ0.001). This association was independent of fat mass, blood pressure, and C-reactive protein, fasting insulin, or LDL cholesterol concentrations. Conclusions-Elevation in leptin was associated with impaired vascular function, independent of the metabolic and inflammatory disturbances associated with obesity. Our observations are consistent with data from experimental models and suggest that high leptin concentration is an important mechanism for the adverse influence of body fatness on CVD.

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Section: Discussionmentioning

confidence: 92%

Section: See P 1904mentioning

confidence: 99%

Influence of Leptin on Arterial Distensibility

et al. 2002

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“…Finally, obesity might increase arterial stiffness through the hormone leptin, which has been shown to promote VSMC proliferation and angiogenesis. 28,29 Obesity is often accompanied by the metabolic syndrome, and substantial improvement of the latter also occurs with weight loss. Interestingly, clinical evidence that improvement of metabolic parameters in obesity reduces vascular stiffening is lacking.…”

Section: Discussionmentioning

confidence: 99%

The effect of a rapid weight loss induced by laparoscopic adjustable gastric banding on arterial stiffness, metabolic and inflammatory parameters in patients with morbid obesity

et al. 2006

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Objective: To determine the effect of drastic weight loss on arterial compliance, inflammatory and metabolic parameters in patients with morbid obesity with and without cardiovascular risk factors who underwent laparoscopic adjustable gastric banding (LAGB). Design: Open prospective study, morbidly obese subjects divided into low-and high-risk group were evaluated before and 4 months after LAGB. Subjects: Forty-one Caucasian subjects aged between 16 and 55 years, with morbid (grade 3) obesity (20 low-risk and 21 highrisk subjects) who underwent LAGB and completed a 16-week follow-up. Measurments: Patients were evaluated at baseline and 4 months after LAGB for body mass index (BMI), arterial blood pressure (BP), metabolic factors including lipid profile, HbA1C, insulin, C-peptide, fibrinogen, hs-C reactive protein (CRP) and Homeostasis model assessment-insulin resistance (HOMA-IR). Arterial elasticity of large and small arteries was evaluated using pulse-wave contour analysis method (HDI CR 2000, Eagan, Minnesota) at baseline and after 4 months. Results: Body mass index reduction induced by LABG, from 43.5575.11 to 35.1074.87 in low-risk patients and from 42.9073.22 to 35.0073.24 in high-risk patients, significantly improved small artery elasticity (SAE) from 6.3072.74 to 7.2571.85, in morbidly obese patients with multiple cardiovascular risk factors (high-risk group). Improvement in SAE was accompanied by improvement of arterial BP, glucose and lipid metabolism, and reduction of CRP values. Conclusion: Although dramatic weight reduction induced by surgical intervention was associated with similar changes in body weight and significant improvement of metabolic and inflammatory parameters in two groups of obese patients, SAE improved only in high-risk patients.

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“…Another growth factor candidate could be leptin, which has been shown to stimulate VSMC proliferation and migration. 41 However, leptin expression is higher in subcutaneous fat than in visceral fat, and its effect on vascular growth may be mediated via circulating levels. In a study in 294 healthy adolescents with a broad range of body mass indexes, higher serum leptin concentrations were associated with impaired arterial distensibility, independently of fat mass or blood pressure.…”

Section: Ectopic Fat Storage In the Heartmentioning

confidence: 99%

Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases

et al. 2004

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In humans and most animal models, the development of obesity leads not only to increased fat depots in classical adipose tissue locations but also to significant lipid deposits within and around other tissues and organs, a phenomenon known as ectopic fat storage. The purpose of this review is to explore the possible locations of ectopic fat in key target-organs of cardiovascular control (heart, blood vessels and kidneys) and to propose how ectopic fat storage can play a role in the pathogenesis of cardiovascular diseases associated with obesity. In animals fed a high-fat diet, cardiac fat depots within and around the heart impair both systolic and diastolic functions, and may in the long-term promote heart failure. Accumulation of fat around blood vessels (perivascular fat) may affect vascular function in a paracrine manner, as perivascular fat cells secrete vascular relaxing factors, proatherogenic cytokines and smooth muscle cell growth factors. Furthermore, high amounts of perivascular fat could mechanically contribute to the increased vascular stiffness seen in obesity. Finally, accumulation of fat in the renal sinus may limit the outflow of blood and lymph from the kidney, which would alter intrarenal physical forces and promote sodium reabsorption and arterial hypertension. Taken together, ectopic fat storage in key target-organs of cardiovascular control may impair their functions, contributing to the increased prevalence of cardiovascular diseases in obese subjects.

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4.P.121 Leptin stimulates rat aortic smooth muscle cell proliferation and migration

Cited by 150 publications

References 0 publications

Influence of Leptin on Arterial Distensibility

Influence of Leptin on Arterial Distensibility

The effect of a rapid weight loss induced by laparoscopic adjustable gastric banding on arterial stiffness, metabolic and inflammatory parameters in patients with morbid obesity

Ectopic fat storage in heart, blood vessels and kidneys in the pathogenesis of cardiovascular diseases

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