Circulating and local visfatin/Nampt/PBEF levels in spontaneously hypertensive rats, stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats

Wang, Pei; Du, Hongwu; Zhang, Ruoyu; Guan, Yongjun; Xu, Tao; Xu, Quan-Yi; Su, Ding‐Feng

doi:10.1007/s12576-010-0103-1

Cited by 20 publications

(15 citation statements)

References 32 publications

(36 reference statements)

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“…A recent animal study showed that visfatin is a myokine, secreted from skeletal muscle cells in a hypertensive rat model (22). In that study serum visfatin levels were not statistically different in hypertensive and normotensive rats.…”

Section: Discussionmentioning

confidence: 71%

Visfatin May Be a Novel Marker for Identifying Stages of Essential Hypertension in Advanced Age Patients

et al. 2012

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Objective Visfatin is a peptide that is secreted from visceral fat. It has been reported to be associated with inflammation and endothelial dysfunction. However, little is known about its function in hypertension. Therefore the aim of the present study was to evaluate visfatin levels in patients with hypertension. Methods We studied forty-six newly diagnosed hypertensive patients and 30 healthy participants. In accordance with blood pressure levels reported in the JNC 7 guidelines, hypertensive patients were divided into 2 groups: stage 1 and stage 2. The control group was divided into 2 groups: normal and prehypertensive. Blood pressure (BP) measurements were obtained from each patient. Serum lipid profile, glucose and visfatin levels were measured. Results The levels of fasting blood glucose (FBG), total cholesterol, triglyceride (TG), low density lipoprotein cholesterol (LDL-C), BMI, waist circumference were significantly higher in the patient group than those in control subjects (p<0.05). The mean visfatin level was significantly higher in hypertensive patients. In the prehypertensive group, the serum visfatin levels were also significantly higher than in participants with normal blood pressure (p:0.043). There was a significantly positive correlation with visfatin and systolic BP, diastolic BP. Conclusion We consider that visfatin may be a marker which may be used to illustrate damage even in prehypertensive stage caused by isolated essential HT.

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Section: Discussionmentioning

confidence: 71%

Visfatin May Be a Novel Marker for Identifying Stages of Essential Hypertension in Advanced Age Patients

et al. 2012

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“…In a recent study, we demonstrated that visfatin, a PVAT‐derived growth factor for vascular smooth muscle cells (VSMC), is highly expressed in PVAT compared with subcutaneous and visceral fat 75 . We also provided evidence that visfatin is involved in cardio‐ and cerebrovascular disease 76–79 . Other studies have shown that visfatin induces inducible nitric oxide synthase and elicits sustained activation of extracellular signal‐regulated kinase (ERK) 1/2 signalling with the induction of NF‐κB in VSMC 80 .…”

Section: Adipokines Inflammation and Cardiovascular Diseasementioning

confidence: 73%

Adipokines in inflammation, insulin resistance and cardiovascular disease

Wang

Miao

2011

Clin Exp Pharma Physio

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1. Obesity is a major determinant of cardiovascular disease (CVD). Studies in the past two decades have shown that adipose tissue is not merely an inert energy reserve of triglycerides, but also an active endocrine organ. 2. Adipose tissue can produce and secrete numerous bioactive peptides and/or proteins termed adipokines. These secretory factors are involved in the regulation of local and systemic inflammation and insulin sensitivity in a paracrine and/or endocrine manner. Inflammation and insulin resistance (IR) play critical roles in the obesity-linked development of CVD, such as atherosclerosis, hypertension and restenosis. 3. In the present minireview, we summarize the relationship between inflammation and IR, as well as their contribution to the development of CVD during adipose tissue dysfunction. In particular, we focus on the effects of various adipokines in pathological processes, which may provide an insight into obesity-linked CVD and facilitate the development of new therapeutic strategies.

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“…This assay has a limit of detection of ≤0.10 µg/L, with interassay and intraassay coefficients of variation of 2.3% and 5.1%, respectively. The homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated using the following formula [31], [32]: HOMA-IR = fasting blood insulin (mIU/L)×fasting blood glucose (mmol/L)/22.5. The quantitative insulin sensitivity check index (QUICKI) was calculated according to the original formula [33] as the inverse log sum of fasting insulin in mIU/L and fasting glucose in mg/dl.…”

Section: Methodsmentioning

confidence: 99%

Chronic Exposure to Nicotine Enhances Insulin Sensitivity through α7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

Guo

Wang

et al. 2012

PLoS ONE

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This study was to investigate the effect of nicotine on insulin sensitivity and explore the underlying mechanisms. Treatment of Sprague-Dawley rats with nicotine (3 mg/kg/day) for 6 weeks reduced 43% body weight gain and 65% blood insulin level, but had no effect on blood glucose level. Both insulin tolerance test and glucose tolerance test demonstrated that nicotine treatment enhanced insulin sensitivity. Pretreatment of rats with hexamethonium (20 mg/kg/day) to antagonize peripheral nicotinic receptors except for α7 nicotinic acetylcholine receptor (α7-nAChR) had no effect on the insulin sensitizing effect of nicotine. However, the insulin sensitizing effect but not the bodyweight reducing effect of nicotine was abrogated in α7-nAChR knockout mice. Further, chronic treatment with PNU-282987 (0.53 mg/kg/day), a selective α7-nAChR agonist, significantly enhanced insulin sensitivity without apparently modifying bodyweight not only in normal mice but also in AMP-activated kinase-α2 knockout mice, an animal model of insulin resistance with no sign of inflammation. Moreover, PNU-282987 treatment enhanced phosphorylation of signal transducer and activator of transcription 3 (STAT3) in skeletal muscle, adipose tissue and liver in normal mice. PNU-282987 treatment also increased glucose uptake by 25% in C2C12 myotubes and this effect was total abrogated by STAT3 inhibitor, S3I-201. All together, these findings demonstrated that nicotine enhanced insulin sensitivity in animals with or without insulin resistance, at least in part via stimulating α7-nAChR-STAT3 pathway independent of inflammation. Our results contribute not only to the understanding of the pharmacological effects of nicotine, but also to the identifying of new therapeutic targets against insulin resistance.

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Circulating and local visfatin/Nampt/PBEF levels in spontaneously hypertensive rats, stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats

Cited by 20 publications

References 32 publications

Visfatin May Be a Novel Marker for Identifying Stages of Essential Hypertension in Advanced Age Patients

Visfatin May Be a Novel Marker for Identifying Stages of Essential Hypertension in Advanced Age Patients

Adipokines in inflammation, insulin resistance and cardiovascular disease

Chronic Exposure to Nicotine Enhances Insulin Sensitivity through α7 Nicotinic Acetylcholine Receptor-STAT3 Pathway

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