Visfatin: Structure, Function and Relation to Diabetes Mellitus and Other Dysfunctions

Adeghate, Ernest

doi:10.2174/092986708785133004

Cited by 158 publications

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“…Visfatin is one of adipocytokines which is mainly secreted from visceral adipose tissue. Different studies showed a direct relationship between PVL, obesity and DMT2 [29][30][31][32]. The positive effects of regular aerobic and resistance exercise in DMT2 patients is well established-included improving glycemic control, improving lipid profile indices and decreasing diabetic complications [33][34][35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Investigation of Plasma Visfatin Changes in Women with Type 2 Diabetes followed by Endurance, Resistance and Combined Exercise: The Role of Lipid Profile, Glycemic Indices and Insulin Resistance

Mehdizadeh¹,

Hamzezadeh²,

Tofighi³

2016

J Diabetes Metab

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Background and purpose: Visfatin is one of insulin-like proteins secreted by adipose tissue associated with obesity and insulin resistance, but the effect of exercise on the levels of this hormone is unclear, despite various studies in this area. The aim of this study was to compare the effects of aerobic, resistance and combined exercises (strength-aerobic) on visfatin changes, glycemic and lipid parameters and evaluation of relationship between visfatin and insulin resistance in women with Diabetes Mellitus Type 2 (DMT2). The recent study differs with other studies in terms of exercise type, sample size, type of subjects and results. Materials and Methods:Forty women with DMT2 were selected by purposive sampling method based on availability then randomly divided into four equal groups; three patient (training) groups including aerobic exercise group (20-50 min/day, with an intensity of 60 to 80% of maximum heart rate), resistance group (3 sets, 10 reps, with an intensity of 50 to 65% of one repetition maximum), combined group (with the same intensity and duration of exercises in aerobic and resistance groups) and no-training group as control group. All patient groups participated in 12-week training program for three sessions per week. Fasting blood samples were collected to evaluate of plasma visfatin levels, insulin, glycated hemoglobin, glucose, cholesterol (Cho), triglycerides, HDL and LDL. To calculate the insulin resistance index HOMA-IR equation was used. Data analysis was performed using two-way ANOVA, Kolmogorov-Smirnov test, Levene's test, multiple linear regressions and post hoc Tukey test.Results: Data analysis showed that the weight index was decreased in aerobic group compared with resistance group. Body fat percentage in combined group was significantly lower than aerobic group and also in aerobic group as compared with control and resistance groups. Waist-to-hip ratio was decreased in aerobic group than combined group. Markers of insulin and insulin resistance reduced in resistance group compared with aerobic and combined groups. LDL index were significantly lower in combined group compared with the resistance and also Cho in resistance group as compared with aerobic and combined groups. There were no significant differences between mean changes of Hb A1c and mean visfatin changes in 4 groups. Conclusions:Even though in the present study; no significant differences were observed in mean changes of Hb A1c and PVL among groups, but each type of exercises had a positive impact on certain parameters in experimental groups. Longitudinal studies with more participants are needed for evaluation of relationship between visfatin and insulin resistance in women with DMT2.

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Section: Discussionmentioning

confidence: 99%

Investigation of Plasma Visfatin Changes in Women with Type 2 Diabetes followed by Endurance, Resistance and Combined Exercise: The Role of Lipid Profile, Glycemic Indices and Insulin Resistance

Mehdizadeh¹,

Hamzezadeh²,

Tofighi³

2016

J Diabetes Metab

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“…Interestingly, as its name implies, visfatin has been characterized as a new adipokine that is mainly expressed in and secreted from visceral fat rather than subcutaneous fat. Visfatin exerts insulin-mimetic effects in stimulating muscle and adipocyte glucose transport and in inhibiting hepatocyte glucose production (Adeghate 2008). Visfatin binds and activates the insulin receptor, thereby inducing receptor phosphorylation and the activation of downstream signaling molecules.…”

Section: Introductionmentioning

confidence: 99%

“…Visfatin binds and activates the insulin receptor, thereby inducing receptor phosphorylation and the activation of downstream signaling molecules. However, visfatin and insulin do not compete for binding to the insulin receptor, which indicates that the two proteins recognize different regions of the receptor (Adeghate 2008). Thus, visfatin might play a role in glucose homeostasis and in the pathogenesis of diabetes.…”

Section: Introductionmentioning

confidence: 99%

Visfatin, a novel adipokine, stimulates glucose uptake through the Ca2+-dependent AMPK–p38 MAPK pathway in C2C12 skeletal muscle cells

Lee¹,

Kim²,

Lee³

et al. 2015

Journal of Molecular Endocrinology

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Visfatin is a novel adipocytokine produced by visceral fat. In the present study, visfatin increased AMP-activated protein kinase (AMPK) phosphorylation in mouse C2C12 skeletal muscle cells. It also increased phosphorylation of the insulin receptor, whose knockdown blocked visfatin-induced AMPK phosphorylation and glucose uptake. Visfatin stimulated glucose uptake in differentiated skeletal muscle cells. However, inhibition of AMPKa2 with an inhibitor or with knockdown of AMPKa2 using siRNA blocked visfatin-induced glucose uptake, which indicates that visfatin stimulates glucose uptake through the AMPKa2 pathway. Visfatin increased the intracellular Ca 2C concentration. STO-609, a calmodulindependent protein kinase kinase inhibitor, blocked visfatin-induced AMPK phosphorylation and glucose uptake. Visfatin-mediated activation of p38 MAPK was AMPKa2-dependent. Furthermore, both inhibition and knockdown of p38 MAPK blocked visfatin-induced glucose uptake. Visfatin increased glucose transporter type 4 (GLUT4) mRNA and protein levels. In addition, visfatin stimulated the translocation of GLUT4 to the plasma membrane, and this effect was suppressed by AMPKa2 inhibition. The present results indicate that visfatin plays an important role in glucose metabolism via the Ca 2C -mediated AMPK-p38 MAPK pathway.

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“…6 This last point could be relevant to the current study because visfatin binds to insulin receptors at a site distinct from insulin and causes hypoglycemia by reducing glucose release from liver cells and stimulating glucose utilization in adipocytes and myocytes. 7 The relationship between RAAS and other human adipokines such as resistin (r), retinol-binding protein 4 (RBP-4) and vaspin is still under investigation. However, it is well known that many of these molecules are associated with or involved in the development of hypertension, both as single risk factors and as components of the metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

Differential effects of candesartan and olmesartan on adipose tissue activity biomarkers in type II diabetic hypertensive patients

et al. 2010

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The aim of this study is to compare the effects of candesartan and olmesartan on insulin sensitivity-related parameters, before and after antihypertensive therapy. After a 4-week washout placebo period, 194 hypertensive (diastolic blood pressure (DBP) X80 mm Hg and systolic blood pressure (SBP) X130 mm Hg) patients with well-controlled type II diabetes were randomized to receive either 8 mg of candesartan once a day (o.d.) or 10 mg olmesartan o.d. and titrated after 1 month to 16 mg candesartan o.d. or 20 mg olmesartan o.d., respectively; the treatment period had a 1-year duration. We evaluated body weight, body mass index, SBP, DBP, glycated hemoglobin, fasting plasma glucose, M value, adiponectin (ADN), resistin (r), retinol-binding protein 4, visfatin, vaspin and high-sensitivity C-reactive protein (Hs-CRP) at their baseline values and after 6 and 12 months of treatment. We observed no variation in body weight or glycemic profile for either treatment. SBP and DBP were significantly reduced by both treatments (from 144 ± 8/88 ± 6 to 126 ± 5/77 ± 4 mm Hg by candesartan (Po0.001) and from 145 ± 9/89 ± 7 to 128 ± 7/79 ± 5 mm Hg by olmesartan (Po0.001)) without any difference between them. Retinol binding protein-4, r, and the vaspin value decreased in the candesartan group but not in olmesartan group. The M value, visfatin and ADN increased with candesartan, whereas no significant variations were observed with olmesartan. Both treatments resulted in a similar reduction in Hs-CRP. Although both therapies resulted in similar reductions in blood pressure, candesartan therapy was more effective than olmesartan therapy in improving insulin sensitivity. Keywords: adipokines; candesartan; olmesartan; type II diabetes mellitus INTRODUCTIONThe renin-angiotensin-aldosteron system (RAAS) is involved in a large number of physiopathological processes leading to hypertension and increased cardiovascular risk. Apparently, the principal mediator of such processes is angiotensin II (AII). 1 Evidence from animal models and cultured skeletal muscle cell line studies indicates that AII can induce insulin resistance, mediated by the impairment of insulin receptor substrate-1-dependent insulin signaling that is reversed by the administration of angiotensin receptor antagonism. 2 In addition, recent literature shows that AII is also strongly involved in adipose tissue metabolism. In fact, both angiotensin type 1 and 2 receptors have been localized to adipocytes, and differences in the regional expression of RAAS components in visceral vs. subcutaneous adipose tissue have been used to explain the link between abdominal obesity and cardiovascular disease. 3 Moreover, AII reduces the adipogenic response of adipocyte progenitor cells; the extent of this reduction correlates directly with the body mass index (BMI) of

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Visfatin: Structure, Function and Relation to Diabetes Mellitus and Other Dysfunctions

Cited by 158 publications

References 0 publications

Investigation of Plasma Visfatin Changes in Women with Type 2 Diabetes followed by Endurance, Resistance and Combined Exercise: The Role of Lipid Profile, Glycemic Indices and Insulin Resistance

Investigation of Plasma Visfatin Changes in Women with Type 2 Diabetes followed by Endurance, Resistance and Combined Exercise: The Role of Lipid Profile, Glycemic Indices and Insulin Resistance

Visfatin, a novel adipokine, stimulates glucose uptake through the Ca2+-dependent AMPK–p38 MAPK pathway in C2C12 skeletal muscle cells

Differential effects of candesartan and olmesartan on adipose tissue activity biomarkers in type II diabetic hypertensive patients

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