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Even Short-Term Telmisartan Treatment Ameliorated Insulin Resistance But Had No Influence on Serum Adiponectin and Tumor Necrosis Factor-Alpha Levels in Hypertensive Patients with Metabolic Syndrome.
Kiyici, S, Guclu, M, Budak, F, Sigirli, D, Tuncel, E
Metabolic syndrome and related disorders. 2019;(3):167-172
Abstract
BACKGROUND We investigated the effect of short-term telmisartan usage in addition to lifestyle changes such as diet and exercise on insulin resistance, lipid metabolism, and serum adiponectin and tumor necrosis factor-alpha (TNF-α) levels in hypertensive patients with metabolic syndrome (MetS). METHODS A total of 36 hypertensive patients with MetS were randomized to telmisartan and control groups in an open-labeled prospective study. RESULTS There were significant decreases in anthropometric variables of patients according to baseline measurements in both groups at the end of the study. Serum insulin level and insulin resistance assessed by homeostasis model assessment-insulin resistance were decreased significantly in the telmisartan group (P = 0.040 and P = 0.034, respectively) compared with the controls, while there was no statistically significant change in the lipid profiles of the two groups. Serum adiponectin level was increased by 19.1% ± 41.7% in the telmisartan group, but intergroup analysis revealed no significant change. There was also no significant change in serum TNF-α level in either group. CONCLUSION It has been observed that even short-term telmisartan treatment had favorable effects on insulin resistance and glucose metabolism compared with lifestyle changes alone. The fundamental effect of telmisartan treatment on insulin resistance renders it a good therapeutic option for hypertensive patients with MetS.
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Resistance training reduces metabolic syndrome and inflammatory markers in older women: A randomized controlled trial.
Tomeleri, CM, Souza, MF, Burini, RC, Cavaglieri, CR, Ribeiro, AS, Antunes, M, Nunes, JP, Venturini, D, Barbosa, DS, Sardinha, LB, et al
Journal of diabetes. 2018;(4):328-337
Abstract
BACKGROUND This study analyzed the effects of a 12-week resistance training (RT) program without dietary interventions on metabolic syndrome (MetS) components and inflammatory biomarkers in older women. METHODS Fifty-three older women (mean [±SD] age 70.4 ± 5.7 years; mean body mass index 26.7 ± 4.0 kg/m2 ) were randomly assigned to a training group (TG; n = 26) that performed 12 weeks of an RT program or a control group (CG; n = 27) that did not perform any type of physical exercise over the same period. Body composition (dual energy X-ray absorptiometry), muscular strength (one-repetition maximum tests), blood pressure (BP), and blood sample measurements were performed before and after intervention. RESULTS After the 12-week period, there were significantly reductions (P < 0.05) in glucose levels (-20.4% vs -0.3%), waist circumference (-1.5% vs +2.0%), and systolic BP (-6.2% vs +0.9%), and complete normalization of MetS prevalence (18% at baseline vs. 0% after 12-weeks RT) in the TG. Moreover, C-reactive protein and tumor necrosis factor-α concentrations decreased in the TG (-28.6% and -21.6%, respectively), but increased in the CG (+34.5% and +13.3%, respectively). In addition there were positive improvements in the MetS Z-score in the TG but not CG (-21.6% vs +13.3%, respectively). CONCLUSION The results suggest that a 12-week RT program seems to effectively reduce MetS components and inflammatory biomarkers in older women, regardless of dietary intervention. The RT-induced adaptations in body composition and inflammatory biomarkers appear to be related to healthy adaptations in risk factors for MetS.
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Polymorphism at the TNF-alpha gene interacts with Mediterranean diet to influence triglyceride metabolism and inflammation status in metabolic syndrome patients: From the CORDIOPREV clinical trial.
Gomez-Delgado, F, Alcala-Diaz, JF, Garcia-Rios, A, Delgado-Lista, J, Ortiz-Morales, A, Rangel-Zuñiga, O, Tinahones, FJ, Gonzalez-Guardia, L, Malagon, MM, Bellido-Muñoz, E, et al
Molecular nutrition & food research. 2014;(7):1519-27
Abstract
SCOPE To examine whether the consumption of a Mediterranean diet (MedDiet), compared with a low-fat diet, interacts with two single nucleotide polymorphisms at the tumor necrosis factor alpha gene (rs1800629, rs1799964) in order to improve triglycerides (TG), glycemic control, and inflammation markers. METHODS AND RESULTS Genotyping, biochemical measurements, dietary intervention, and oral fat load test meal were determined in 507 metabolic syndrome (MetS) patients selected from all the subjects included in CORDIOPREV clinical trial (n = 1002). At baseline, G/G subjects (n = 408) at the rs1800629 polymorphism, showed higher fasting and postprandial TG (p = 0.003 and p = 0.025, respectively), and high sensitivity C-reactive protein (hsCRP) (p = 0.003) plasma concentrations than carriers of the minor A-allele (G/A + A/A) (n = 99). After 12 months of MedDiet, baseline differences between genotypes disappeared. The decrease in TG and hsCRP was statistically significant in G/G subjects (n = 203) compared with carriers of the minor A-allele (p = 0.005 and p = 0.034, respectively) (n = 48). No other gene-diet interactions were observed in either diet. CONCLUSION These results suggest that the rs1800629 at the tumor necrosis factor alpha gene interacts with MedDiet to influence TG metabolism and inflammation status in MetS subjects. Understanding the role of gene-diet interactions may be the best strategy for personalized treatment of MetS.
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Behavior of insulin sensitivity and its relation to leptin and tumor necrosis factor-alpha in obese women undergoing liposuction: 6-month follow-up.
Robles-Cervantes, JA, Martínez-Abundis, E, González-Ortiz, M, Cárdenas-Camarena, L, Hernández-Salazar, E, Olvera-Ozuna, R
Obesity surgery. 2007;(9):1242-7
Abstract
BACKGROUND Metabolic syndrome is a group of pathological processes which involve insulin resistance, a biochemical and molecular disorder. Obesity appears to be the most frequent clinical component in metabolic syndrome. Subcutaneous fat, independent from visceral fat, is still controversial as a marker of the pathophysiology of insulin resistance. METHODS An open parallel-group clinical trial was performed of 12 women (age 30-40 years), with BMI from 30-33 kg/m2 and fasting glucose < or =110 mg/dl. 6 women were included in the "liposuction plus diet" group, and 6 were included in the "diet-only" group. Metabolic profile, including insulin tolerance test (ITT), leptin and tumor necrosis factor alpha (TNFalpha), was performed at baseline, 1 and 6 months in both groups. Subcutaneous and visceral fat was quantified with spiral tomography at baseline and after 6 months. Friedman and Wilcoxon test were used for intra-group differences, Mann-Whitney U for differences between groups, and Spearman test for correlation, with significance set at P<0.05. RESULTS No difference existed between groups regarding clinical characteristics and metabolic profile. In the liposuction group, the increase in insulin sensitivity was (3.8+/-0.86, 3.1+/-0.85, 4.5+/-1.02 %/min, P=0.08. Insulin sensitivity did not correlate with subcutaneous fat, leptin, or TNFalpha. Leptin diminished at 1 month (52.7+/-6.04 vs 31.6+/-11.9), P=0.028, and correlated with the subcutaneous fat (r=0.957). In the diet-only group, TNFalpha diminished at 6 months, P=0.046. CONCLUSION Subcutaneous abdominal fat correlates with leptin; nevertheless, it is a weak marker for TNFalpha and insulin sensitivity.
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Effects of TNF-alpha neutralization on adipocytokines and skeletal muscle adiposity in the metabolic syndrome.
Lo, J, Bernstein, LE, Canavan, B, Torriani, M, Jackson, MB, Ahima, RS, Grinspoon, SK
American journal of physiology. Endocrinology and metabolism. 2007;(1):E102-9
Abstract
In a prior study, we have shown that tumor necrosis factor (TNF)-alpha neutralization improves inflammatory markers and total adiponectin in patients with the metabolic syndrome, without improving insulin sensitivity. In this study, we sought to extend our understanding of the effects of TNF-alpha neutralization in this human model of obesity by investigating the responses of high-molecular-weight (HMW) adiponectin, resistin, leptin, and muscle adiposity to etanercept in patients with the metabolic syndrome. Fifty-six men and women with the metabolic syndrome enrolled in a double-blind randomized placebo-controlled trial. Circulating concentrations of total and HMW adiponectin, resistin, and leptin were determined at baseline and after 4 wk of treatment with etanercept. Muscle adiposity was measured by computed tomography (CT). Although etanercept increased total adiponectin concentration, the HMW form, which is thought to mediate insulin sensitivity, was unchanged. Thus the ratio of HMW to total adiponectin decreased following etanercept treatment compared with placebo (-0.03 +/- 0.03 vs. 0.06 +/- 0.03, P = 0.02). Resistin tended to decrease in the etanercept-treated group compared with placebo (-0.6 +/- 0.7 vs. 1.2 +/- 0.7 ng/ml, P = 0.06), whereas leptin was not altered. Etanercept decreased muscle attenuation on CT [-0.61 +/- 0.64 Hounsfield units (HU) vs. 1.54 +/- 0.77 HU in placebo, P = 0.04], suggesting an increase in muscle adiposity. Together, these results demonstrate that neutralization of TNF-alpha in obese humans results in differential effects on critical adipokines and body composition indexes. These findings may help to explain the lack of effect on insulin sensitivity and extend our knowledge of the biological effects of TNF-alpha neutralization in obesity.
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6.
Diet but not aerobic exercise training reduces skeletal muscle TNF-alpha in overweight humans.
Ferrier, KE, Nestel, P, Taylor, A, Drew, BG, Kingwell, BA
Diabetologia. 2004;(4):630-7
Abstract
AIMS/HYPOTHESIS Our aim was to test the hypothesis that TNF-alpha protein levels in skeletal muscle are important in mediating the improvements in glucose homeostasis that are associated with diet and exercise regimens intended to reduce cardiovascular risk. METHODS We recruited 20 people with a body mass index of 32.1 +/- 1.2 kg/m2 (mean +/- SEM) and one other component of the metabolic syndrome. The average age was 51.2 +/- 8.1 years (mean +/- SD). Of the 20 subjects, 6 were men and 14 were women. All subjects completed an 8-week control period, followed by randomisation to 8 weeks of moderate cycling exercise (30 min, three times per week) or to a diet with the following characteristics: low in saturated fat, high in fibre, low glycaemic index, rich in complex carbohydrates. RESULTS Diet induced a small reduction in body mass index (3.0 +/- 0.7%, p<0.05), although weight loss was not intended. Exercise training increased maximum oxygen consumption by 12 +/- 6% (p<0.05). Both interventions reduced fasting plasma insulin levels by about 20%. Diet reduced skeletal muscle TNF-alpha protein by 54 +/- 10% (p<0.05), an effect that was independent (p=0.94 in covariate analysis) of the small concurrent weight loss (-2.8 +/- 0.7 kg). Levels of GLUT4 protein were unchanged in the diet group. In contrast, exercise training did not significantly change TNF-alpha protein expression, but GLUT4 protein expression increased by 105 +/- 37% (p<0.05). CONCLUSIONS/INTERPRETATION These data indicate that the metabolic benefits of a diet aimed at cardiovascular risk reduction are associated with a decrease in skeletal muscle TNF-alpha protein.