scholarly journals Ezetimibe combined with standard diet and exercise therapy improves insulin resistance and atherosclerotic markers in patients with metabolic syndrome

2014 ◽  
Vol 6 (3) ◽  
pp. 325-333 ◽  
Author(s):  
Kyoko Ohbu‐Murayama ◽  
Hisashi Adachi ◽  
Yuji Hirai ◽  
Mika Enomoto ◽  
Ako Fukami ◽  
...  
2013 ◽  
Vol 77 (11) ◽  
pp. 2807-2815 ◽  
Author(s):  
Yasushi Matsuzawa ◽  
Seigo Sugiyama ◽  
Koichi Sugamura ◽  
Hitoshi Sumida ◽  
Hirofumi Kurokawa ◽  
...  

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 339
Author(s):  
María de la Fuente-Fernández ◽  
Daniel González-Hedström ◽  
Sara Amor ◽  
Antonio Tejera-Muñoz ◽  
Nuria Fernández ◽  
...  

The incidence of metabolic syndrome (MetS) is increasing worldwide which makes necessary the finding of new strategies to treat and/or prevent it. The aim of this study was to analyze the possible beneficial effects of a carob fruit extract (CSAT+®) on the cardiometabolic alterations associated with MetS in mice. 16-week-old C57BL/6J male mice were fed for 26 weeks either with a standard diet (chow) or with a diet rich in fats and sugars (HFHS), supplemented or not with 4.8% of CSAT+®. CSAT+® supplementation reduced blood glucose, Homeostatic Model Assessment of Insulin Resistance (HOMA-IR) and circulating levels of total cholesterol, low-density lipoprotein (LDL) cholesterol (LDL-c), insulin, and interleukin-6 (IL-6). In adipose tissue and skeletal muscle, CSAT+® prevented MetS-induced insulin resistance, reduced macrophage infiltration and the expression of pro-inflammatory markers, and up-regulated the mRNA levels of antioxidant markers. Supplementation with CSAT+® prevented MetS-induced hypertension and decreased the vascular response of aortic rings to angiotensin II (AngII). Moreover, treatment with CSAT+® attenuated endothelial dysfunction and increased vascular sensitivity to insulin. In the heart, CSAT+® supplementation reduced cardiomyocyte apoptosis and prevented ischemia-reperfusion-induced decrease in cardiac contractility. The beneficial effects at the cardiovascular level were associated with a lower expression of pro-inflammatory and pro-oxidant markers in aortic and cardiac tissues.


2009 ◽  
Vol 297 (3) ◽  
pp. R587-R592 ◽  
Author(s):  
Melissa J. Romero-Aleshire ◽  
Maggie K. Diamond-Stanic ◽  
Alyssa H. Hasty ◽  
Patricia B. Hoyer ◽  
Heddwen L. Brooks

Factors comprising the metabolic syndrome occur with increased incidence in postmenopausal women. To investigate the effects of ovarian failure on the progression of the metabolic syndrome, female B6C3F1 mice were treated with 4-vinylcyclohexene diepoxide (VCD) and fed a high-fat (HF) diet for 16 wk. VCD destroys preantral follicles, causing early ovarian failure and is a well-characterized model for the gradual onset of menopause. After 12 wk on a HF diet, VCD-treated mice had developed an impaired glucose tolerance, whereas cycling controls were unaffected [12 wk AUC HF mice 13,455 ± 643 vs. HF/VCD 17,378 ± 1140 mg/dl/min, P < 0.05]. After 16 wk on a HF diet, VCD-treated mice had significantly higher fasting insulin levels (HF 5.4 ± 1.3 vs. HF/VCD 10.1 ± 1.4 ng/ml, P < 0.05) and were significantly more insulin resistant (HOMA-IR) than cycling controls on a HF diet (HF 56.2 ± 16.7 vs. HF/VCD 113.1 ± 19.6 mg/dl·μU/ml, P < 0.05). All mice on a HF diet gained more weight than mice on a standard diet, and weight gain in HF/VCD mice was significantly increased compared with HF cycling controls. Interestingly, even without a HF diet, progression into VCD-induced menopause caused a significant increase in cholesterol and free fatty acids. Furthermore, in mice fed a standard diet (6% fat), insulin resistance developed 4 mo after VCD-induced ovarian failure. Insulin resistance following ovarian failure (menopause) was prevented by estrogen replacement. Studies here demonstrate that ovarian failure (menopause) accelerates progression into the metabolic syndrome and that estrogen replacement prevents the onset of insulin resistance in VCD-treated mice. Thus, the VCD model of menopause provides a physiologically relevant means of studying how sex hormones influence the progression of the metabolic syndrome.


2017 ◽  
Vol 14 (1) ◽  
pp. 10 ◽  
Author(s):  
Fiqhi Cahyaningrum Rahmawati ◽  
Kis Djamiatun ◽  
Nyoman Suci

Background: The metabolic syndrome often begins with insulin resistance characterized by hyperinsulinemia and hyperglycemia. Synbiotic yoghurt tanduk banana contains probiotic and prebiotic FOS can improve insulin resistance in metabolic syndrome.Objective: To prove the effect of synbiotic yoghurt tanduk banana can reduce blood glucose levels and insulin levels in metabolic syndrome rats.Method: True-experimental study with randomized controlled group pre-post test design in male wistar rats. Eighteen samples were induced to become metabolic syndrome with high fat fructose diet for 2 weeks and they were divided into 3 groups: control (K) was given standard diet, treatment group 1 (P1), and treatment group 2 (P2) were given sinbiotic yoghurt tanduk banana dose of 0.009 ml/g body weight (BW)/day and 0.018 ml/g BW/day for 2 weeks.Results: The paired t-test showed there were differences of blood glucose levels and insulin levels before and after treatment in P2 group. The Kruskal Wallis test showed there were differences of mean blood glucose levels inter group after treatment (p<0.05). The One-way Anova test showed there were differences of mean insulin levels inter group after treatment (p<0.05). Conclusion: Synbiotic yoghurt tanduk banana can reduce blood glucose levels and insulin levels in metabolic syndrome rat with effective dose is 0.018 ml/grBW/day.


2021 ◽  
Vol 12 (3) ◽  
pp. 3305-3315

One of the main health problems is metabolic syndrome (MetS). Its incidence elevates with age leading to a higher risk of evolving chronic diseases and cancer. Obesity and insulin resistance was considered the most vital components in its pathogenesis for a long time. This study aims to evaluate serum novel adipokine and myokine to establish the irrelation of insulin resistance and their impact on metabolic syndrome. Four groups of rats were included; the control group (C) fed with a standard diet, the second group (CI) fed on a standard diet and injected daily with irisin (100ng/ ml) till the end of the experiment. The third group (MetS group) fed on the HCHF diet for 20 weeks and served as a control group. Rats in the fourth group (MetS+I group) were fed on the HCHF diet until they become obese and diabetic, then injected daily with irisin (100ng/ ml) till the end of the experiment and served as a treated group. Serum levels of obesity and diabetes indices were significantly increased while HDL was significantly decreased in the metabolic syndrome group, but after treatment with irisin, their levels were improved. Both adropin and irisin were significantly decreased, while IL-6 was significantly increased in the same group that was enhanced after irisin treatment. In conclusion, this study demonstrated that lower irisin correlates with the increased risk of increased risk of insulin resistance and MetS. In addition, our results suggested that irisin could have a potential role in glucose metabolism. The relations among increased levels of circulating irisin, insulin resistance, and MetS prevalence may be elucidated with a physiological compensatory contrivance.


2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Irena Markova ◽  
Denisa Miklankova ◽  
Martina Hüttl ◽  
Petr Kacer ◽  
Jelena Skibova ◽  
...  

Introduction. The development of metabolic syndrome-associated renal dysfunction is exacerbated by a number of factors including dyslipidemia, ectopic deposition of lipids and their toxic metabolites, impairment of lipid metabolism, and insulin resistance. Renal dysfunction is also affected by the production of proinflammatory and profibrotic factors secreted from adipose tissue, which can in turn directly impair kidney cells and potentiate insulin resistance. In this study, we investigated the manifestation of renal lipid accumulation and its effect on renal dysfunction in a model of metabolic syndrome—the hereditary hypertriglyceridemic rat (HHTg)—by assessing microalbuminuria and targeted urinary proteomics. Male Wistar control rats and HHTg rats were fed a standard diet and observed over the course of ageing at 3, 12, and 20 months of age. Results. Chronically elevated levels of triglycerides in HHTg rats were associated with increased levels of NEFA during OGTT and over a period of 24 hours (+80%, P<0.01). HHTg animals exhibited qualitative changes in NEFA fatty acid composition, represented by an increased proportion of saturated fatty acids (P<0.05) and a decreased proportion of n-3 PUFA (P<0.01). Ectopic lipid deposition in the kidneys of HHTg rats—triglycerides (+30%) and cholesterol (+10%)—was associated with markedly elevated microalbuminuria as ageing increased, despite the absence of microalbuminuria at the young age of 3 months in these animals. According to targeted proteomic analysis, 3-month-old HHTg rats (in comparison to age-matched controls) exhibited increased urinary secretion of proinflammatory parameters (MCP-1, IL-6, IL-8, P<0.01) and decreased urinary secretion of epidermal growth factor (EGF, P<0.01) before manifestation of microalbuminuria. Elevation in the urinary secretion of inflammatory cytokines can be affected by increased relative expression of MCP-1 in the renal cortex (P<0.05). Conclusions. Our results confirm dyslipidemia and ectopic lipid accumulation to be key contributors in the development of metabolic syndrome-associated renal dysfunction. Assessing urinary secretion of proinflammatory cytokines and epidermal growth factor can help in detecting early development of metabolic syndrome-associated renal dysfunction.


2016 ◽  
Author(s):  
Ann-Kristin Picke ◽  
Lykke Sylow ◽  
Lisbeth L V Moller ◽  
Rasmus Kjobsted ◽  
Erik Richter ◽  
...  

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