Factors involved in rosuvastatin induction of insulin sensitization in rats fed a high fat diet

Heras, Natalia de las; Valero-Muñoz, María; Ballesteros, Sandra; Gómez-Hernández, Almudena; Martín-Fernández, Beatriz; Blanco-Rivero, Javier; Cachofeiro, Victoria; Benito, Manuel; Balfagón, Gloria; Lahera, Vicente

doi:10.1016/j.numecd.2012.11.009

Cited by 24 publications

(19 citation statements)

References 29 publications

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“…Dietary factors, especially hypercaloric diets, are the main contributors to the aetiology of MtS [28]. Chronic consumption of HFD induces overweight along with metabolic and cardiovascular alterations, such as insulin resistance, dyslipidemia or hypertension, among others, being all of these symptoms of the MtS [3,4]. Interestingly, studies in animal models demonstrated that HFD intake is related to gut dysbiosis [29,30].…”

Section: Discussionmentioning

confidence: 99%

“…NO in the vascular tissue is predominantly released from the endothelium, and it has been demonstrated that the decrease in endothelial NO release in obesity and MtS is the main factor for endothelial dysfunction [3,48]. Aside from endothelium, NO is also released from perivascular nitrergic innervation and this release is altered in situations in which vascular resistance is decreased [47,49].…”

Section: Discussionmentioning

confidence: 99%

“…Water intake was comparable among groups (Table 1). 3 Food and water intake were measured every two days in the last 4 weeks of the experimental procedure coinciding with the administration of the synbiotic. 4 Serum total cholesterol (TC), triglycerides /TG), high density lipoproteins (HDL) and low density lipoproteins (LDL) were analysed at the end of the experimental period of 12 weeks.…”

Section: The Effect Of Hfd and Synbiotic Supplementation On The Body mentioning

confidence: 99%

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Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A

et al. 2020

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A high fat diet (HFD) intake is crucial for the development and progression of metabolic syndrome (MtS). Increasing evidence links gut dysbiosis with the metabolic and vascular alterations associated with MtS. Here we studied the use of a combination of various probiotic strains together with a prebiotic (synbiotic) in a commercially available Prodefen® Plus. MtS was induced by HFD (45%) in male Wistar rats. Half of the MtS animals received Prodefen® Plus for 4 weeks. At 12 weeks, we observed an increase in body weight, together with the presence of insulin resistance, liver steatosis, hypertriglyceridemia and hypertension in MtS rats. Prodefen® Plus supplementation did not affect the body weight gain but ameliorated all the MtS-related symptoms. Moreover, the hypertension induced by HFD is caused by a diminished both nitric oxide (NO) functional role and release probably due to a diminished neuronal nitric oxide synthase (nNOS) activation by protein kinase A (PKA) pathway. Prodefen® Plus supplementation for 4 weeks recovered the NO function and release and the systolic blood pressure was returned to normotensive values as a result. Overall, supplementation with Prodefen® Plus could be considered an interesting non-pharmacological approach in MtS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: The Effect Of Hfd and Synbiotic Supplementation On The Body mentioning

confidence: 99%

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Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A

et al. 2020

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“…It has been also reported that adiponectin and SIRT-1 play an important role in the regulation of mitochondrial function in the same mouse model. 40,[130][131][132][133][134][135] Therefore, the common mechanisms for skeletal muscle mitochondrial abnormalities could be involved in diabetes and HF. Conclusions: The number of patients with HF is on the rise and the development of new treatment strategies for HF is a critical issue.…”

Section: Hf and Diabetes Mellitusmentioning

confidence: 99%

Skeletal Muscle Abnormalities in Heart Failure

et al. 2015

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Exercise capacity is lowered in patients with heart failure, which limits their daily activities and also reduces their quality of life. Furthermore, lowered exercise capacity has been well demonstrated to be closely related to the severity and prognosis of heart failure. Skeletal muscle abnormalities including abnormal energy metabolism, transition of myofibers from type I to type II, mitochondrial dysfunction, reduction in muscular strength, and muscle atrophy have been shown to play a central role in lowered exercise capacity. The skeletal muscle abnormalities can be classified into the following main types: 1) low endurance due to mitochondrial dysfunction; and 2) low muscle mass and muscle strength due to imbalance of protein synthesis and degradation. The molecular mechanisms of these skeletal muscle abnormalities have been studied mainly using animal models. The current review including our recent study will focus upon the skeletal muscle abnormalities in heart failure.

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“…In contrast to the effects on the zinc-dependent class I and II HDACs, numerous cell and animal based studies have reported that statins upregulate the expression of sirtuin 1 (SIRT1), a NAD1-dependent class III HDAC (Ota et al, 2010;Tabuchi et al, 2012;de las Heras et al, 2013;Kawai et al, 2013;Kok et al, 2013;Du et al, 2014;Gong et al, 2014). SIRT1 has a broad substrate specificity: in addition to histone residues H1K26, H3K9, H3K14, and H4K16 (Zhang and Kraus, 2010), it can deacetylate numerous other proteins, including p53, FOXO, and PGC1a (Lavu et al, 2008).…”

Section: Effects Of Statins On Histone Acetylationmentioning

confidence: 99%

Pleiotropic and Adverse Effects of Statins—Do Epigenetics Play a Role?

Allen

Mamotte

2017

J Pharmacol Exp Ther

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Statins are widely used to prevent major cardiovascular events by lowering serum cholesterol. There is evidence that statins have pleiotropic effects-that is, cholesterol-independent effects-that may also confer protection from cardiovascular disease and potentially numerous other pathologies, including cancer. Statins also have a number of well described adverse effects, including myopathy, rhabdomyolysis, liver damage, and type 2 diabetes. This paper examines the evidence of epigenetic modifications as a contributory factor to the pleiotropic and adverse effects of statins. In vitro and animal studies have shown that statins can inhibit histone deacetylase activity and increase histone acetylation. Similarly, there is evidence that statins may inhibit both histone and DNA methyltransferases and subsequently demethylate histone residues and DNA, respectively. These changes have been shown to alter expression of various genes, including tumor suppressor genes and genes thought to have anti-atherosclerotic actions. Statins have also been shown to influence the expression of numerous microRNAs that suppress the translation of proteins involved in tumorigenesis and vascular function. Whether the adverse effects of statins may also have an epigenetic component has been less widely studied, although there is evidence that microRNA expression may be altered in statin-induced muscle and liver damage. As epigenetics and microRNAs influence gene expression, these changes could contribute to the pleiotropic and adverse effects of statins and have long-lasting effects on the health of statin users.

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Factors involved in rosuvastatin induction of insulin sensitization in rats fed a high fat diet

Cited by 24 publications

References 29 publications

Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A

Beneficial Effect of a Multistrain Synbiotic Prodefen® Plus on the Systemic and Vascular Alterations Associated with Metabolic Syndrome in Rats: The Role of the Neuronal Nitric Oxide Synthase and Protein Kinase A

Skeletal Muscle Abnormalities in Heart Failure

Pleiotropic and Adverse Effects of Statins—Do Epigenetics Play a Role?

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