Metformin and atorvastatin combination further protect the liver in type 2 diabetes with hyperlipidaemia

Matafome, Paulo; Louro, Teresa; Rodrigues, Lisa; Crisóstomo, Joana; Nunes, Elsa; Amaral, Carlos; Monteiro, Pedro; Cipriano, Augusta; Seiça, Raquel

doi:10.1002/dmrr.1157

Cited by 64 publications

(51 citation statements)

References 36 publications

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“…In one study of fatty liver pathogenesis, type 2 diabetic mice fed with a high-fat diet developed increased levels of markers of inflammation and oxidative stress, including C-reactive protein, interleukin-6 and tumor necrosis factor-α. 30 The combinatorial use of atorvastatin and metformin attenuated these effects to a significantly greater degree than either drug alone. Another study found that the proapoptotic and anti-survival effects of an AMPK activator similar to metformin on malignant melanoma cell lines were enhanced by combination with simvastatin or fluvastatin.…”

Section: Discussionmentioning

confidence: 98%

Synergism between metformin and statins in modifying the risk of biochemical recurrence following radical prostatectomy in men with diabetes

Danzig

Kotamarti

Ghandour

et al. 2014

Prostate Cancer Prostatic Dis

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The combination of statins and metformin in men undergoing RP for prostate cancer (PCa) may be associated with a lower BCR risk than would be predicted based on the independent effects of both medications. A synergism between these two agents is biologically plausible based on our current understanding of their diverse molecular pathways of action. The results of future clinical trials involving the use of either medication in men with PCa should be carefully assessed for confirmatory evidence of such a relationship.

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Section: Discussionmentioning

confidence: 98%

Synergism between metformin and statins in modifying the risk of biochemical recurrence following radical prostatectomy in men with diabetes

Danzig

Kotamarti

Ghandour

et al. 2014

Prostate Cancer Prostatic Dis

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“…Therefore, these models are unable to facilitate systematic examination of the effect of timed onset of diabetes added to a high-fat diet or to a metabolic syndrome phenotype; however, interventions targeting hyperglycemia in diabetes, for example, can be trialled in them. To date, these interventions are relatively few and include hepatic antisteatotic and systemic antiinflammatory effects of a selective dipeptidyl peptidase-IV (DPP-IV) inhibitor in a murine diabetes model (126), statin therapy with either metformin (127) or insulin (128) in db/db fat-fed mice, and peroxisome proliferator-activated receptor (PPAR)-␣ agonist treatment in the foz/foz cholesterol-fed model (129). This limited series of studies is collated in Table 2 and collectively implicates dyslipidemia, insulin resistance, and possibly hyperglycemia in effects of type 2 diabetes on NAFLD and its progression.…”

Section: Pathogenic Mechanisms In the Relationship Of Nafld Andmentioning

confidence: 99%

Diabetes and Nonalcoholic Fatty Liver Disease: A Pathogenic Duo

et al. 2012

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Recent data increasingly support a complex interplay between the metabolic condition diabetes mellitus and the pathologically defined nonalcoholic fatty liver disease (NAFLD). NAFLD predicts the development of type 2 diabetes and vice versa, and each condition may serve as a progression factor for the other. Although the association of diabetes and NAFLD is likely to be partly the result of a "common soil," it is also probable that diabetes interacts with NAFLD through specific pathogenic mechanisms. In particular, through interrelated metabolic pathways currently only partly understood, diabetes appears to accelerate the progression of NAFLD to nonalcoholic steatohepatitis, defined by the presence of necroinflammation, with varying degrees of liver fibrosis. In the research setting, obstacles that have made the identification of clinically significant NAFLD, and particularly nonalcoholic steatohepatitis, difficult are being addressed with the use of new imaging techniques combined with risk algorithms derived from peripheral blood profiling. These techniques are likely to be used in the diabetes population in the near future. This review examines the pathogenic links between NAFLD and diabetes by exploring the epidemiological evidence in humans and also through newer animal models. Emerging technology to help screen noninvasively for differing pathological forms of NAFLD and the potential role of preventive and therapeutic approaches for NAFLD in the setting of diabetes are also examined.

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“…Thus, for controlling blood glucose level and cholesterol level, combination therapy has become undoubtedly well-appreciated [26] [27]. As a result, combination therapy is being regarded as the most efficient remedy, on account of their potentiality to revive the function of the pancreas with an improved insulin output, to slacken the intestinal absorption of glucose, to process the metabolites in insulin dependent pathways [28] and by inhibiting the enzyme HMG-CoA (3-hydroxy-3-methyl-glutaryl-coenzyme A reductase) reductase to cease the cholesterol biosynthetic route [29].…”

Section: Introductionmentioning

confidence: 99%

Comparison of the Hypoglycemic, Hypolipidemic and Hepatoprotective Effects of<i> Asparagus racemosus</i> Linn. in Combination with Gliclazide and Pioglitazone on Alloxan-Induced Diabetic Rats

Mamun¹,

Hossain²,

Islam³

et al. 2017

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In recent years, the popularity of medicinal plants as a remedy has been increased manifold due to having minimal adverse effects. The current study aimed to compare the hypoglycemic, hypolipidemic and hepatoprotective effects of the ethanolic extract of Asparagus racemosus (EEAR) Linn. alone and combinedly with conventional antidiabetic agents (gliclazide and pioglitazone) in alloxan-induced diabetic rats. Diabetes was induced in male Wister albino rats by the administration of single intra-peritoneal injection of alloxan monohydrate (120 mg/kg b.w.). Effect of oral administration of two different doses of EEAR (200 and 400 mg/kg b.w.), gliclazide (10 mg/kg b.w.) and pioglitazone (10 mg/70kg/b.w.) alone for 2 weeks and a combination of EEAR (200 mg/kg b.w.) with either gliclazide (10 mg/kg b.w.) or pioglitazone (10 mg/70kg/b.w.) for 2 weeks were examined on hypoglycemic activity on 0 treatment as compared to that of disease control rats, gliclazide treated rats and pioglitazone treated rats. Proposed adjunct therapy also markedly (p < 0.001; p < 0.01, p < 0.001) improved serum TG, HDL and LDL level with insignificant change in VLDL and TC level while comparing with groups receiving gliclazide treated rats and pioglitazone treated rats. Administration of different doses of EEAR markedly (p < 0.05, p < 0.01, p < 0.001; p < 0.05, p < 0.01; p < 0.05) reduced the activity of TC, TG, LDL, VLDL and HDL cholesterol levels in a dose-dependent approach with respect to that of gliclazide treated rats and pioglitazone treated rats. The effect of combination therapy significantly (p < 0.001; p < 0.001; p < 0.01, p < 0.001) decreased the SGOT, SGPT and TP hepatic enzyme levels when compared to disease control rats, gliclazide treated rats and pioglitazone treated rats indicated improvement in liver dysfunctions. Administration of different doses of EEAR noticeably (p < 0.05, p < 0.01, p < 0.001; p < 0.05, p < 0.01; p < 0.05, p < 0.01) reduced the liver enzymes level including SGOT, SGPT and TP in a dose-dependent manner as compared to the disease control rats, gliclazide treated rats and pioglitazone treated rats. The maximum survival rate (100%) was observed in rats of combination treated rats. No significant changes in the body weight and organ weight to body weight ratio were observed except the groups that were given combined therapy showed improvement in the liver and pancreas weight. Our study suggests that the EEAR potentiates the activity of gliclazide and pioglitazone in controlling blood glucose levels, modifies the lipid profile and improves in liver dysfunction on alloxan-induced diabetic rats.

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Metformin and atorvastatin combination further protect the liver in type 2 diabetes with hyperlipidaemia

Abstract: our data provides evidence of a greater benefit with a combination of atorvastatin and metformin in improving liver injury in type 2 diabetes with hyperlipidaemia.

Cited by 64 publications

References 36 publications

Synergism between metformin and statins in modifying the risk of biochemical recurrence following radical prostatectomy in men with diabetes

Synergism between metformin and statins in modifying the risk of biochemical recurrence following radical prostatectomy in men with diabetes

Diabetes and Nonalcoholic Fatty Liver Disease: A Pathogenic Duo

Comparison of the Hypoglycemic, Hypolipidemic and Hepatoprotective Effects of<i> Asparagus racemosus</i> Linn. in Combination with Gliclazide and Pioglitazone on Alloxan-Induced Diabetic Rats

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Metformin and atorvastatin combination further protect the liver in type 2 diabetes with hyperlipidaemia

Abstract: our data provides evidence of a greater benefit with a combination of atorvastatin and metformin in improving liver injury in type 2 diabetes with hyperlipidaemia.

Cited by 64 publications

References 36 publications

Synergism between metformin and statins in modifying the risk of biochemical recurrence following radical prostatectomy in men with diabetes

Synergism between metformin and statins in modifying the risk of biochemical recurrence following radical prostatectomy in men with diabetes

Diabetes and Nonalcoholic Fatty Liver Disease: A Pathogenic Duo

Comparison of the Hypoglycemic, Hypolipidemic and Hepatoprotective Effects of&lt;i&gt; Asparagus racemosus&lt;/i&gt; Linn. in Combination with Gliclazide and Pioglitazone on Alloxan-Induced Diabetic Rats

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Comparison of the Hypoglycemic, Hypolipidemic and Hepatoprotective Effects of<i> Asparagus racemosus</i> Linn. in Combination with Gliclazide and Pioglitazone on Alloxan-Induced Diabetic Rats