Effects of acetyl‐L‐carnitine and oxfenicine on aorta stiffness in diabetic rats

Chang, Kuo‐Chu; Tseng, Chuen-Den; Lu, Shao-Chun; Liang, Jin–Tung; Wu, Ming-Shiou; Tsai, Ming-Shian; Hsu, Kwan-Lih

doi:10.1111/j.1365-2362.2010.02358.x

Cited by 7 publications

(19 citation statements)

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“…Oxfenicine (4-Hydroxy-L-phenylglycine) has been successfully used as an inhibitor of fatty acid oxidation, but with contradictory outcomes [22,23]. A few studies have reported negative outcomes associated with the experimental use of oxfenicine in healthy lean animals [23][24][25][26]. The underlying mechanism(s) for these effects remain unclear.…”

Section: Introductionmentioning

confidence: 97%

Effect of Chronic CPT-1 Inhibition on Myocardial Ischemia-Reperfusion Injury (I/R) in a Model of Diet-Induced Obesity

Maarman

Marais

Lochner

et al. 2012

Cardiovasc Drugs Ther

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Section: Introductionmentioning

confidence: 97%

Effect of Chronic CPT-1 Inhibition on Myocardial Ischemia-Reperfusion Injury (I/R) in a Model of Diet-Induced Obesity

Maarman

Marais

Lochner

et al. 2012

Cardiovasc Drugs Ther

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“…Previous work from our laboratory demonstrated that OXF, but not ALC, elevates R p in the diabetic peripheral arteries, which parallels its increase in plasma levels of FFA [17]. By contrast, ALC attenuates the diabetes-related arterial stiffening and cardiac hypertrophy through its ability to reduce aorta levels of MDA/TABRS in the DM.…”

Section: Discussionmentioning

confidence: 61%

“…Thus, the reduced plasma FFA and cardiac MDA levels from ALC may be responsible for the prevention of diabetes-related damage in the myocardial contractility. By contrast, in the absence of any significant changes in cardiac MDA content, the already high plasma levels of FFA augmented when the DM was treated with OXF [17]. OXF might accordingly be expected to exert no benefit to the diabetic heart and even worsen the contractile status of the LV.…”

Section: Discussionmentioning

confidence: 94%

“…Conversely, oxfenicine (OXF) is a well-characterized CPT-1 inhibitor that can reduce the accumulation of long-chain acyl-carnitine to enhance glucose metabolism [16]. Our team demonstrated in the past that ALC, but not OXF, attenuated arterial stiffening by reducing aorta levels of malondialdehyde (MDA) in insulin-deficient rats [17]. MDA is a highly toxic byproduct formed by lipid oxidation-derived free radicals, which can react with collagen to form MDA-collagen cross-links with profound cardiovascular risk [18], [19].…”

Section: Introductionmentioning

confidence: 99%

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Acetyl-l-Carnitine and Oxfenicine on Cardiac Pumping Mechanics in Streptozotocin-Induced Diabetes in Male Wistar Rats

Wang

et al. 2013

PLoS ONE

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IntroductionIn the treatment of patients with diabetes, one objective is an improvement of cardiac metabolism to alleviate the left ventricular (LV) function. For this study, we compared the effects of acetyl-l-carnitine (one of the carnitine derivatives) and of oxfenicine (a carnitine palmitoyltransferase-1 inhibitor) on cardiac pumping mechanics in streptozotocin-induced diabetes in male Wistar rats, with a particular focus on the pressure-flow-volume relationship.MethodsDiabetes was induced by a single tail vein injection of 55 mg kg−1 streptozotocin. The diabetic animals were treated on a daily basis with either acetyl-L-carnitine (1 g L−1 in drinking water) or oxfenicine (150 mg kg−1 by oral gavage) for 8 wk. They were also compared with untreated age-matched diabetic controls. LV pressure and ascending aortic flow signals were recorded to calculate the maximal systolic elastance (E max) and the theoretical maximum flow (Q max). Physically, E max reflects the contractility of the myocardium as an intact heart, whereas Q max has an inverse relationship with the LV internal resistance.ResultsWhen comparing the diabetic rats with their age-matched controls, the cardiodynamic condition was characterized by a decline in E max associated with the unaltered Q max. Acetyl-l-carnitine (but not oxfenicine) had reduced cardiac levels of malondialdehyde in these insulin-deficient animals. However, treating with acetyl-l-carnitine or oxfenicine resulted in an increase in E max, which suggests that these 2 drugs may protect the contractile status from deteriorating in the diabetic heart. By contrast, Q max showed a significant fall after administration of oxfenicine, but not with acetyl-L-carnitine. The decrease in Q max corresponded to an increase in total vascular resistance when treated with oxfenicine.ConclusionsAcetyl-l-carnitine, but not oxfencine, optimizes the integrative nature of cardiac pumping mechanics by preventing the diabetes-induced deterioration in myocardial intrinsic contractility associated with unaltered LV internal resistance.

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“…Considering the role of oxidative stress in this process, antioxidant treatment can be expected to reduce/ prevent organ damages in DM. It has been shown in recent studies that antioxidant agents such as apocynin, lipoic acid, simvastatin,coenzyme Q10 and acetyl L-carnitine have positive effects in DM (5)(6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%

Quercetin, a Powerful Antioxidant Bioflavonoid, Prevents Oxidative Damage in Different Tissues of Long-Term Diabetic Rats

Edremitlioğlu¹,

Andiç²,

Korkut³

2012

Balkan Med J

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Objective: The role of oxidant damage on the development of end-organ injuries caused by diabetic rat is well known. The aim of this study is to examine the effect of quercetin, which is a strong antioxidant bioflavonoid, on oxidant damage and antioxidant capacity in various organs in the case of medium-term or long-term diabetic rat.Material and Methods: Forty-eight male Wistar rats were divided into five groups, namely, control group, diabetic group of 8-weeks, diabetic group of 16-weeks, quercetin treated diabetic group of 8-weeks, and quercetin treated diabetic group of 16-weeks. At the end of the experiment, malondialdehyde levels, superoxide dismutase, catalase, and glutathione peroxidase activities were measured in the lung, aorta, heart, spleen, liver, and kidney tissues.Results: MDA levels were elevated in all tissues except in the lung in non-treated diabetic groups. Quercetin treatment increased the antioxidant enzyme capacities and considerably reduced oxidant damage. Conclusion:We suggest that quercetin has a protective effect on the aorta, heart, brain, liver, and kidneys from oxidant damage in the case of mediumterm or long-term diabetic rat. It can be argued that quercetin is effective by increasing the antioxidant defence capacity in this process.

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Effects of acetyl‐L‐carnitine and oxfenicine on aorta stiffness in diabetic rats

Abstract: Acetyl-L-carnitine, but not oxfenicine, attenuates aortic stiffening and cardiac hypertrophy, possibly through its decrease of lipid oxidation-derived MDA/TBARS in the rats with insulin deficiency.

Cited by 7 publications

References 47 publications

Effect of Chronic CPT-1 Inhibition on Myocardial Ischemia-Reperfusion Injury (I/R) in a Model of Diet-Induced Obesity

Effect of Chronic CPT-1 Inhibition on Myocardial Ischemia-Reperfusion Injury (I/R) in a Model of Diet-Induced Obesity

Acetyl-l-Carnitine and Oxfenicine on Cardiac Pumping Mechanics in Streptozotocin-Induced Diabetes in Male Wistar Rats

Quercetin, a Powerful Antioxidant Bioflavonoid, Prevents Oxidative Damage in Different Tissues of Long-Term Diabetic Rats

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