The propionyl-l-carnitine hypothesis: An alternative approach to treating heart failure

Ferrari, Roberto; Giuli, Federica De

doi:10.1016/s1071-9164(97)90018-x

Cited by 35 publications

(17 citation statements)

References 41 publications

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“…This has been shown experimentally in hypertrophied hearts (Schonekess et al, 1995) and post-ischaemically (Loster et al, 1999;Felix et al, 2001). However, not all studies have shown a universal benefit for cardiac function (Ferrari and De Giuli, 1997). As predicted from Fig.…”

Section: Fuel Usesupporting

confidence: 56%

Carnitine acyltransferases and their influence on CoA pools in health and disease

Ramsay

Zammit

2004

Molecular Aspects of Medicine

126

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Section: Fuel Usesupporting

confidence: 56%

Carnitine acyltransferases and their influence on CoA pools in health and disease

Ramsay

Zammit

2004

Molecular Aspects of Medicine

126

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“…reported that l ‐carnitine released from PLC metabolism increased the CoA‐SH/acetyl‐CoA ratio by stimulating the mitochondrial efflux of pyruvate‐generated acetyl‐CoA in the form of acetyl carnitine in a reaction mediated by carnitine acetyl transferase. Conversely, the propionyl‐CoA formed in the mitochondria from PLC can be converted into succinyl‐CoA, in a reaction mediated by propionyl‐CoA carboxylase, thus increasing, with an anaplerotic reaction, the flux through the Krebs cycle and the energy yielding utilization of acetyl‐CoA in the absence of oxygen consumption 60,61 . Accordingly, the reversal of CDDP‐induced depletion of total carnitine and ATP in kidney tissues by PLC could be a secondary event following an increase in long‐chain fatty utilization, with a consequent increase in ATP production.…”

Section: Discussionmentioning

confidence: 99%

REVERSAL OF CISPLATIN‐INDUCED CARNITINE DEFICIENCY AND ENERGY STARVATION BY PROPIONYL‐l‐CARNITINE IN RAT KIDNEY TISSUES

Aleisa

Al-Majed

Al-Yahya

et al. 2007

Clin Exp Pharma Physio

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1. The present study examined whether propionyl-L-carnitine (PLC) could prevent the development of cisplatin (CDDP)-induced acute renal failure in rats. 2. Forty adult male Wistar albino rats were divided into four groups. Rats in the first group were injected daily with normal saline (2.5 mL/kg, i.p.) for 10 consecutive days, whereas the second group received PLC (250 mg/kg, i.p.) for 10 consecutive days. Animals in the third group were injected daily with normal saline for 5 consecutive days before and after a single dose of CDDP (7 mg/kg, i.p.). Rats in the fourth group received a combination of PLC (250 mg/kg, i.p.) for 5 consecutive days before and after a single dose of CDDP (7 mg/kg, i.p.). On Day 6 following CDDP treatment, animals were killed and serum and kidneys were isolated for analysis. 3. Injection of CDDP resulted in a significant increase in serum creatinine, blood urea nitrogen (BUN), thiobarbituric acid-reactive substances (TBARS) and total nitrate/nitrite (NO(x)), as well as a significant decrease in reduced glutathione (GSH), total carnitine, ATP and ATP/ADP in kidney tissues. 4. Administration of PLC significantly attenuated the nephrotoxic effects of CDDP, manifested as normalization of the CDDP-induced increase in serum creatinine, BUN, TBARS and NO(x) and the CDDP-induced decrease in total carnitine, GSH, ATP and ATP/ADP in kidney tissues. 5. Histopathological examination of kidney tissues from CDDP-treated rats showed severe nephrotoxicity, in which 50-75% of glomeruli and renal tubules exhibited massive degenerative changes. Interestingly, administration of PLC to CDDP-treated rats resulted in a significant improvement in glomeruli and renal tubules, in which less than 25% of glomeruli and renal tubules exhibited focal necrosis. 6. Data from the present study suggest that PLC prevents the development of CDDP-induced acute renal injury by a mechanism related, at least in part, to the ability of PLC to increase intracellular carnitine content, with a consequent improvement in mitochondrial oxidative phosphorylation and energy production, as well as its ability to decrease oxidative stress. This will open new perspectives for the use of PLC in the treatment of renal diseases associated with or secondary to carnitine deficiency.

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“…Patients with HF, particularly those treated with diuretics, may become deficient in vitamins and micronutrients. Several nutritional supplements (e.g., coenzyme Q10, carnitine, taurine, and antioxidants) and hormonal therapies (e.g., growth hormone or thyroid hormone) have been proposed for the treatment of HF (424)(425)(426)(427)(428)(429). Aside from replen-ACC/AHA Practice Guidelines ACC -www.acc.org AHA -www.americanheart.org term treatment of HF, even in its advanced stages.…”

Section: Drugs and Interventions Of Unproved Value And Not Recommendedmentioning

confidence: 99%

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult

Hunt¹

2005

Journal of the American College of Cardiology

1,873

357

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The propionyl-l-carnitine hypothesis: An alternative approach to treating heart failure

Cited by 35 publications

References 41 publications

Carnitine acyltransferases and their influence on CoA pools in health and disease

Carnitine acyltransferases and their influence on CoA pools in health and disease

REVERSAL OF CISPLATIN‐INDUCED CARNITINE DEFICIENCY AND ENERGY STARVATION BY PROPIONYL‐l‐CARNITINE IN RAT KIDNEY TISSUES

ACC/AHA 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure in the Adult

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