Carnitine – ABC CARDIOL

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Editorial

L-Carnitine Supplementation in the Diabetic Heart

Filipe Welson Leal Pereira et al. Sergio Alberto Rupp de Paiva

Carnitine is a non-essential nutrient, which is derived from amino acids. The main food source of carnitine is red meat, poultry and dairy products. Part of the carnitine can be produced endogenously, from lysine and methionine mainly by the liver and kidneys. It acts primarily as an enzymatic cofactor for the transport of long-chain fatty acids from the cytoplasm into the mitochondria, and subsequent degradation to beta-oxidation, being a very important energy metabolism pathway. Therefore, carnitine is essential as fuel for muscles, and more than 95% of the total body carnitine is found in skeletal muscle. The liver, heart, brain and kidneys have the remainder of the body’s carnitine reserves or are able to synthesize it. This distribution shows the importance of carnitine in these organs. L-carnitine supplementation has been studied in sarcopenia, in liver diseases, in heart failure, in kidney diseases and in neurological diseases.^,

Most studies have shown the benefit of L-carnitine on cardiovascular risk factors. L-carnitine supplementation reduces hypertension, hyperlipidemia, hyperglycemia, insulin-dependent diabetes mellitus, insulin resistance, obesity, inflammation and oxidative stress.^{, –}

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Original Article

Novel Cardioprotective Effect of L-Carnitine on Obese Diabetic Mice: Regulation of Chemerin and CMKLRI Expression in Heart and Adipose Tissues

Rezvan Amiri et al. Mohammad Reza Tabandeh Seyed Ahmad Hosseini

Abstract

Background

L-carnitine (LC) has many beneficial effects on diabetic animals and humans, but its regulatory effect on chemerin as an inflammatory cytokine, and its receptor in diabetes status is unknown.

Objectives

The present study aimed to investigate the regulatory effect of LC on the expression of chemerin and chemokine-like receptor I (CMKLRI) in adipose and cardiac tissues of diabetic mice.

Methods

Sixty NMARI mice were divided into four groups including control, diabetic, diabetic + LC supplementation and control + LC supplementation. Diabetes was induced by feeding the animals a high-calorie diet for 5 weeks and injection of Streptozotocin. The animals were treated with 300 mg/kg LC for 28 days. On days 7, 14, and 28 after treatment, the mRNA and protein levels of chemerin and CMKLRI in the cardiac and adipose tissues of the animals were determined using qPCR analysis and ELISA. Insulin resistance indices were also measured in all experimental groups. Differences with p <0.05 were considered significant.

Results

Chemerin and CMKLRI expressions levels were increased in cardiac and adipose tissues of diabetic mice on days 14 and 28 after diabetes induction, concurrent with the incidence of insulin resistance and increased levels of circulating chemerin (p<0.05). The treatment with LC caused a significant decrease in the expression of both genes in studied tissues and the reduction of insulin resistance symptoms and serum chemerin levels (p<0.05).

Conclusion

The results suggest that LC treatment were able to downregulate the expression of chemerin and CKLR1 in cardiac and adipose tissues of obese, diabetic experimental animals.