Effects of Early Resveratrol Intervention on Skeletal Muscle Mitochondrial Function and Redox Status in Neonatal Piglets with or without Intrauterine Growth Retardation.

Kang Cheng,Tian Wang,Hao Zhang,Simian Li,Zhihua Song,Ting Wang,Lili Zhang

doi:10.1155/2020/4858975

Abstract

Skeletal muscle mitochondrial malfunction of offspring induced by intrauterine growth retardation (IUGR) may be a contributor to growth restriction and metabolic disorder at various periods of life. This study explored the effects of IUGR and resveratrol (RSV) on mitochondrial function and redox status in the longissimus dorsi muscle (LM) of piglets during the sucking period. A total of 36 pairs of IUGR and normal birth weight male piglets were orally fed with either 80 mg RSV/kg body weight/d or 0.5% carboxymethylcellulose sodium during days 7-21 after birth. The results showed that RSV treatment improved anomalous mitochondrial morphology, increased adenosine triphosphate and glycogen contents, and enhanced nicotinamide adenine dinucleotide/reduced form of nicotinamide-adenine dinucleotide ratio in the LM of IUGR piglets. Moreover, the IUGR-induced increased malondialdehyde and protein carbonyl concentrations, abnormal mtDNA number, and suppressed genes expression of mitochondrial biogenesis such as nuclear respiratory factor 1, estrogen-related receptor alpha, and polymerase gamma in the LM were restored to some extent by RSV treatment. Additionally, RSV increased mitochondrial complex V activity in the LM of piglets. Collectively, RSV administration alleviated the LM mitochondrial dysfunction and oxidative damage of IUGR piglets.

Highlights

Offspring affected by a low birth weight (LBW) after suffering processes of intrauterine growth retardation (IUGR) is receiving increased attention in both human medicine and animals production, owing to the short-term and long-term repercussions of LBW [1]
Epidemiological and animal studies have found that IUGR offspring exhibited impaired skeletal muscle growth and development as well as abnormal glucose metabolism [5,6,7], which may be associated with a mitochondrial malfunction in skeletal muscle
Piglets suffering from IUGR exhibited the diminished levels of ATP and NAD+, reduced NAD+/NADH ratio, and increased NADH content in the longissimus dorsi muscle (LM) (P < 0:05, Figure 3)

Summary

Introduction

Offspring affected by a low birth weight (LBW) after suffering processes of intrauterine growth retardation (IUGR) is receiving increased attention in both human medicine and animals production, owing to the short-term (incremental morbidity and mortality of neonates) and long-term repercussions of LBW (decreased growth patterns, health status, and performance of individuals) [1]. The main reason for IUGR is the decrease of nutrients and oxygen to the fetus by the placenta [2]. Epidemiological and animal studies have found that IUGR offspring exhibited impaired skeletal muscle growth and development as well as abnormal glucose metabolism [5,6,7], which may be associated with a mitochondrial malfunction in skeletal muscle. Limited information about skeletal muscle mitochondrial redox status in IUGR offspring was available, which needs to be investigated in the present study. Oxidative Medicine and Cellular Longevity improving the mitochondrial function and redox status in skeletal muscle may be a potential strategy to alleviate the negative effects of IUGR on growth and metabolism

Methods

Results

Conclusion