Dietary supplementation with β-hydroxy-β-methylbutyrate calcium during the early postnatal period accelerates skeletal muscle fibre growth and maturity in intra-uterine growth-retarded and normal-birth-weight piglets

Abstract

Intra-uterine growth restriction (IUGR) impairs postnatal growth and skeletal muscle development in neonatal infants. This study evaluated whether dietary β-hydroxy-β-methylbutyrate Ca (HMB-Ca) supplementation during the early postnatal period could improve muscle growth in IUGR neonates using piglets as a model. A total of twelve pairs of IUGR and normal-birth-weight (NBW) male piglets with average initial weights (1·85 (SEM 0·36) and 2·51 (SEM 0·39) kg, respectively) were randomly allotted to groups that received milk-based diets (CON) or milkbased diets supplemented with 800 mg/kg HMB-Ca (HMB) during days 7-28 after birth. Blood and longissimus dorsi (LD) samples were collected and analysed for plasma amino acid content, fibre morphology and the expression of genes related to muscle development. The results indicate that, regardless of diet, IUGR piglets had a significantly decreased average daily weight gain (ADG) compared with that of NBW piglets (P < 0·05). However, IUGR piglets fed HMB-Ca had a net weight and ADG similar to that of NBW piglets fed the CON diet. Irrespective of body weight (BW), HMB-Ca supplementation markedly increased the type II fibre cross-sectional area and the mRNA expression of mammalian target of rapamycin (mTOR), insulin-like growth factor-1 and myosin heavy-chain isoform IIb in the LD of piglets (P < 0·05). Moreover, there was a significant interaction between the effects of BW and HMB on mTOR expression in the LD (P < 0·05). In conclusion, HMB-Ca supplementation during the early postnatal period could improve skeletal muscle growth and maturity by accelerating fast-twitch glycolytic fibre development in piglets.

Postnatal development of skeletal muscle in pigs with intrauterine growth restriction: morphofunctional phenotype and molecular mechanisms

“…It is well established that muscle fiber number, which is determined at the fetal stage, is a crucial component of postnatal growth, and postnatal skeletal muscle development is mainly attributable to the increase in muscle fiber size, with no net formation of new muscle fibers (Brameld et al 2000;Yan et al 2013). Since the number of muscle fibers formed during the fetal stage is dependent on the number of available myogenic progenitor cells, and their proliferation is highly sensitive to nutrient availability in utero (Yan et al 2013 Similar to previous studies (Alvarenga et al 2013;Wan et al 2016) where growth rates of different birth weight pigs were investigated, IUGR gilts showed lower body weights throughout the postnatal development period. This may be attributable to the lower muscle fiber number observed in IUGR piglets at birth, as a positive correlation between muscle fiber number and performance traits has been previously reported (Oksbjerg et al 2013;Madsen et al 2017).…”

A metabolite of leucine (β-hydroxy-β-methylbutyrate) given to sows during pregnancy alters bone development of their newborn offspring by hormonal modulation

“…Oral administration of LEU or HMB enhances protein synthesis not only in skeletal muscle but also in other tissues [1, 5]. Moreover, multiple clinical studies show that HMB counteracts protein degradation in many pathological conditions like AIDS trauma bed rest, cancer cachexia, or IUGR [3, 6]. Many in vitro studies have been conducted to examine the mechanism of HMB action [3].…”

Overcoming nature’s paradox in skeletal muscle to optimise animal production

“…Leucine, as a standalone nutritional intervention, is not effective in preventing muscle wasting. In contrast, some studies in rapidly growing young pigs fed a protein-restricted diet have shown that feeding with leucine (or its metabolite b-hydroxymethylbutyrate) can enhance growth (Wan et al 2016;Zheng et al 2016). Using porcine myoblasts, in vitro studies have suggested that leucine induces a fast-to-slow fibretype transition via AMP-activated protein kinase/SIRT1mediated (Chen et al 2019) or FOXO1-mediated (Zhang et al 2019) signalling.…”