Transfer of β-hydroxy-β-methylbutyrate from sows to their offspring and its impact on muscle fiber type transformation and performance in pigs

Background： Previous studies suggested that supplementation of lactating sows with β-hydroxy-β-methylbutyrate（HMB） could improve the performance of weaning pigs, but there were little information in the muscle fiber type transformation of the offspring and the subsequent performance in pigs from weaning through finishing in response to maternal HMB consumption. The purpose of this study was to determine the effect of supplementing lactating sows with HMB on skeletal muscle fiber type transformation and growth of the offspring during d 28 and180 after birth. A total of 20 sows according to their body weight were divided into the control（CON, n = 10） or HMB groups（HMB, n = 10）. Sows in the HMB group were supplemented with β-hydroxy-β-methylbutyrate calcium（HMB-Ca） 2 g/kg feed during d 1 to 27 of lactation. After weaning, 48 mixed sex piglets were blocked by sow treatment and fed standard diets for post-weaning, growing, finishing periods. Growth performance was recorded during d 28 to 180 after birth. Pigs were slaughtered on d 28（n = 6/treatment） and 180（n = 6/treatment） postnatal and the longissimus dorsi（LD） was collected, respectively.Results： The HMB-fed sows during lactation showed increased HMB concentration（P ＆lt; 0.05） in milk and LD of weaning piglets（P ＆lt; 0.05）. In addition, offsprings in HMB group had a higher finishing BW and lean percentage than did pigs in CON group（P ＆lt; 0.05）, meanwhile, compared with pigs from sows fed the CON diet, pigs from sows fed HMB diet showed higher type Ⅱ muscle fiber cross-sectional area（CSA）, elevated myosin heavy chain（MyHC） Ⅱb and Sox6 mRNA, and fast-MyHC protein levels in LD（P ＆lt; 0.05）.Conclusions： HMB supplemented to sow diets throughout lactation increases the levels of HMB in maternal milk and skeletal muscle of pigs during d 28 after birth and promotes subsequent performance of pigs between d 28 and 180 of age by enhancing glycolytic muscle fiber transformation.

β-hydroxy-β-methylbutyrate Improves Chronic Renal Failure-Induced Sarcopenia in SD Rats by Regulating Autophagy

Background Chronic renal failure-induced sarcopenia(CRF-S)seriously affects public health by increasing morbidity and mortality.This study evaluated the therapeutic effects ofβ-hydroxy-β-methylbutyrate acid(HMB)and the underlying mechanism in an adenine-induced CRF-S rat model.Methods Sprague Dawley rats were divided into control,model(CRF-S),and HMB treatment(CRF-S+HMB)groups.The rats in the CRF-S group received 250 mg/kg/d adenine by oral gavage every day for 14 days,followed by administration every other day until the 28th day.In the CRF-S+HMB group,each rat was given 320 mg/kg/d HMB by oral gavage starting from 7 days prior to adenine treatment,and this treatment was maintained for a total of 35 days.The body weight,right anterior tibial muscle weight,blood serum parameters,gastrocnemius muscle and renal tissue histology,and expression of autophagy-related transcripts and proteins were evaluated.Results A rat model of CRF-S was successfully established via adenine gavage,as indicated by reduced body weight and muscle weights,and markers of sarcopenia.There were increased mRNA levels of LC3B,Beclin1,Ulk1,Atg5,Atg7,Atg13 and vps-34,and increased protein expression levels of LC3B and P62.In the rats with HMB intervention,the body weight,right anterior tibial weight and gastrocnemius muscle histology were not significantly different from those in the control group,and the expression levels of autophagy-related proteins(LC3B and P62)were consistent with those in the control group.Conclusion We successfully established a rat model of CRF-S using adenine administered via oral gavage,and observed that HMB treatment prevented CRF-S.