Effects of branched-chain amino acid supplementation in dams fed a low-protein diet on muscle growth and mitochondrial oxidative capacity in obese offspring

BCAA;low protein diet;mouse offspring;high-fat diet;muscle;mitochondria;641

생활과학대학 식품영양학과 ;

University:서울대학교 대학원

关键词: BCAA;    low protein diet;    mouse offspring;    high-fat diet;    muscle;    mitochondria;    641;   

Others  :  http://s-space.snu.ac.kr/bitstream/10371/142174/3/000000149700.pdf

美国|英语

来源: Seoul National University Open Repository

【 摘 要 】

Maternal low protein (LP) diet has been reported to have a negative impact on the onset of metabolic diseases in adulthood, which is related to growth retardation during fetal development. Branched-chain amino acids (BCAA), especially leucine, activates mechanistic target of rapamycin pathway that stimulate protein synthesis, and it is known that the circulating level of BCAA is reduced in the dams fed an LP diet. It suggests that maternal BCAA supplementation could relieve the growth retardation and this restoration could affect muscle oxidative capacity through alterations of muscle fiber distribution, and finally cause changes in response to high-fat diet. To test, female ICR mice were fed a normal protein (NP, 20% casein), low protein (LP, 10% casein), LP with 2% BCAA or 2% alanine (Ala) diet two weeks prior to mating and throughout gestation and lactation. Male offspring were challenged with high fat (45% kcal from fat) diet after weaning to 25 weeks of age. Gastrocnemius muscle weight and Pax7 mRNA expression level, a satellite cell marker, were decreased by maternal LP feeding, but were reversed by BCAA and Ala supplementation. Furthermore, maternal LP consumption reduced total ribosomal protein S6 level, a marker of ribosome biogenesis, which was increased in the LP+BCAA and LP+Ala groups. However, the markers related to the high-fat diet induced atrophy, such as ER stress, were not changed by maternal LP diet. HOMA-IR, an index of systemic insulin resistance, was significantly lower in the LP group compared with the NP group, but the effect of maternal BCAA supplementation was not observed. Moreover, there were no changes in the mitochondrial oxidative capacity of gastrocnemius and soleus muscle. In conclusion, maternal BCAA supplementation has protective effects on the damaged muscle growth and these effects were mediated by increasing satellite cell number and ribosome biogenesis. However, the specific effect of BCAA on muscle growth was not observed.