Whey peptide ingestion suppresses body fat accumulation in senescence-accelerated mouse prone 6 (SAMP6).

PURPOSE: Body weight in young growing and young adult animals was reduced by a high dietary density of whey protein concentrate; however, it is unclear whether dietary proteins similarly affect body weight in aging animals. Here, we examined whether whey protein or whey peptide ingestion suppressed body fat accumulation and affected protein expression and phosphorylation in skeletal muscle in aging mice.

METHODS: Twenty-six male senescence-accelerated mouse prone 6 (SAMP6) mice were assigned randomly to three dietary treatment groups: 18.7% casein control (CON), 18.7% whey protein (WPR), and 18.7% whey peptide (WPE). After 28 weeks of treatment, skeletal tissues were dissected and weighed for analysis. Western blotting was performed to examine the expression of AMP-activated protein kinase (AMPK), acetyl-CoA carboxylase (ACC), and adipose triglyceride lipase (ATGL) in quadriceps muscles.

RESULTS: Body (CON: 47.6 ± 2.2 g, WPR: 48.2 ± 2.7 g, WPE: 38.3 ± 2.0 g) and relative white adipose tissue (CON: 38.5 ± 3.5 mg/g, WPR: 43.8 ± 4.0 mg/g, WPE: 21.1 ± 4.4 mg/g) weights were lower in the WPE group compared with the other two groups (p < 0.05), and no significant differences were observed between the CON and WPR groups. The relative weights of tibialis anterior muscle (CON: 1.04 ± 0.04 mg/g, WPR: 0.97 ± 0.03 mg/g, 1.23 ± 0.05 mg/g) and gastrocnemius muscle (CON: 3.02 ± 0.12 mg/g, WPR: 2.92 ± 0.15 mg/g, WPE: 3.65 ± 0.18 mg/g) were higher in the WPE group compared with the other groups (p < 0.05). The phosphorylation of AMPK (WPR: 1.03 ± 0.11, WPE: 1.36 ± 0.12; fold change from control) and ACC (WPR: 1.08 ± 0.07, WPE: 1.18 ± 0.05; fold change from control) in WPE was higher than in CON (p < 0.05). There were no significant differences in the expression levels of ATGL among the three groups.

CONCLUSIONS: These data suggest that a normal (or moderate excess) dietary density of whey peptide attenuates body fat accumulation via upregulation of fatty acid oxidation in skeletal muscle in aging mice.