Effects of Whey Peptide Supplementation on Sarcopenic Obesity in High-Fat Diet-Fed Mice

Abstract

The incidence of sarcopenic obesity gradually increased in parallel with the aged population. This research examined the effects of whey peptide (WP) supplementation with/without resistant exercise (RE) on sarcopenic obesity. Male 8-month-old C57BL/6J mice were fed a control diet (10 kcal% fat) or a high-fat diet (60 kcal% fat) for 8 weeks. High-fat diet-fed mice were randomly divided into four groups: obesity control group (OB), RE (RE only), WP (WP only), and WPE (RE and WP). WP supplementation (1500 mg/day/kg B.W.) gavage and RE (ladder climbing, five times weekly, 8−10 repetitions, 10−20% B.W. load) were conducted for an additional 8 weeks. Protein and mRNA levels of markers related to energy, protein, and lipid metabolism were analyzed in skeletal muscle and adipose tissue by one-way analysis of variance (ANOVA). WP supplementation regardless of RE significantly suppressed the increasing fat mass (p = 0.016) and decreasing lean mass (p = 0.014) and alleviated abnormal morphological changes in skeletal muscle and adipose tissue (p < 0.001). In adipose tissue, WP supplementation regardless of RE ameliorated dysregulated energy metabolism and contributed to the reduction in adipocyte differentiation (PPAR-γ (p = 0.017), C/EBPα (p = 0.034)). In skeletal muscle, WP supplementation regardless of RE alleviated energy metabolism dysregulation and resulted in down-regulated protein degradation (Atrogin-1 (p = 0.003), MuRF1 (p = 0.006)) and apoptosis (Bax) (p = 0.004). Taken together, the current study elucidated that WP supplementation regardless of RE has potential anti-obesity and anti-sarcopenic effects in sarcopenic obesity.

Keywords: adipocyte differentiation; adipogenesis; protein degradation; resistant exercise; sarcopenic obesity; whey peptide.

Figure 1

Experimental design. X: non-exercise; O: exercise.

Figure 2

The incremental intensity load applied to the resistant exercise.

Figure 3

Effects of WP supplementation and RE on adipose tissue and skeletal muscle morphology (×200) in sarcopenic obese mice. (A) Adipose tissue morphology, (B) Mean adipocytes size (um), (C) Gastrocnemius morphology, and (D) Mean myofibers area (%). Values are means ± SEMs, n = 3–4. Mean values with the same superscript letter (a, b and c) are not significantly different (p < 0.05).

Figure 4

Effects of WP supplementation and RE on adipose tissue adipokines, lipid and energy metabolism in sarcopenic obese mice. (A) Adipokines (B) Lipid metabolism, and (C) Energy metabolism. Values are means ± SEMs, n = 6–8. Mean values with the same superscript letter (a and b) are not significantly different (p < 0.05). PPAR-γ, peroxisome proliferator-activated receptors γ; C/EBPα, CCAAT-enhancer-binding proteins α; AMPK, AMP-activated protein kinase; PGC-1α, proliferator-activated receptor-gamma coactivator 1-alpha. N.S.—Not significant.

Figure 5

Effects of WP supplementation and RE on skeletal muscle protein and energy metabolism in sarcopenic obese mice. (A) Protein metabolism and (B) Energy metabolism. Values are means ± SEMs, n = 6–8. Mean values with the same superscript letter (a, b and c) are not significantly different (p < 0.05). Bax, bcl-2-like protein 4; Bcl-xL, B-cell lymphoma–extra large; FoxO3a, forkhead box O3; Atrogin-1, muscle atrophy F-box gene; MuRF1, E3 ubiquitin–protein ligase; S6K1, ribosomal protein S6 kinase beta-1: IGF-1, insulin-like growth factor I; Akt, protein kinase B. N.S.—Not significant.

Figure 5

Effects of WP supplementation and RE on skeletal muscle protein and energy metabolism in sarcopenic obese mice. (A) Protein metabolism and (B) Energy metabolism. Values are means ± SEMs, n = 6–8. Mean values with the same superscript letter (a, b and c) are not significantly different (p < 0.05). Bax, bcl-2-like protein 4; Bcl-xL, B-cell lymphoma–extra large; FoxO3a, forkhead box O3; Atrogin-1, muscle atrophy F-box gene; MuRF1, E3 ubiquitin–protein ligase; S6K1, ribosomal protein S6 kinase beta-1: IGF-1, insulin-like growth factor I; Akt, protein kinase B. N.S.—Not significant.