Green tea extracts ameliorate high-fat diet–induced muscle atrophy in senescence-accelerated mouse prone-8 mice

Abstract

Muscle atrophy (loss of skeletal muscle mass) causes progressive deterioration of skeletal function. Recently, excessive intake of fats was suggested to induce insulin resistance, followed by muscle atrophy. Green tea extracts (GTEs), which contain polyphenols such as epigallocatechin gallate, have beneficial effects on obesity, hyperglycemia, and insulin resistance, but their effects against muscle atrophy are still unclear. Here, we found that GTEs prevented high-fat (HF) diet–induced muscle weight loss in senescence-accelerated mouse prone-8 (SAMP8), a murine model of senescence. SAMP8 mice were fed a control diet, an HF diet, or HF with 0.5% GTEs (HFGT) diet for 4 months. The HF diet induced muscle weight loss with aging (measured as quadriceps muscle weight), whereas GTEs prevented this loss. In HF diet–fed mice, blood glucose and plasma insulin concentrations increased in comparison with the control group, and these mice had insulin resistance as determined by homeostasis model assessment of insulin resistance (HOMA-IR). In these mice, serum concentrations of leukocyte cell–derived chemotaxin 2 (LECT2), which is known to induce insulin resistance in skeletal muscle, were elevated, and insulin signaling in muscle, as determined by the phosphorylation levels of Akt and p70 S6 kinases, tended to be decreased. In HFGT diet–fed mice, these signs of insulin resistance and elevation of serum LECT2 were not observed. Although our study did not directly show the effect of serum LECT2 on muscle weight, insulin resistance examined using HOMA-IR indicated an intervention effect of serum LECT2 on muscle weight, as revealed by partial correlation analysis. Accordingly, GTEs might have beneficial effects on age-related and HF diet–induced muscle weight loss, which correlates with insulin resistance and is accompanied by a change in serum LECT2.

Experimental Models of Sarcopenia: Bridging Molecular Mechanism and Therapeutic Strategy

“…For example, gosha-jinki-gan alleviated skeletal muscle atrophy through Akt/FoxO4/MuRF1-and AMPK/PGC-1α-associated mitochondrial dysfunction in SAMP8 mice [146]. Furthermore, high-fat-diet-fed SAMP8 mice exhibited susceptibility to aging-related muscle wasting, and the muscle weight was decreased by 15.3% at 6 months of age compared with that at 2 months of age [147]. Several observations suggested that the use of SAMP strains is cost-effective for sarcopenia research.…”

“…Guo et al showed that the number of type II muscle fibers, which are predominant in gastrocnemius muscles, reached a peak at 7 months of age and then declined gradually in SAMP8 mice [ 145 ]. Consequently, SAMP8 mice have been used to investigate novel sarcopenia therapeutics and assess their efficacy [ 120 , 146 , 147 ]. For example, gosha-jinki-gan alleviated skeletal muscle atrophy through Akt/FoxO4/MuRF1- and AMPK/PGC-1α-associated mitochondrial dysfunction in SAMP8 mice [ 146 ].…”

Green Tea Extracts Attenuate Brain Dysfunction in High-Fat-Diet-Fed SAMP8 Mice

“…The animal experiments described in this study were carried out simultaneously with those described in our recent publication [19]. In brief, male SAMR1 (Number of samples, N = 24) and SAMP8 ( N = 56) mice were obtained from Japan SLC, Inc. (Hamamatsu, Japan).…”

“…Calorie-based average daily amount of food intake per mouse (kcal/mouse/day) did not differ significantly among the groups and was 17.00 (SAMR1; Cont), 17.06 (SAMP8; Cont), 19.06 (SAMP8; HF), and 18.13 (SAMP8; HFGT). Although no significant difference in body weight was observed among any groups of mice at 6 months of age, the HF group of SAMP8 mice had insulin resistance, as assessed by homeostasis model assessment of insulin resistance (HOMA-IR) [19].…”

“…Green tea extracts (GTEs), which contain high concentrations of polyphenols such as epigallocatechin gallate (EGCg), have been extensively evaluated for their effects on obesity, type 2 diabetes, insulin resistance, and hyperglycemia in humans and rodents [13,14,15,16,17,18,19,20]. The mechanisms responsible for the effects of GTEs on obesity-related diseases may rely on increasing glucose and lipid oxidation [17,21,22,23,24], anti-oxidative stress [13,14], and anti-inflammatory effects [14,15].…”