Reduction of diet-induced obesity by a combination of tea-catechin intake and regular swimming

Abstract

Objective: Obesity is a metabolic disorder resulting from imbalance between metabolizable energy intake and energy expenditure. It is known to be a strong risk factor for lifestyle-related diseases. Here, we investigated the effects of long-term intake of tea catechins (Cat) in combination with regular exercise (Ex) on the development of obesity in C57BL/6 mice. Design: We compared body weight, adipose tissue mass, plasma parameters and b-oxidation activity in mice fed a low-fat diet (5% triglyceride (TG); LF), a high-fat diet (30% TG; HF), a HF diet supplemented with 0.5% (w/w) tea Cat, a HF diet in addition to swimming Ex or a HF diet plus 0.5% tea Cat in addition to swimming Ex (Cat þ Ex) for 15 weeks. Oxygen consumption and respiratory quotients were measured using indirect calorimetry. Results: Tea-Cat intake in combination with swimming Ex suppressed HF diet-induced body-weight gain by 18 and 22%, respectively, compared to Ex and tea-Cat intake on their own. Visceral fat accumulation and the development of hyperinsulinemia and hyperleptinemia were also reduced in the HF þ Cat þ Ex group. Muscular b-oxidation activity in this group was 69 and 52% higher, respectively, than that in the HF and HF þ Cat groups. Lipid oxidation, determined using indirect calorimetry, was higher in the HF þ Cat þ Ex group, suggesting increased lipid utilization at the individual level. Conclusion: These results indicate that intake of tea Cat, together with regular Ex helps to reduce diet-induced obesity. This effect might be attributed, at least in part, to the activation of whole-body energy metabolism.

Tea catechin ingestion combined with habitual exercise suppresses the aging-associated decline in physical performance in senescence-accelerated mice

“…On the other hand, it is not clear whether catechin intake alone improves endurance capacity. Based on the results of the present study and a previous study (28), the effect of catechins alone might be limited because catechin intake alone had no marked effect on muscle metabolism, including fatty acid ␤-oxidation activity and mRNA expression. Rather, catechins seem to exert their main effects by stimulating hepatic lipid catabolism (26,28,39), which leads to reduced liver and abdominal fat weight and a lower plasma insulin level ( Table 2, 3).…”

“…Moreover, tea catechins are proposed to be neuroprotective agents against progressive neurodegenerative disorders such as Parkinson's and Alzheimer's diseases (45). Thus, there is a growing interest in the application of tea catechins for disease prevention and treatment (49).We have been investigating the nutritional functions of tea catechins and demonstrated that long-term intake of tea catechins is beneficial for reducing diet-induced obesity in humans (30) and mice (26,28,39). More recently, we demonstrated that habitual intake of catechin-rich green tea extract (GTE) improves both swimming and running endurance capacity in normally-aging BALB/c mice (27,29).…”

Epigallocatechin-3-gallate (EGCG), A Green Tea Polyphenol, Suppresses Hepatic Gluconeogenesis through 5′-AMP-activated Protein Kinase

“…1,2). EGCG has been shown to be involved in regulation of a variety of metabolic processes and has been used as an anti-obesity reagent in animal models and in humans (3)(4)(5)(6). Although its effectiveness in the treatment of human diabetes has not been established, EGCG has been shown in rodents to be effective in preventing the development of Type I diabetes and treatment of Type II diabetes (7,8).…”

Aqueous Extract of Kotahla Himbutu (Salacia reticulata) Stems Promotes Oxygen Comsumption and Supresses Body Fat Accumulation in Mice

“…22,23) Therefore, physical and pharmacological approaches that lead to sympathetic activation have been recommended for the management of obesity. 24) High doses of tea catechins are reported to inhibit catechol-o-methyltransferase (the enzyme that degrades catecholamines) in vitro 25) and increase VO 2 in HF diet-fed C57BL/6J mice, 26) but it remains unclear as to whether a KTE component is involved in the catechol pathway. In our previous study, KTE upregulated the expression levels of the genes associated with catecholamine metabolism, thus increasing the expression of catechol-o-methyltransferase and monoamine oxidase A (enzymes that degrade catecholamines) in C57BL/6J mice.…”