<P>The cortex of <I>Cinnamomum</I><I>cassia</I> Presl (Cinnamomi Cortex: CC) has commonly been used for weight control in traditional medicines, but without a scientific basis. Therefore, this study was undertaken to inve...
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https://www.riss.kr/link?id=A107434213
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2017
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SCIE,SCOPUS
학술저널
1017-1031(15쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<P>The cortex of <I>Cinnamomum</I><I>cassia</I> Presl (Cinnamomi Cortex: CC) has commonly been used for weight control in traditional medicines, but without a scientific basis. Therefore, this study was undertaken to inve...
<P>The cortex of <I>Cinnamomum</I><I>cassia</I> Presl (Cinnamomi Cortex: CC) has commonly been used for weight control in traditional medicines, but without a scientific basis. Therefore, this study was undertaken to investigate the anti-obesity effect of CC extract in a high-fat diet (HFD)-induced obese mouse model and in C2C12 mouse skeletal muscle cells. Male C57BL/6 mice were fed a normal diet or a HFD for 16 consecutive weeks, and orally administered CC extract (100 or 300<TEX>$ \,$</TEX>mg/kg) or metformin (250<TEX>$ \,$</TEX>mg/kg; positive control) daily for 16 weeks. CC extract administration significantly decreased body weights, food intakes, and serum levels of glucose, insulin, total cholesterol and ALT levels, prevented oral glucose tolerance and insulin resistance, inhibited the protein expressions of MyHC and PGC1<TEX>$ \alpha $</TEX> and the phosphorylation of AMPK, suppressed lipid accumulation in liver, decreased adipocyte size and increased muscle mass in obese mice. For this <I>in vitro</I> study, C2C12 myoblasts were differentiated into the myotubes for five days, and then treated with CC extract (0.1 or 0.2<TEX>$ \,$</TEX>mg/ml) for 24<TEX>$ \,$</TEX>h. CC extract significantly increased ATP levels by increasing the mRNA expressions of mitochondrial biogenesis-related factors, such as, PGC1<TEX>$ \alpha $</TEX>, NRF-1, and Tfam, and the phosphorylations of AMPK and ACC. Our results suggest CC extract controls weight gain in obese mice by inhibiting lipid accumulation and increasing energy expenditure, and that its action mechanism involves the up-regulation of mitochondrial biogenesis in skeletal muscle cells.</P>