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논문 기본 정보

자료유형
학술저널
저자정보
Sun Yan (Department of Endocrinology, Heji Hospital Affilicated to Changzhi Medical College, Changzhi, Shanxi 046011, China) Qu Hai (독립연구자) Niu Xiaohong (Department of Endocrinology, Heji Hospital Affilicated to Changzhi Medical College, Changzhi, Shanxi 046011, China) Li Ting (Department of Endocrinology, Heji Hospital Affilicated to Changzhi Medical College, Changzhi, Shanxi 046011, China) Wang Lijuan (Department of Endocrinology, Heji Hospital Affilicated to Changzhi Medical College, Changzhi, Shanxi 046011, China) Peng Hairui (Department of Endocrinology, Heji Hospital Affilicated to Changzhi Medical College, Changzhi, Shanxi 046011, China)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제28권 제1호
발행연도
2024.1
수록면
1 - 10 (10page)
DOI
10.4196/kjpp.2024.28.1.1

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초록· 키워드

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Type 2 diabetes mellitus (T2DM) is characterized by hyperglycemia and dyslipidemia. Carvacrol (CAR) has demonstrated the potential to mitigate dyslipidemia. This study aims to investigate whether CAR can modulate blood glucose and lipid levels in a T2DM rat model by regulating short-chain fatty acids (SCFAs) and the GPR41/43 pathway. The T2DM rat model was induced by a high-fat diet combined with low-dose streptozocin injection and treated with oral CAR and/or mixed antibiotics. Fasting blood glucose, oral glucose tolerance, and insulin tolerance tests were assessed. Serum lipid parameters, hepatic and renal function indicators, tissue morphology, and SCFAs were measured. In vitro, high glucose (HG)-induced IEC-6 cells were treated with CAR, and optimal CAR concentration was determined. HG-induced IEC-6 cells were treated with SCFAs or/and GPR41/43 agonists. CAR significantly reduced blood lipid and glucose levels, improved tissue damage, and increased SCFA levels in feces and GPR41/43 expression in colonic tissues of T2DM rats. CAR also at tenuated HG-induced apoptosis of IEC-6 cells and enhanced GPR41/43 expression. Overall, these findings suggest that CAR alleviates blood lipid and glucose abnormalities in T2DM rats by modulating SCFAs and the GPR41/43 pathway.

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