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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2025.4
- 수록면
- 200 - 214 (15page)
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초록· 키워드
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BACKGROUND/OBJECTIVES: p-Coumaric acid (CA), a 4-hydroxycinnamic acid derivative, is widely distributed in nature and exerts various beneficial biological effects. However, the effects of CA on metabolic abnormalities triggered by excessive fructose intake, such as dyslipidemia, hyperglycemia, non-alcoholic fatty liver disease (NAFLD), and insulin resistance, have not been sufficiently investigated. Our objective was to investigate whether CA ameliorates high-fructose diet (HFrD)-induced metabolic dysregulation.
MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks.
RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns.
CONCLUSION: Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.
MATERIALS/METHODS: Golden Syrian hamsters were randomly assigned to 3 groups and were fed diets containing 60% cornstarch (CON group), 60% fructose (HFrD group), or 60% fructose with CA (0.02%) (HFrD+CA group) for 5 weeks.
RESULTS: HFrD feeding significantly increased the levels of plasma triglyceride, apolipoprotein (apo)-CIII, fasting blood glucose, and homeostatic model assessment insulin resistance, and tended to increase plasma total cholesterol (TC) and low-density lipoprotein/very low-density lipoprotein cholesterol (LDL/VLDL-C) compared with the CON group. In HFrD-fed hamsters, CA supplementation significantly decreased plasma TC, LDL/VLDL-C, apo-CIII, and fasting blood glucose levels. Moreover, CA significantly decreased the hepatic lipid levels and fibrosis induced by HFrD. The plasma and hepatic lipid-lowering effects of CA were associated with decreased enzyme activity and mRNA expression of genes involved in fatty acid, triglyceride, and cholesterol synthesis as well as increased activity of carnitine palmitoyltransferase, a rate-limiting enzyme in fatty acid oxidation, in the liver. CA-treated hamsters also exhibited decreased hepatic gluconeogenic enzyme activity and increased hepatic glycolytic enzyme activity, with mRNA expression changes similar to these activity patterns.
CONCLUSION: Our findings indicate that CA potentially improves metabolic abnormalities associated with excessive fructose intake, such as hyperglycemia, dyslipidemia, and NAFLD.
목차
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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