Allomyrina dichotoma larva extract attenuates free fatty acid-induced lipotoxicity in pancreatic beta cellsAllomyrina dichotoma larva extract attenuates free fatty acid-induced lipotoxicity in pancreatic beta cells
- Other Titles
- Allomyrina dichotoma larva extract attenuates free fatty acid-induced lipotoxicity in pancreatic beta cells
- Authors
- 김경; Kwak Min-Kyu; 배공덕; 박은영; 백동재; 김철영; 장세은; 전희숙; 오윤신
- Issue Date
- Jun-2021
- Publisher
- KOREAN NUTRITION SOC
- Keywords
- Diabetes mellitus; apoptosis; insulin-secreting cells; nitric oxide; oxidative stress
- Citation
- Nutrition Research and Practice, v.15, no.3, pp.294 - 308
- Journal Title
- Nutrition Research and Practice
- Volume
- 15
- Number
- 3
- Start Page
- 294
- End Page
- 308
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/81523
- DOI
- 10.4162/nrp.2021.15.3.294
- ISSN
- 1976-1457
- Abstract
- BACKGROUD/OBJECTIVES: Allomyrina dichotoma larva (ADL), one of the many edible insects recognized as future food resources, has a range of pharmacological activities. In a previous study, an ADL extract (ADLE) reduced the hepatic insulin resistance of high-fat diet (HFD)-induced diabetic mice. On the other hand, the associated molecular mechanisms underlying pancreatic beta-cell dysfunction remain unclear. This study examined the effects of ADLE on palmitate-induced lipotoxicity in a beta cell line of a rat origin, INS-1 cells.
MATERIALS/METHODS: ADLE was administered to high-fat diet treated mice. The expression of apoptosis-related molecules was measured by Western blotting, and reactive oxidative stress generation and nitric oxide production were measured by DCH-DA fluorescence and a Griess assay, respectively.
RESULTS: The administration of ADLE to HFD-induced diabetic mice reduced the hyperplasia, 4-hydroxynonenal levels, and the number of apoptotic cells while improving the insulin levels compared to the HFD group. Treatment of INS-1 cells with palmitate reduced insulin secretion, which was attenuated by the ADLE treatment. Furthermore, the ADLE treatment prevented palmitate-induced cell death in INS-1 cells and isolated islets by reducing the apoptotic signaling molecules, including cleaved caspase-3 and PARP, and the Bax/Bcl2 ratio. ADLE also reduced the levels of reactive oxygen species generation, lipid accumulation, and nitrite production in palmitate-treated INS-1 cells while increasing the ATP levels. This effect corresponded to the decreased expression of inducible nitric oxide synthase (iNOS) mRNA and protein.
CONCLUSIONS: ADLE helps prevent lipotoxic beta-cell death in INS-1 cells and HFD-diabetic mice, suggesting that ADLE can be used to prevent or treat beta-cell damage in glucose intolerance during the development of diabetes.
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