Omega-3 Polyunsaturated Fatty Acids May Attenuate Streptozotocin-Induced Pancreatic beta-Cell Death via Autophagy Activation in Fat1 Transgenic Mice.
10.3803/EnM.2015.30.4.569
- Author:
Won Min HWANG
1
;
Dong Ho BAK
;
Dong Ho KIM
;
Ju Young HONG
;
Seung Yun HAN
;
Keun Young PARK
;
Kyu LIM
;
Dong Mee LIM
;
Jae Gu KANG
Author Information
1. Division of Nephrology, Department of Internal Medicine, Konyang University College of Medicine, Daejeon, Korea.
- Publication Type:Original Article
- Keywords:
Omega 3 fatty;
Beta cell;
Fat-1 transgenic mice
- MeSH:
Animals;
Autophagy*;
Blood Glucose;
Cell Death;
Chronic Disease;
Cicatrix;
Diet, High-Fat;
Dietary Fats;
Drinking;
Eosine Yellowish-(YS);
Fatty Acids, Omega-3;
Fatty Acids, Unsaturated*;
Fibrosis;
Hematoxylin;
Hyperglycemia;
Islets of Langerhans;
Mice;
Mice, Transgenic*;
Pancreas;
Phenotype;
Polydipsia;
Streptozocin
- From:Endocrinology and Metabolism
2015;30(4):569-575
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Inflammatory factors and beta-cell dysfunction due to high-fat diets aggravate chronic diseases and their complications. However, omega-3 dietary fats have anti-inflammatory effects, and the involvement of autophagy in the etiology of diabetes has been reported. Therefore, we examined the protective effects of autophagy on diabetes using fat-1 transgenic mice with omega-3 self-synthesis capability. METHODS: Streptozotocin (STZ) administration induced beta-cell dysfunction in mice; blood glucose levels and water consumption were subsequently measured. Using hematoxylin and eosin (H&E) and Masson's trichrome staining, we quantitatively assessed STZ-induced changes in the number, mass, and fibrosis of pancreatic islets in fat-1 and control mice. We identified the microtubule-associated protein 1A/1B light chain 3-immunoreactive puncta in beta-cells and quantified p62 levels in the pancreas of fat-1 and control mice. RESULTS: STZ-induced diabetic phenotypes, including hyperglycemia and polydipsia, were attenuated in fat-1 mice. Histological determination using H&E and Masson's trichrome staining revealed the protective effects of the fat-1 expression on cell death and the scarring of pancreatic islets after STZ injection. In the beta-cells of control mice, autophagy was abruptly activated after STZ treatment. Basal autophagy levels were elevated in fat-1 mice beta-cells, and this persisted after STZ treatment. Together with autophagosome detection, these results revealed that n-3 polyunsaturated fatty acid (PUFA) enrichment might partly prevent the STZ-related pancreatic islet damage by upregulating the basal activity of autophagy and improving autophagic flux disturbance. CONCLUSION: Fat-1 transgenic mice with a n-3 PUFA self-synthesis capability exert protective effects against STZ-induced beta-cell death by activating autophagy in beta-cells.
