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KMID : 0356620150300040567
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Journal of Korean Society of Endocrinology
2015 Volume.30 No. 4 p.567 ~ p.575
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Omega-3 Polyunsaturated Fatty Acids May Attenuate Streptozotocin-Induced Pancreatic β-Cell Death via Autophagy Activation in Fat1 Transgenic Mice
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:Hwang Won-Min
:Bak Dong-Ho/:Kim Dong-Ho/:Han Seung-Yun/:Park Keun-Young/:Lim Kyu/:Lim Kyu/:Kang Jae-Gu
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Abstract
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Background : Inflammatory factors and β-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 β-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 β-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 β-cells of control mice, autophagy was abruptly activated after STZ treatment. Basal autophagy levels were elevated in fat-1 mice β-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 β-cell death by activating autophagy in β-cells.
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KEYWORD
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Omega 3 fatty, Beta cell, Fat-1 transgenic mice
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