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Endocrinol Metab (Seoul). 2015 Dec;30(4):569-75. doi: 10.3803/EnM.2015.30.4.569.

Omega-3 Polyunsaturated Fatty Acids May Attenuate Streptozotocin-Induced Pancreatic β-Cell Death via Autophagy Activation in Fat1 Transgenic Mice.

Author information

1
Division of Nephrology, Department of Internal Medicine, Konyang University College of Medicine, Daejeon, Korea.
2
Myunggok Research Institute, Konyang University College of Medicine, Daejeon, Korea.
3
Department of Anatomy, Konyang University College of Medicine, Daejeon, Korea.
4
Division of Endocrinology, Department of Internal Medicine, Konyang University College of Medicine, Daejeon, Korea.
5
Department of Biochemistry, Chungnam National University School of Medicine, Daejeon, Korea.
6
Cancer Research Institute, Chungnam National University School of Medicine, Daejeon, Korea.
7
Division of Endocrinology, Department of Internal Medicine, Konyang University College of Medicine, Daejeon, Korea. mdldm@hanmail.net.

Abstract

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.

KEYWORDS:

Beta cell; Fat-1 transgenic mice; Omega 3 fatty

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