Diabetes type 1 (T1D) characterized by destruction of pancreatic β-cells results in inadequate insulin production and hyperglycaemia. Generation of reactive oxygen species and glycosylation end-products stimulates toxic impacts on T1D. Dietary w-3 fatty acids present in Fish oil (FO) might be helpful in the prevention of oxidative stress and lipid peroxidation, thus, beneficial against T1D. But how the cellular secretion from β-cells under influence of FO affects the glucose homeostasis of peri-pancreatic cells is poorly understood. In the current study, we aimed to introduce an in vitro model for T1D and evaluate its effectiveness in respect of alloxan treatment to pancreatic Min6 cells. We use alloxan in the Min6 pancreatic β-cell line to induce cellular damage related to T1D. Further treatment with FO was seen to prevent cell death by alloxan and induce mRNA expression of both insulin 1 and insulin 2 isoforms under low-glucose conditions. From the first part of the study, it is clear that FO is effective to recover Min6 cells from the destructive effect of alloxan, and it worked best when given along with alloxan or given after alloxan treatment regime. FO-induced secretion of molecules from Min6 was clearly shown to regulate mRNA expression of key enzymes of carbohydrate metabolism in peri-pancreatic cell types. This is a pilot study showing that an improved in vitro approach of using Min6 along with muscle cells (C2C12) and adipose tissue cells (3T3-L1) together to understand the crosstalk of molecules could be used to check the efficacy of an anti-diabetic drug.
Keywords: Alloxan; Fish oil; Glucose metabolism; Insulin; Peri-pancreatic tissue; Type I diabetes.
© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.