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Sesamol Alleviated Lipotoxicity-Induced Dysfunction in MIN6 Cells via Facilitating Cellular Senescence Caused by
Yan Xie1, Yongyan Tang1, Jinxin Yang1
1Department of Nutrition and Food Hygiene, Xiangya School of Public Health, Central South University, Changsha, China.
Abstract:
Obesity is found to be a significant risk factor for type 2 diabetes mellitus (T2DM), attributed to lipotoxicity-induced β-cell dysfunction. However, the specific mechanism involved in the process remains incompletely unclarified. The current study demonstrated lipotoxicity resulted in the activation of ER stress, which increased the protein level of TXNIP, thereby inducing senescence-assiciated dysfunction in MIN6 cells under high fat environment. And we also found sesamol, a natural functional component extracted from sesame, was able to alleviate senescence-associated β-cell dysfunction induced by lipotoxicity by inhibiting ER stress and TXNIP. Our findings provided novel insights into senescence-related T2DM and propose innovative therapeutic approaches for utilizing sesamol in the treatment of T2DM in the obese elderly population.
Insights
Obesity causes type 2 diabetes mellitus (T2DM) via lipotoxicity. Sesamol, a sesame extract, combats this by reducing ER stress and TXNIP, protecting pancreatic beta cells and offering a potential T2DM treatment.
Area of Science:
- Endocrinology and Metabolism
- Cellular Biology
- Nutraceutical Research
Background:
- Obesity is a major risk factor for type 2 diabetes mellitus (T2DM).
- Lipotoxicity-induced pancreatic beta-cell dysfunction is implicated, but mechanisms are unclear.
- Understanding these mechanisms is crucial for developing effective T2DM therapies.
Purpose of the Study:
- To elucidate the role of endoplasmic reticulum (ER) stress and TXNIP in lipotoxicity-driven beta-cell dysfunction.
- To investigate the potential of sesamol, a natural compound, in mitigating this dysfunction.
- To explore sesamol as a therapeutic agent for T2DM in obese individuals.
Main Methods:
- Induction of lipotoxicity in MIN6 cells using a high-fat environment.
- Assessment of ER stress markers and TXNIP protein levels.
- Evaluation of sesamol's effects on beta-cell function and senescence markers.
Main Results:
- Lipotoxicity activated ER stress and increased TXNIP protein levels in MIN6 cells.
- This led to senescence-associated dysfunction in beta cells.
- Sesamol treatment inhibited ER stress and TXNIP, alleviating lipotoxicity-induced beta-cell dysfunction.
Conclusions:
- ER stress and TXNIP upregulation are key mediators of lipotoxicity-induced beta-cell senescence in T2DM.
- Sesamol demonstrates therapeutic potential for T2DM by targeting ER stress and TXNIP.
- Findings support sesamol as a novel treatment for T2DM in obese elderly populations.
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