ArticleEndocrinology and metabolism (Seoul, Korea)2018
Pioglitazone Attenuates Palmitate-Induced Inflammation and Endoplasmic Reticulum Stress in Pancreatic β-Cells.
Article in Endocrinology and metabolism (Seoul, Korea), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 29 citations in OpenAlex.
- PPAR-γ Activation Alleviates Intestinal Dysfunction and Lactose Malabsorption in Experimental Food Allergy Rats.Nutrients · 2026Article
- Research progress on endoplasmic reticulum homeostasis in acute kidney injury.Frontiers in pharmacology · 2025Review
- Nr1h4 and Thrb ameliorate ER stress and provide protection in the MPTP mouse model of Parkinson's.Life science alliance · 2024Article
- Peroxisome proliferator-activated receptors as targets to treat metabolic diseases: Focus on the adipose tissue, liver, and pancreas.World journal of gastroenterology · 2023Review
- Nicotinamide N-methyltransferase upregulation contributes to palmitate-elicited peroxisome proliferator-activated receptor transactivation in hepatocytes.American journal of physiology. Cell physiology · 2023Article
- Prosthetic vascular grafts engineered to combat calcification: Progress and future directions.Biotechnology and bioengineering · 2023Review
- Metformin promotes osteogenic differentiation and prevents hyperglycaemia-induced osteoporosis by suppressing PPARγ expression.Acta biochimica et biophysica Sinica · 2023Article
- Obesity, diabetes mellitus, and cardiometabolic risk: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2023.Obesity pillars · 2023Article
- Chemical inducer of regucalcin attenuates lipopolysaccharide-induced inflammatory responses in pancreatic MIN6 β-cells and RAW264.7 macrophages.FEBS open bio · 2022Article
- Activation of PPARPPAR research · 2022Article
- Current Status of Endoplasmic Reticulum Stress in Type II Diabetes.Molecules (Basel, Switzerland) · 2021Review
- JunD Regulates Pancreatic β-Cells Function by Altering Lipid Accumulation.Frontiers in endocrinology · 2021Article
- Mechanisms of impaired pancreatic β‑cell function in high‑fat diet‑induced obese mice: The role of endoplasmic reticulum stress.Molecular medicine reports · 2020Article
- Recent Insights Into Mechanisms of β-Cell Lipo- and Glucolipotoxicity in Type 2 Diabetes.Journal of molecular biology · 2020Review
- Article
- Changes of MODY signal pathway genes in the endoplasmic reticulum stress in INS-1-3 cells.PloS one · 2018Article
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Authors and funding
10 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundThe nuclear receptor peroxisome proliferator-activator gamma (PPARγ) is a useful therapeutic target for obesity and diabetes, but its role in protecting β-cell function and viability is unclear.
methodsTo identify the potential functions of PPARγ in β-cells, we treated mouse insulinoma 6 (MIN6) cells with the PPARγ agonist pioglitazone in conditions of lipotoxicity, endoplasmic reticulum (ER) stress, and inflammation.
resultsPalmitate-treated cells incubated with pioglitazone exhibited significant improvements in glucose-stimulated insulin secretion and the repression of apoptosis, as shown by decreased caspase-3 cleavage and poly (adenosine diphosphate [ADP]-ribose) polymerase activity. Pioglitazone also reversed the palmitate-induced expression of inflammatory cytokines (tumor necrosis factor α, interleukin 6 [IL-6], and IL-1β) and ER stress markers (phosphor-eukaryotic translation initiation factor 2α, glucose-regulated protein 78 [GRP78], cleaved-activating transcription factor 6 [ATF6], and C/EBP homologous protein [CHOP]), and pioglitazone significantly attenuated inflammation and ER stress in lipopolysaccharide- or tunicamycin-treated MIN6 cells. The protective effect of pioglitazone was also tested in pancreatic islets from high-fat-fed KK-Ay mice administered 0.02% (wt/wt) pioglitazone or vehicle for 6 weeks. Pioglitazone remarkably reduced the expression of ATF6α, GRP78, and monocyte chemoattractant protein-1, prevented α-cell infiltration into the pancreatic islets, and upregulated glucose transporter 2 (Glut2) expression in β-cells. Moreover, the preservation of β-cells by pioglitazone was accompanied by a significant reduction of blood glucose levels.
conclusionAltogether, these results support the proposal that PPARγ agonists not only suppress insulin resistance, but also prevent β-cell impairment via protection against ER stress and inflammation. The activation of PPARγ might be a new therapeutic approach for improving β-cell survival and insulin secretion in patients with diabetes mellitus.
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