ArticleAmerican journal of physiology. Endocrinology and metabolism2013
Dysfunctional mitochondrial bioenergetics and oxidative stress in Akita(+/Ins2)-derived β-cells.
Article in American journal of physiology. Endocrinology and metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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36 citing papers in PubMed, 45 citations in OpenAlex.
- Metabolic Programming of β-Cell Fate, State, and Function through Time and Space.Physiology (Bethesda, Md.) · 2026Review
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- Fucoidan: An Update on Function, Role in Human Health and Applications.Chemical biology & drug design · 2026Review
- Renalase inhibition defends against acute and chronic β cell stress by regulating cell metabolism.Molecular metabolism · 2025Article
- Fucoidan alleviated autoimmune diabetes in NOD mice by regulating pancreatic autophagy through the AMPK/mTOR1/TFEB pathway.Iranian journal of basic medical sciences · 2024Article
- β Cell Stress and Endocrine Function During T1D: What Is Next to Discover?Endocrinology · 2023Article
- Cathepsin D overexpression in the nervous system rescues lethality and AActa pharmaceutica Sinica. B · 2023Article
- Unfolded Protein Response Differentially Modulates the Platelet Phenotype.Circulation research · 2022Article
- Acute inhibition of OGA sex-dependently alters the networks associated with bioenergetics, autophagy, and neurodegeneration.Molecular brain · 2022Article
- Therapeutic Potential of Different Natural Products for the Treatment of Alzheimer's Disease.Oxidative medicine and cellular longevity · 2022Review
- OGT Regulates Mitochondrial Biogenesis and Function via Diabetes Susceptibility Gene Pdx1.Diabetes · 2021Article
- Nuclear receptor binding factor 2 (NRBF2) is required for learning and memory.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- α-Hemolysin of uropathogenic E. coli regulates NLRP3 inflammasome activation and mitochondrial dysfunction in THP-1 macrophages.Scientific reports · 2020Article
- Traditional Chinese medicine for anti-Alzheimer's disease: berberine and evodiamine fromChinese medicine · 2020Review
- Chronic intermittent electronic cigarette exposure induces cardiac dysfunction and atherosclerosis in apolipoprotein-E knockout mice.American journal of physiology. Heart and circulatory physiology · 2019Article
- Feasibility of cellular bioenergetics as a biomarker in porphyria patients.Molecular genetics and metabolism reports · 2019Article
- Characterization of Novel Nonobese Type 2 Diabetes Rat Model with Enlarged Kidneys.Journal of diabetes research · 2019Article
- Article
- Insulin mutations impair beta-cell development in a patient-derived iPSC model of neonatal diabetes.eLife · 2018Article
- Methods for assessing mitochondrial quality control mechanisms and cellular consequences in cell culture.Redox biology · 2018Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Insulin release from pancreatic β-cells plays a critical role in blood glucose homeostasis, and β-cell dysfunction leads to the development of diabetes mellitus. In cases of monogenic type 1 diabetes mellitus (T1DM) that involve mutations in the insulin gene, we hypothesized that misfolding of insulin could result in endoplasmic reticulum (ER) stress, oxidant production, and mitochondrial damage. To address this, we used the Akita(+/Ins2) T1DM model in which misfolding of the insulin 2 gene leads to ER stress-mediated β-cell death and thapsigargin to induce ER stress in two different β-cell lines and in intact mouse islets. Using transformed pancreatic β-cell lines generated from wild-type Ins2(+/+) (WT) and Akita(+/Ins2) mice, we evaluated cellular bioenergetics, oxidative stress, mitochondrial protein levels, and autophagic flux to determine whether changes in these processes contribute to β-cell dysfunction. In addition, we induced ER stress pharmacologically using thapsigargin in WT β-cells, INS-1 cells, and intact mouse islets to examine the effects of ER stress on mitochondrial function. Our data reveal that Akita(+/Ins2)-derived β-cells have increased mitochondrial dysfunction, oxidant production, mtDNA damage, and alterations in mitochondrial protein levels that are not corrected by autophagy. Together, these findings suggest that deterioration in mitochondrial function due to an oxidative environment and ER stress contributes to β-cell dysfunction and could contribute to T1DM in which mutations in insulin occur.
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