ReviewAnalytical cellular pathology (Amsterdam)2015
The Role of Organelle Stresses in Diabetes Mellitus and Obesity: Implication for Treatment.
Review in Analytical cellular pathology (Amsterdam), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Advances regarding the mechanism of endoplasmic reticulum stress in diabetic kidney disease and pharmacological interventions (Review).Molecular medicine reports · 2026Review
- GLP-1 receptor and Mitochondria-ER Contact Sites: an emerging mechanism of metabolic regulation.Frontiers in physiology · 2026Review
- Deciphering the complex interplay of risk factors in type 2 diabetes mellitus: A comprehensive review.Metabolism open · 2024Review
- On the use of QDE-SVM for gene feature selection and cell type classification from scRNA-seq data.PloS one · 2023Article
- Ticagrelor alleviates high-carbohydrate intake induced altered electrical activity of ventricular cardiomyocytes by regulating sarcoplasmic reticulum-mitochondria miscommunication.Molecular and cellular biochemistry · 2021Article
- Comparison of endoplasmic reticulum stress and mitochondrial biogenesis responses after 12 weeks of treadmill running and ladder climbing exercises in the cardiac muscle of middle-aged obese rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- The role of endoplasmic reticulum-mitochondria contact sites in the control of glucose homeostasis: an update.Cell death & disease · 2018Review
- Obesity Exacerbates Sepsis-Induced Oxidative Damage in Organs.Inflammation · 2016Article
- An Updated Mini Review of Vitamin D and Obesity: Adipogenesis and Inflammation State.Open access Macedonian journal of medical sciences · 2016Review
- Does bariatric surgery improve adipose tissue function?Obesity reviews : an official journal of the International Association for the Study of Obesity · 2016Review
- The influence of oxidative stress and autophagy cross regulation on pregnancy outcome.Cell stress & chaperones · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The type 2 diabetes pandemic in recent decades is a huge global health threat. This pandemic is primarily attributed to the surplus of nutrients and the increased prevalence of obesity worldwide. In contrast, calorie restriction and weight reduction can drastically prevent type 2 diabetes, indicating a central role of nutrient excess in the development of diabetes. Recently, the molecular links between excessive nutrients, organelle stress, and development of metabolic disease have been extensively studied. Specifically, excessive nutrients trigger endoplasmic reticulum stress and increase the production of mitochondrial reactive oxygen species, leading to activation of stress signaling pathway, inflammatory response, lipogenesis, and pancreatic beta-cell death. Autophagy is required for clearance of hepatic lipid clearance, alleviation of pancreatic beta-cell stress, and white adipocyte differentiation. ROS scavengers, chemical chaperones, and autophagy activators have demonstrated promising effects for the treatment of insulin resistance and diabetes in preclinical models. Further results from clinical trials are eagerly awaited.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.