ReviewEuropean journal of nutrition2021
Endoplasmic reticulum stress as the basis of obesity and metabolic diseases: focus on adipose tissue, liver, and pancreas.
Review in European journal of nutrition, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 78 citations in OpenAlex.
- Targeting the IRE1α/XBP1 pathway in type 2 diabetes mellitus: from ER stress signaling to therapeutic opportunity.Molecular biology reports · 2026Review
- Molecular Mechanisms of Obesity-Associated Oxidative Stress and Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- Cross-species metabolic profiling of follicular compartments in obesity.Life medicine · 2026Article
- Interplay between MASLD, obesity and type 2 diabetes: epidemiology, shared pathways and clinical implications.BMJ open gastroenterology · 2026Review
- Fish Oil Alters the Metabolome, Antioxidative Potential, and Secretory Profile of Visceral Adipose Tissue in Mice with High-Fat Diet-Induced Obesity Compared with Other Dietary Fat Sources.Molecules (Basel, Switzerland) · 2026Article
- Endoplasmic reticulum stress as a mechanistic link between nutrition and inflammatory bowel disease.Frontiers in nutrition · 2026Review
- From NAFPD to MAFPD: a literature review of implications of a nomenclature change.Hepatobiliary surgery and nutrition · 2025Review
- Beyond fructolysis: ketohexokinase orchestrates ER proteostasis in nutrient-stressed hepatocytes.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
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- Impact of Maternal High-Fat Diet on Offspring Cardiovascular-Kidney-Metabolic Health: Spotlight on Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
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- Excess Fructose Intake Activates Hyperinsulinemia and Mitogenic MAPK Pathways in Association With Cellular Stress, Inflammation, and Apoptosis in the Pancreas of Rats.Molecular nutrition & food research · 2025Article
- Mechanism of PI3K/Akt‑mediated mitochondrial pathway in obesity‑induced apoptosis (Review).Biomedical reports · 2025Review
- Modulation of endoplasmic reticulum stress-induced insulin resistance by the low-carbohydrate high-fat ketogenic diet.Frontiers in nutrition · 2025Review
- Role of metabolic conditions in cardiorenal diseases: initiating pathways and therapeutic targeting.Frontiers in nutrition · 2025Review
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- Irisin: A Multifaceted Hormone Bridging Exercise and Disease Pathophysiology.International journal of molecular sciences · 2024Review
- Brown and Beige Adipose Tissue: One or Different Targets for Treatment of Obesity and Obesity-Related Metabolic Disorders?International journal of molecular sciences · 2024Review
- Mesenchymal Stem Cell-Derived Exosomes Attenuate Hepatic Steatosis and Insulin Resistance in Diet-Induced Obese Mice by Activating the FGF21-Adiponectin Axis.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Obesity challenges lipid and carbohydrate metabolism. The resulting glucolipotoxicity causes endoplasmic reticulum (ER) dysfunction, provoking the accumulation of immature proteins, which triggers the unfolded protein reaction (UPR) as an attempt to reestablish ER homeostasis. When the three branches of UPR fail to correct the unfolded/misfolded proteins, ER stress happens. Excessive dietary saturated fatty acids or fructose exhibit the same impact on the ER stress, induced by excessive ectopic fat accumulation or rising blood glucose levels, and meta-inflammation. These metabolic abnormalities can alleviate through dietary interventions. Many pathways are disrupted in adipose tissue, liver, and pancreas during ER stress, compromising browning and thermogenesis, favoring hepatic lipogenesis, and impairing glucose-stimulated insulin secretion within pancreatic beta cells. As a result, ER stress takes part in obesity, hepatic steatosis, and diabetes pathogenesis, arising as a potential target to treat or even prevent metabolic diseases. The scientific community seeks strategies to alleviate ER stress by avoiding inflammation, apoptosis, lipogenesis suppression, and insulin sensitivity augmentation through pharmacological and non-pharmacological interventions. This comprehensive review aimed to describe the contribution of excessive dietary fat or sugar to ER stress and the impact of this adverse cellular environment on adipose tissue, liver, and pancreas function.
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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.