Is Oxidative Stress the Pathogenic Mechanism Underlying Insulin Resistance, Diabetes, and Cardiovascular Disease? The Common Soil Hypothesis Revisited
Open accessAbstract
Type 2 diabetes is a worldwide increasing disease resulting from the interaction between a subject’s genetic makeup and lifestyle. In genetically predisposed subjects, the combination of excess caloric intake and reduced physical activity induces a state of insulin resistance. When beta cells are no longer able to compensate for insulin resistance by adequately increasing insulin production, impaired glucose tolerance appears, characterized by excessive postprandial hyperglycemia. Impaired glucose tolerance may evolve into overt diabetes. These 3 conditions, ie, insulin resistance, impaired glucose tolerance, and overt diabetes, are associated with an increased risk of cardiovascular disease. Because all these conditions are also accompanied by the presence of an oxidative stress, this article proposes oxidative stress as the pathogenic mechanism linking insulin resistance with dysfunction of both beta cells and endothelium, eventually leading to overt diabetes and cardiovascular disease. This hypothesis, moreover, may also contribute to explaining why treating cardiovascular risk with drugs, such as calcium channel blockers, ACE inhibitors, AT-1 receptor antagonists, and statins, all compounds showing intracellular preventive antioxidant activity, results in the onset of new cases of diabetes possibly being reduced.
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MDA is a marker of oxidative stress and lipid peroxidation, processes implicated in vascular injury and diabetic complications.
“malondialdehyde (MDA) is a marker of oxidative stress and lipid peroxidation, processes implicated in vascular injury and diabetic complications [9].”
From Effects of <scp>GLP</scp> ‐1 Receptor Agonists and Dual <scp>GIP</scp> / <scp>GLP</scp> ‐1 Receptor Agonists on Inflammatory and Metabolic Biomarkers in Type 2 Diabetes: A Systematic Review and Meta‐Analysis (2026) · cites this paper as [9]
The section “Oxidative Stress as a Common Pathogenic Factor for the Dysfunction of Beta and Endothelial Cells” links oxidative stress to endothelial dysfunction in hyperglycemia. However, searches for malondialdehyde and lipid peroxidation found no passage identifying MDA as a marker of either process. The paper supports the vascular-damage context, not the specific MDA claim. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe reduction in MDA supports a concomitant decrease in oxidative stress and lipid peroxidation.
“The reduction in MDA supports a concomitant decrease in oxidative stress and lipid peroxidation [9].”
From Effects of <scp>GLP</scp> ‐1 Receptor Agonists and Dual <scp>GIP</scp> / <scp>GLP</scp> ‐1 Receptor Agonists on Inflammatory and Metabolic Biomarkers in Type 2 Diabetes: A Systematic Review and Meta‐Analysis (2026) · cites this paper as [9]
The therapeutic-implications section discusses reducing oxidative stress, but does not connect that reduction to MDA or lipid peroxidation. Searches of our full-text copy for “MDA,” “malondialdehyde,” and “lipid peroxidation” found no passage supporting the claimed interpretation of an MDA reduction. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIn these conditions oxidative stress may arise from excess superoxide anion production in mitochondria, which inactivates nitric oxide and yields peroxynitrite.
“The production of oxidative stress in such conditions may involve the overgeneration of superoxide anion (O 2 Ϫ ) at the mitochondrial level, which in turn inactivates nitric oxide (NO), producing peroxynitrite, a potent long-lived oxidant.”
The preferential use of the liver to dispose a significant amount of the ingested glucose during first pass, along with a 60-70% hepatic clearance of insulin, protect the peripheral circulation from excessive hyperglycemia/hyperinsulinemia in the postprandial period.
“The preferential use of the liver to dispose a significant amount of the ingested glucose during first pass, along with a 60–70% hepatic clearance of insulin, protect the peripheral circulation from excessive hyperglycemia/hyperinsulinemia in the postprandial period [35,36,37,38,39,40,41,42,43].”
From Effects of diet, lifestyle, Chrononutrition and alternative dietary interventions on postprandial Glycemia and insulin resistance (2022) · cites this paper as [37]
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- Authors
- Ceriello, A., & Motz, E.
- Affiliations
- University of Udine (IT)
- ORCID
- Ceriello, Antonio
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2004-05
- Volume
- 24
- Issue
- 5
- Pages
- 816-823
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2087882379
- Cited by
- 1,378
- References
- 94
- Citations by year
- 2026: 27 · 2025: 32 · 2024: 34 · 2023: 29 · 2022: 52 · 2021: 54 · 2020: 76 · 2019: 75 · 2018: 75 · 2017: 66 · 2016: 74 · 2015: 73 · 2014: 85 · 2013: 72 · 2012: 85
- FWCI
- 7.27
- Type
- journal article
- Language
- en
- Open access
- Licence
- other-oa
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Keywords
- oxidative stress, insulin resistance, type 2 diabetes, impaired glucose tolerance, cardiovascular disease, beta-cell dysfunction, endothelial dysfunction, postprandial hyperglycemia, antioxidant drugs, calcium channel blockers, ACE inhibitors, statins, pathophysiological mechanisms
- MeSH terms
- Insulin Secretion, Aged, Antioxidants, Cardiovascular Diseases, Diabetes Mellitus, Type 2, Endothelium, Vascular, Energy Metabolism, Humans, Hypoglycemic Agents, Inflammation, Insulin, Insulin Resistance, Islets of Langerhans, Middle Aged, Models, Biological, Incidence, Reactive Oxygen Species, Glucose Intolerance, Oxidative Stress, Overnutrition
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