Research
Hormonal
Chronic low-grade inflammation, driven by obesity and ectopic lipid deposition, impairs insulin signaling and beta-cell function through pathways like NF-κB, JNK, and oxidative stress.
Inflammation is not just a symptom of diabetes; it is a cause. Excess fat, especially around organs (ectopic fat), triggers inflammation that blocks insulin from working and damages insulin-producing cells. Managing weight and diet reduces this inflammation.
GoodSupportsHIGH confidence
Inflammation, ectopic lipid deposition, endoplasmic reticulum stress (ERS), and oxidative stress are involved in the onset and progression of T2D and TOD by impairing insulin sensitivity and/or β cell dysfunction, reciprocal with metabolic disorders.
Why this rating
Detailed molecular pathways (NF-κB, JNK, ROS) are described with citations.
Source
Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy
Xi Lu et al. · Signal Transduction and Targeted Therapy · 2024
DOI 10.1038/s41392-024-01951-9
narrative_reviewCited 485×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
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- Obesity (or preobesity) is a primary upstream risk factor for Type 2 Diabetes, contributing to more than 50% of global T2D disability-adjusted life years.Strong
- Type 2 diabetes should be managed as a component of Metabolic Dysfunction Syndrome (MDS) rather than solely as a hyperglycemic disorder, requiring holistic protection of target organs against all MDS-related metabolic disorders.Good
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