Research
Hormonal
Chronic inflammation in pancreatic islets, driven by macrophage infiltration and proinflammatory cytokines (IL-1β, IL-23, IL-24), causes beta-cell dysfunction and reduced glucose-stimulated insulin secretion (GSIS) in Type 2 Diabetes.
In Type 2 Diabetes, inflammation inside the pancreas damages the insulin-producing beta cells. This isn't just about insulin resistance; the pancreas itself gets inflamed, reducing its ability to secrete insulin when needed. Protecting beta cells from inflammation is a key therapeutic target.
GoodSupportsHIGH confidence
Several reports have shown islet inflammation can also be etiologically important in causing beta-cell dysfunction in T2DM. The expression of proinflammatory cytokines (such as IL-1beta, IL-33, IL-23, and IL-24) and macrophage infiltration is increased in the islets of obese/T2DM patients...
Why this rating
Strong evidence from rodent models and human islet studies, though human validation is less extensive than for adipose/liver.
Source
Chronic tissue inflammation and metabolic disease
Yun Sok Lee et al. · Genes & Development · 2021
DOI 10.1101/gad.346312.120
narrative_reviewCited 310×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Macrophage accumulation and polarization towards a proinflammatory (M1-like) state in adipose tissue is the dominant mechanism driving insulin resistance in obesity.Strong
- Chronic tissue inflammation, driven by obesity-induced macrophage accumulation and proinflammatory cytokine release, is a major etiologic cause of insulin resistance and beta-cell dysfunction in metabolic disease.Good
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