Research
Hormonal
Insulin resistance and obesity increase the secretory demand on beta-cells, which accelerates the formation of cytotoxic IAPP aggregates and amyloid deposition.
Managing insulin resistance through weight loss or exercise may reduce the 'secretory demand' on beta-cells, thereby slowing the accumulation of toxic amyloid proteins that destroy insulin-producing cells.
GoodSupportsHIGH confidence
(cid:1)-cell dysfunction seems to be an important prerequisite for islet amyloid formation, with increased secretory demand from obesity and/or insulin resistance acting to further increase islet amyloid deposition.
Why this rating
Supported by transgenic mouse models fed high-fat diets.
Source
Islet Amyloid: A Critical Entity in the Pathogenesis of Type 2 Diabetes
Rebecca L. Hull et al. · The Journal of Clinical Endocrinology & Metabolism · 2004
DOI 10.1210/jc.2004-0405
narrative_reviewCited 584×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Islet amyloid polypeptide (IAPP) aggregation into small soluble oligomers causes beta-cell death via membrane disruption and oxidative stress, contributing to the loss of beta-cell mass in type 2 diabetes.Good
- Small, soluble IAPP oligomers (prefibrillar assemblies) are the primary cytotoxic species responsible for beta-cell death, whereas mature amyloid fibrils are less cytotoxic.Good
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