Research

Hormonal

Loss-of-function mutations in the zinc transporter SLC30A8 (ZnT8) reduce the risk of type 2 diabetes in humans, likely by preventing the formation of toxic human islet amyloid polypeptide (hIAPP) oligomers through altered insulin oligomerization dynamics.

Do not assume zinc supplementation is a cure-all for diabetes. While deficiency is a risk factor, the paper suggests that genetic variations in zinc transport (ZnT8) significantly impact diabetes risk, and excessive zinc intake may actually worsen metabolic markers. Focus on overall nutrient balance rather than high-dose supplementation without medical guidance.

ModerateQualifiesMEDIUM confidence
Interestingly, these new findings appear to be consistent with the finding that rare loss-of-function mutations in ZnT8 are associated with reduced T2DM risk in humans [27]. ... The theory of altered hIAPP aggregation in β cells in response to altered ZnT8 function is a promising but still correlative hypothesis at this point.
Ayako Fukunaka et al. · International Journal of Molecular Sciences · 2018

Why this rating

The paper is a review; the specific hIAPP mechanism is described as a 'promising but still correlative hypothesis' requiring validation in transgenic mice.

Source

Role of Zinc Homeostasis in the Pathogenesis of Diabetes and Obesity

Ayako Fukunaka et al. · International Journal of Molecular Sciences · 2018

DOI 10.3390/ijms19020476

narrative_reviewCited 256×
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DOI resolved against Crossref · corpus check 2026-06-10

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