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.
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.
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
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