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Normally, the level of this substance should decrease after injection but in people with Rotor syndrome, this decrease is slower than normal without any secondary increase which is seen in Dubin-Johnson syndrome

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Mounting evidence positions redox imbalance not merely as a secondary phenomenon but as a primary driver of the disease continuum - from initial -cell dysfunction to devastating micro- and macro-vascular complications

This finding is consistent with a previous study in which mice lacking TRPM5 function exhibited a decline in glucose tolerance and an impaired GSIS [31, 32]