Misfolded insulin may be quietly driving diabetes — SkimNews
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- BiP and p58IPK must work together to fold proinsulin in pancreatic beta cells, according to a study published June 1, 2026 in the Proceedings of the National Academy of Sciences by Sanford Burnham Prebys and University of Michigan researchers.
- Removing p58IPK from two cell lines caused misfolded proinsulin to accumulate, and mice engineered to lack p58IPK produced smaller amounts of both proinsulin and insulin.
- Reintroducing p58IPK improved proinsulin folding and transport, but only when BiP was also present — BiP acting alone could not compensate.
- Lead author Insook Jang compared BiP working solo to "a single tennis player trying to play a doubles match."
- Senior author Randal J. Kaufman said no current diabetes medications target proinsulin folding, making the coordinated activity of BiP a promising early-intervention target.
- The study was supported by the NIH, NIDDK, NCI, and Breakthrough T1D (formerly JDRF).
Why it matters: No current diabetes medication targets the protein-folding failures that progressively damage beta cells — a gap the researchers explicitly flag. If drug developers can influence the BiP-p58IPK partnership, they could intervene earlier in diabetes to preserve insulin-producing cells rather than only managing blood sugar after beta-cell function has already declined.
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