A study published in June 2026 shows that misfolded proinsulin proteins can stress insulin-producing cells and reduce insulin output. Researchers identified key helper proteins that support proper folding and may offer a new treatment approach.
Researchers from Sanford Burnham Prebys Medical Discovery Institute and the University of Michigan published their findings on June 1, 2026, in the Proceedings of the National Academy of Sciences. The work details how beta cells in the pancreas rely on binding immunoglobulin protein, or BiP, and its cochaperone p58IPK to fold proinsulin correctly.
When p58IPK was removed from cell lines and mice, misfolded proinsulin built up and insulin production fell. Restoring p58IPK improved folding only when BiP was also present at normal levels.
"Like a single tennis player trying to play a doubles match, we found that BiP cannot just go it alone," said lead author Insook Jang. Senior author Randal J. Kaufman noted that strengthening this system could protect cells early in diabetes.
Current treatments do not target protein folding. The study suggests that supporting BiP and its partners might preserve beta cell function, though further research is needed.
