It’s hard to change entrenched ideas in science.

Protein is the genetic material.

Genes are continuous and immobile.

The genome consists of 120,000 genes; no, 80,000; no, 60,000; no, 20,325.

What we know about the natural world changes as we learn more. That’s why there’s no such thing as scientific “proof,” just evidence, hypotheses, and, rarely, enough findings to support a theory. Science is evidence-based, from observations and experiments. We don’t “believe” in evolution or climate change as if it is a religion. Yet presenting evidence that challenges a long-held idea can be difficult for a researcher.

Bryon Petersen, PhD, director of the Pediatric Stem Cell Research and Hepatic Disorders Child Health Research Institute at the University of Florida is in the uncomfortable position of challenging dogma, knows that well. His findings suggest that type 1 diabetes (T1D) might not directly be autoimmune in origin, and that tracking blood glucose might not be the only way to manage the disease.

His team has just published a paper in the journal Laboratory Investigation, “Suppression of islet homeostasis protein thwarts diabetes mellitus progression,” that puts a little-known molecule on the radar: islet homeostasis protein, aka IHoP.

People with type 1 diabetes make too much IHoP. Plus, experiments in mice and humans show that decreasing IHoP restores blood glucose control and increases the number of insulin-producing beta cells in the pancreas. Perhaps most importantly, excess IHoP is in the blood of patients, making it a possible new biomarker for T1D.


The pancreas is a dual gland. The exocrine part makes and sends enzymes into digestive juice in the small intestine. That’s not the part important in diabetes.