Rate Of Cellular Energy Production Lower In Persons At Risk For Type 2 Diabetes

The new research by Gerald Shulman, M.D., professor of internalmedicine, endocrinology, and senior author of the study, indicates thata decreased ability to burn sugars and fats efficiently is an early andcentral part of the diabetes problem. The new data also suggest thatthe basic defect lies within the mitochondria, which are the energyfactories inside cells that produce most of the chemical power neededto sustain life.

The young adults studied by the research team are theoffspring of parents who have type 2 diabetes, adding support to theidea that the risk can be inherited and that the problem begins wellbefore diabetes symptoms become evident. The researchers observed thatthe mitochondria in the subjects' muscle cells responded poorly toinsulin stimulation. Normal mitochondria react to insulin by boostingproduction of an energy-carrying molecule, ATP, by 90 percent. But themitochondria from the insulin-resistant people they tested only boostedATP production by five percent.

Among their findings was also evidence for a severe reductionin the amount of insulin stimulated phosphorus transport into themuscle cells of the insulin-resistant participants. This also points toa dramatic defect in insulin signaling and may explain the observedabnormalities in insulin-stimulated power production in theinsulin-resistant study subjects. Phosphorus is a key element in themithochondrion's complex energy-production process.

The co-authors were Kitt Petersen and Sylvie Dufour.

PLoS Medicine 2: www.plosmedicine.org (September 2005)