Using small groups of eight rats, they found that the rats who received Avandia prior to the start of any rise in blood sugars, usually seen at 8 to 10 weeks of age, did not loose beta cell mass. The treated animals also did not develop diabetes. Avandia and other glitazones like Actos, and the no-longer available Rezulin, work by sensitizing cells to insulin. TNF and other inflammatory cytokines are believed to cause insulin resistance, but they also appear to be a major cause of beta cell death in both Type 1 and Type 2 diabetes. Cytokine inhibitors have been indirectly tested for their ability to protect beta cells.
Cytokines cause cell death through an excess production of oxidizing agents and nitric oxide.
Antioxidants , such as superoxide dismutase and catalase, are believed likely to add additional protection when added to agents that reduce cytokines. Human clinical trials will be required to test whether this Zucker fatty rat study translates to humans, and whether Avandia and other glitazones can succeed where every other diabetes medication has failed. We suggest that, if research funds are allocated to study this promising area, the placebo and treatment arms each be split to test another protective mechanism, such as a combined group of antioxidants. Heart disease is not an unusual complication of insulin resistance and diabetes. However, a new study suggests that this link may actually be genetic.