A small study conducted at the University at Buffalo has discovered that insulin injections exert a strong anti-inflammatory effect in patients with type 1 diabetes. Furthermore, the study revealed that small amounts of glucose result in inflammation.
The study included ten patients with type 1 diabetes who were infused with either 2 units per hour of insulin with 100 ml 5% dextrose/hr or just the dextrose, or normal saline at 100ml/hr for 4 hours following an overnight fast. The study was repeated on three separate days total. Blood samples were collected at 0, 2, 4, and 6 hours.
Results indicated a significant decrease in CRP levels, a circulating proinflammatory mediator, by 27 +/ 9% at 6 hours following insulin infusion. There was no significant change in CRP levels following the dextrose or saline infusions. In addition, a significant reduction by 23 +/7% in reactive oxygen species generation by polymorphonuclear neutrophils (PMN) was observed at 6 hours following insulin infusion. Contrarily, at 6 hours following the dextrose infusion, an increase of 59 +/18% was observed.
The effect works by suppressing a pro-inflammatory protein known as HMG-B1, which facilitates the synthesis of additional messenger proteins that induce even further inflammation when secreted and released by the injured cell.
The investigators published a similar study in patients with type 2 diabetes, which also showed insulin’s anti-inflammatory properties. However, an important difference between the two is the timing of the anti-inflammatory effect. According to data from both studies, insulin’s anti-inflammatory effects take roughly 6 hours, as opposed to only two hours in patients with type 2 diabetes and obese patients.
These investigators now plan to shift their focus to studying meals taken with and without insulin in type 1 diabetics, so that they can better understand what missing even a single insulin injection at mealtime means to these patients.
Insulin infusion suppresses while glucose infusion induces Toll-like receptors and high-mobility group-B1 protein expression in mononuclear cells of type 1 diabetes patients. Am J Physiol Endocrinol Metab April 15, 2013 304:E810-E818; published ahead of print February 12, 2013, doi:10.1152/ajpendo.00566.2012