Well not quite all, but new research suggests that a population of brain cells have a role to play in triggering the non-insulin-dependent form of the disease.
Writing in this week's Nature, Laura Parton and her colleagues at Harvard describe how they have identified glucose-sensitive neurones in the brain's hypothalamus which become excited when blood sugar levels rise. Since the hypothalamus controls energy balance and metabolism, the researchers wondered whether these glucose-sensing cells could also play a role in diabetes. To find out they genetically deactivated the glucose sensor used by these nerve cells and studied their how this affected blood chemistry in a group of experimental mice. Despite each having a perfectly normal pancreas capable of making normal levels of insulin, the animals developed a condition similar to the human pre-diabetic state known as "impaired glucose tolerance"; in other words they couldn't control their blood sugar levels correctly.
Next the team explored what role these cells might play in the association between diabetes and obesity. Two groups of identical, normal mice were given either a healthy diet or fed the rodent equivalent of high-calorie junk food. As expected the over-fed mice became obese, and when they did so the glucose-sensing cells in their brains stopped responding normally to blood sugar. The mice of the same age on the healthy diet, meanwhile, showed normal responses. Since shutting off these cells produced a diabetic-like state in the first group of mice, it may be that this is what links obesity with diabetes. "The discovery that defects in glucose-sensing by the brain could help lead to new therapeutic strategies", points out Brad Lowell, who led the study.