Here I'll point out interesting research, suggesting that excess fat in the pancreas, and really nowhere else, is the cause of type 2 diabetes. Of course the only way to gain that pancreatic fat is the standard method of eating enough to put on a lot of excess visceral fat tissue and other fat tissue throughout the body, a path that shortens life expectancy, raises the risk of all of the common age-related conditions, and increases lifetime medical expenses. Visceral fat is metabolically active and causes increased chronic inflammation, among other issues, and inflammation contributes to the progression of degenerative aging. The important point to take away from this backdrop is that developing type 2 diabetes is a lifestyle choice, and so is the maintenance of the condition; even after pushing through metabolic syndrome into full-blown diabetes, a patient can choose to turn back by losing weight. It is frankly amazing that so few do, given the harms, pains, inconvenience, and cost of suffering this condition.
There are other types of diabetes that are not choices. Type 1 diabetes is an autoimmune condition that rarely emerges in later life. It is an unfortunate happenstance that, like all forms of autoimmunity, is still comparatively poorly understand. There is only a collection of theories regarding its origins rather than anything more concrete at this time. The immune system is enormously complex and incompletely mapped, as are its failure modes. Of late researchers have proposed a type 4 age-related diabetes produced by a different sort of immune system dysregulation, quite capable of arising in older people without excess fat tissue. Again this may well be happenstance, the result of a lifetime of cell and tissue damage producing disarray in complex bodily systems.
Returning to type 2 diabetes and this recent research, if the cause lies specifically in pancreatic fat, then this might go some way towards explaining the differing susceptibility across the population of people who have chosen to gain excess fat tissue. Some fraction becomes diabetic, the rest do not. If there is significant variation in the degree to which becoming overweight leads to fat in the pancreas, based on genetics or environmental factors such as level of physical activity for example, then that would be enough to produce the observed outcome.
Type 2 diabetes is caused by fat accumulating in the pancreas - and that losing less than one gram of fat through weight loss reverses the diabetes, researchers have shown. In a trial, 18 people with Type 2 diabetes and 9 people who did not have diabetes were measured for weight, fat levels in the pancreas and insulin response before and after bariatric surgery. The patients with Type 2 diabetes had been diagnosed for an average of 6.9 years, and all for less than 15 years. The people with Type 2 diabetes were found to have increased levels of fat in the pancreas.
The participants in the study had all been selected to have gastric bypass surgery for obesity and were measured before the operation then again eight weeks later. After the operation, those with Type 2 diabetes were immediately taken off their medication. Both groups lost the same amount of weight, around 13% of their initial body weight. Critically, the pool of fat in the pancreas did not change in the non-diabetics but decreased to a normal level in those with Type 2 diabetes.
"For people with Type 2 diabetes, losing weight allows them to drain excess fat out of the pancreas and allows function to return to normal. So if you ask how much weight you need to lose to make your diabetes go away, the answer is one gram! But that gram needs to be fat from the pancreas. At present the only way we have to achieve this is by calorie restriction by any means - whether by diet or an operation."
This study determined whether the decrease in pancreatic triacylglycerol during weight loss in type 2 diabetes mellitus (T2DM) is simply reflective of whole-body fat or specific to diabetes and associated with the simultaneous recovery of insulin secretory function. Individuals listed for gastric bypass surgery who had T2DM or normal glucose tolerance (NGT) matched for age, weight, and sex were studied before and 8 weeks after surgery. Pancreas and liver triacylglycerol were quantified.
Weight loss after surgery was similar, as was the change in fat mass. Pancreatic triacylglycerol did not change in NGT but decreased in the group with T2DM. First-phase insulin response to a stepped intravenous glucose infusion did not change in NGT but normalized in T2DM. We conclude that the fall in intrapancreatic triacylglycerol in T2DM, which occurs during weight loss, is associated with the condition itself rather than decreased total body fat.