Although the results of recent research bring us a step closer to confirming the effect of bariatric surgery on the incidence of de-novo type 2 diabetes, many questions still remain unanswered. Whether altered anatomy after bariatric surgery provides continued protection against de-novo type 2 diabetes in the case of weight regain remains an open question. Can bariatric surgery reduce the risk of type 2 diabetes in obese people?
Anything that helps reduce obesity, including from the consumption of a balanced diet and exercise to more invasive procedures, such as surgery.
As for the de novo type 2 diabetes, it is a matter of how one views the entire process. The clinical pronouncement of this disease usually happens well after many changes that have already happened over a period of time, in some cases years. For example, many of the subjects in high risk group for type 2 diabetes who are not clinically diabetic yet, tend to have abnormal glucose tolerance profile and varying degree of insulin resistance. Clinical onset of type 2 diabetes is based on an agreed upon set of values whereas the disease is a slow progression of events which eventually results in the clinical onset.
Early improvement of type 2 diabetes following bariatric surgery is clearly linked to the anatomical-structural changes brought by surgery, but there is now some data indicating that weight loss may play an important role in maintaining the benefits achieved.
Moreover, it is necessary to differentiate the two major types of postsurgical refractory diabetes. They may be persistant (no postoperative remission at all) or de novo (initial remission followed by resurgence). Persistant appears to be more linked to previous diabetic profile (duration, use of insulin) and de novo might be associated with insufficient late postoperative incretin/adipokyne response. Weight loss failure and/or regain must play a role in both cases.
While studies indicate that there is a definite reduction in the risk of type2 diabetes in obese people undergoing bariatric surgery, whether the risk reduction is due to calorie restricted diet alone or due to postoperative endocrine changes, i.e., reduced ghrelin secretion or augmented GLP-1 and PYY output, is still not clearly known.
Another pending question about this theme is how long the postsurgical gastrointestinal hormone response is sustained following surgery. Several prospective studies has shown decreasing rates of diabetes reversal over time, especially within the longer follow-up groups. Whether this is linked to decrease of incretin response, weight regain, unknown features of insulin resistance, etc., it is to be researched.
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