The current issue of Surgery for Obesity and Related Diseases is entirely dedicated to the widespread problem of Diabetes. There are 422 million diabetics in the world making Diabetes one of the epidemic diseases of our time. Traditionally, type 2 Diabetes has always been considered a medical problem. Diabetes, however, is most likely a surgical disease. The common association between obesity and type 2 diabetes has long been established. It has been accepted that obesity leads to peripheral insulin resistance which causes a rise in blood glucose levels. This in turns elicits increased insulin secretion. As insulin resistance worsens, hyperglycemia further stimulates insulin secretion leading eventually to pancreatic islet cells burnout and overt diabetes.
The advent of bariatric and metabolic surgery has challenged this causative theory. Dr. Walter Pories was first to publish in 1995 a study on the immediate normalization of blood glucose level within 24 hours of gastric bypass surgery prior to any significant weight loss. Numerous publications followed this initial landmark study and demonstrated that the manipulation of the gastro-intestinal tract results in altered neuro-hormonal signals that improve blood sugar control independent of weight loss. The amelioration of diabetes following metabolic surgery like gastric bypass and sleeve gastrectomy was dramatic when compared to current medical treatment protocol. The exact mechanisms for diabetes resolution and sometimes cure following weight loss surgery are still not fully understood. However, the theoretical framework for diabetes development has been set. Peripheral insulin resistance, due to fat accumulation in muscle and adipose tissue, is less likely to be the cause of type 2 diabetes. Rather, insulin resistance is a consequence of type 2 diabetes. It has long been established that insulin is secreted into the portal system in a pulsatile fashion. Loss of this pulsatile insulin secretion is the first step in type 2 diabetes development. Indeed, many studies have shown that patients with pre-diabetes or increased glucose intolerance have lost their pulsatile insulin secretion. The loss of this delicate mechanism slowly results in increased central and peripheral insulin resistance which in turn exacerbates hyperglycemia. Hyperglycemia further stimulates insulin secretion leading eventually to islet cell fatigue and burnout. Manipulation of the gastro-intestinal tract in the form of gastric bypass or sleeve surgery seems to break this vicious circle leading to restoration of islet cell pulsatile insulin secretion. Today, there are no studies on the pulsatile insulin secretion following gastric bypass surgery or sleeve gastrectomy that I am aware of. Such studies, however, are crucial to improving our understanding of type 2 diabetes development and treatment.
In conclusion, surgical manipulation of the gastrointestinal tract leads to altered gut motility and neuro-hormonal secretion. These changes have dramatic effect on several organs in the body including the pancreas. Studying the pulsatile insulin secretion of pancreatic islet cells following weight loss surgery may help uncover a potential causative etiology of type 2 diabetes.