Type 2 diabetes mellitus is a metabolic disorder characterized by insulin resistance and progressive failure of pancreatic beta cells, resulting in hyperglycemia. Obesity, is one of the potent risk factor for type 2 diabetes, contributes to its development by inducing insulin resistance and inflammation, which in turn impair glucose regulation. Bariatric surgery is a weight loss surgery, used as a last resort to treat people who are dangerously obese (carrying an abnormally excessive amount of body fat). This surgery is used to treat people with potentially life-threatening obesity that will not respond to non-surgical treatments, such as lifestyle and dietary changes or modifications. According to guidelines from the National Institutes of Health, the current indications for bariatric surgery include a BMI of 40 kg/m2 or higher, or a BMI between 35 and 40 kg/m2 with at least two obesity-related comorbidities. The guidelines suggest that bariatric surgery be discussed with all severely obese patients (BMI > 35 kg/m2) with type 2 diabetes who have not been able to lose weight with other weight-control approaches.
In bariatric surgery, weight loss is usually achieved by reducing the size of the stomach with an implanted medical device (gastric banding) or through removal of a portion of the stomach (sleeve gastrectomy or biliopancreatic diversion with duodenal switch) or by resecting and re-routing the small intestines to a small stomach pouch (gastric bypass surgery). But not all bariatric procedures have the same effect on weight and diabetes.
The recent researches revealed that after bariatric surgery, patients lose more weight than with traditional weight-loss methods—up to 25% of their total body weight. Furthermore, of those with type 2 diabetes, 87% achieve at least better glucose control and need fewer antidiabetic medications, and an average of 78% achieve normal glycemic control without taking any antidiabetic medications at all.
There are three major mechanisms or theory that explains how bariatric surgery reverses diabetes. 1st theory indicates weight loss increases insulin sensitivity. The negative energy balance and weight loss after bariatric surgery reduce insulin resistance. Consequently, the beta cells can rest because they don’t need to produce as much insulin. Usually observed after both gastric restrictive procedures and gastric bypass procedures. 2nd theory reflects that bariatric surgery lessens insulin resistance by reducing “lipotoxicity,” a condition related to dysregulated fatty acid flux, lipid metabolites in tissues, and direct and indirect effects of hormones secreted by adipocytes. The strongest evidence for this theory comes from Bikman et al, who found that insulin sensitivity increased after Roux-en-Y surgery more than expected from weight loss alone. One year after surgery, even though they remained anthropometrically obese (BMI > 30 kg/m2), the patients had insulin sensitivity levels similar to those in a control group of lean people (BMI < 25 kg/m2).
The third theory is likely the most relevant and relates to various hormones secreted by the gut in response to food. Surgical exclusion of the duodenum in the Roux-en-Y procedure and of the duodenum and jejunum in biliopancreatic diversion result in altered relative distribution of CHO and fat absorption. The “hindgut hypothesis” raised by Cummings et al, suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances, which account for the reversal of hyperglycemia and obesity. In contrast, the “foregut hypothesis” raised by Rubino et al, suggests that nutrient interactions in the duodenum are diabetogenic and, hence, bypassing the duodenum would reverse this defect.
Strong evidence now exists that bariatric surgery increases life expectancy and that this is largely attributable to reduction in CVD risk factors such as diabetes and cancer. Recent studies have found that the long-term death rate is 32% to 73% lower for patients undergoing bariatric surgery than in matched controls who do not undergo surgery. A decrease in the death rate related to diabetes has played an important role in these results.
REFERENCES
The recent researches revealed that after bariatric surgery, patients lose more weight than with traditional weight-loss methods—up to 25% of their total body weight. Furthermore, of those with type 2 diabetes, 87% achieve at least better glucose control and need fewer antidiabetic medications, and an average of 78% achieve normal glycemic control without taking any antidiabetic medications at all.
There are three major mechanisms or theory that explains how bariatric surgery reverses diabetes. 1st theory indicates weight loss increases insulin sensitivity. The negative energy balance and weight loss after bariatric surgery reduce insulin resistance. Consequently, the beta cells can rest because they don’t need to produce as much insulin. Usually observed after both gastric restrictive procedures and gastric bypass procedures. 2nd theory reflects that bariatric surgery lessens insulin resistance by reducing “lipotoxicity,” a condition related to dysregulated fatty acid flux, lipid metabolites in tissues, and direct and indirect effects of hormones secreted by adipocytes. The strongest evidence for this theory comes from Bikman et al, who found that insulin sensitivity increased after Roux-en-Y surgery more than expected from weight loss alone. One year after surgery, even though they remained anthropometrically obese (BMI > 30 kg/m2), the patients had insulin sensitivity levels similar to those in a control group of lean people (BMI < 25 kg/m2).The third theory is likely the most relevant and relates to various hormones secreted by the gut in response to food. Surgical exclusion of the duodenum in the Roux-en-Y procedure and of the duodenum and jejunum in biliopancreatic diversion result in altered relative distribution of CHO and fat absorption. The “hindgut hypothesis” raised by Cummings et al, suggests that accelerated transit of concentrated nutrients (particularly glucose) to the distal intestine results in increased production of insulinotropic and appetite-controlling substances, which account for the reversal of hyperglycemia and obesity. In contrast, the “foregut hypothesis” raised by Rubino et al, suggests that nutrient interactions in the duodenum are diabetogenic and, hence, bypassing the duodenum would reverse this defect.
Strong evidence now exists that bariatric surgery increases life expectancy and that this is largely attributable to reduction in CVD risk factors such as diabetes and cancer. Recent studies have found that the long-term death rate is 32% to 73% lower for patients undergoing bariatric surgery than in matched controls who do not undergo surgery. A decrease in the death rate related to diabetes has played an important role in these results.
REFERENCES
- Adams TD, Gress RE, Smith SC, et al. Long-term mortality after gastric bypass surgery. N Engl J Med 2007; 357:753–761.
- Bikman BT, Zheng D, Pories WJ, et al. Mechanism for improved insulin sensitivity after gastric bypass surgery. J Clin Endocrinol Metab 2008;93:4656–4663.
- Buchwald H, Avidor Y, Braunwald E, et al. Bariatric surgery: a systematic review and meta-analysis. JAMA 2004; 292:1724–1737.
- Buchwald H, Estok R, Fahrbach K, et al. Weight and type 2 diabetes after bariatric surgery: systematic review and meta-analysis. Am J Med 2009;122:248–256.
- Consensus Development Conference Panel. NIH conference. Gastrointestinal surgery for severe obesity. Ann Intern Med 1991; 115:956–961.
- Cummings DE, Overduin J, Foster-Schubert KE. Gastric bypass for obesity: mechanisms of weight loss and diabetes resolution. J Clin Endocrinol Metab 2004; 89:2608–2615.
- DeFronzo RA. Pathogenesis of type 2 diabetes mellitus. Med Clin North Am 2004; 88:787–835.
- Kashyap SR, Defronzo RA. The insulin resistance syndrome: physiological considerations. Diab Vasc Dis Res 2007; 4:13–19.
- Mokdad AH, Ford ES, Bowman BA, et al. Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA 2003; 289:76–79.
- Rubino F, Forgione A, Cummings DE, et al.The mechanism of diabetes control after gastrointestinal bypass surgery reveals a role of the proximal small intestine in the pathophysiology of type 2 diabetes. Ann Surg 2006;244:741–749.
- Sjöström L, Narbro K, Sjöström CD, et al., Swedish Obese Subjects Study. Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med 2007; 357:741–752.
- Unger RH. Minireview: weapons of lean body mass destruction: the role of ectopic lipids in the metabolic syndrome. Endocrinology 2003;144:5159–5165.
