Metabolic Effects of Gastric Bypass Surgery: Is It All About Calories?

Abstract

Bariatric surgery is an efficient method to induce weight loss and also, frequently, remission of type 2 diabetes (T2D). Unpaired studies have shown bariatric surgery and dietary interventions to differentially affect multiple hormonal and metabolic parameters, suggesting that bariatric surgery causes T2D remission at least partially via unique mechanisms. In the current study, plasma metabolite profiling was conducted in patients with (n = 10) and without T2D (n = 9) subjected to Roux-en-Y gastric bypass surgery (RYGB). Mixed-meal tests were conducted at baseline, after the presurgical very-low-calorie diet (VLCD) intervention, immediately after RYGB, and after a 6-week recovery period. Thereby, we could compare fasted and postprandial metabolic consequences of RYGB and VLCD in the same patients. VLCD yielded a pronounced increase in fasting acylcarnitine levels, whereas RYGB, both immediately and after a recovery period, resulted in a smaller but opposite effect. Furthermore, we observed profound changes in lipid metabolism following VLCD but not in response to RYGB. Most changes previously associated with RYGB were found to be consequences of the presurgical dietary intervention. Overall, our results question previous findings of unique metabolic effects of RYGB and suggest that the effect of RYGB on the metabolite profile is mainly attributed to caloric restriction.

Is type 2 diabetes an adiposity-based metabolic disease? From the origin of insulin resistance to the concept of dysfunctional adipose tissue

“…Lower geneƟc risk Higher geneƟc risk result was further corroborated in two recent studies that compared the metabolic effects of a VLCD versus Roux-en-Y gastric bypass in type 2 diabetic patients; the metabolic improvements were identical in the two group, ruling out any mechanism intrinsic to the surgical operation and confirming the reversibility of type 2 diabetes [85,86]. These data strengthen the concept that type 2 diabetes is caused by a chronic condition of positive energy balance with the consequent deposition of caloric surplus in liver and pancreas when adipocytes become dysfunctional.…”

Metabolomic signatures after bariatric surgery – a systematic review

“…The reduction in BCAA has been attributed to a combination of multiple factors including decreased protein intake; decreased amino acids absorption; increased BCAA catabolism and decreased protein catabolism as a consequence of insulin sensitivity improvement and metabolic amelioration [3]. The upregulation of BCAAs catabolism is supported by the consistent postoperative decline of specific subproducts of BCAAs' mitochondrial oxidation, namely short chain acylcarnitine's C3 and C5 [17,18,28,30,43]. Although BCAAs decrease after both restrictive and malabsorptive surgeries [17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][35][36][37], parallel arm studies reported a greater effect of RYGB in BCAAs levels [27,31].…”

“…After BPD, most saturated and unsaturated SMs were found to be decreased [47]. A decrease in saturated SMs levels [43,50] and increase in unsaturated SMs levels [37,43,50] after RYGB was identified by the majority of studies, Likewise, an increase in ketone bodies (3-hydroxybutyrate and acetoacetate) levels was also identified after bariatric surgery [19,27,37,38,43,51]. Although, carboxylic acids and ketone bodies levels were only observed or were more pronounced in short-term period after surgery [22,27].…”

“…Acylcarnitines are esters of L-carnitine and fatty acids. The short chain AC acetylcarnitines were reported to increase rapidly after interventions and to remain elevated for 6 to 12 months after bariatric surgery [17,21,28,32,37,43]. Contrarily, the short chain acylcarnitines derived from the branched chain amino acids (BCAAs) catabolism, C3 and C5, were shown to decrease after bariatric surgery [17,18,28,30,33,34,43].…”

“…The short chain AC acetylcarnitines were reported to increase rapidly after interventions and to remain elevated for 6 to 12 months after bariatric surgery [17,21,28,32,37,43]. Contrarily, the short chain acylcarnitines derived from the branched chain amino acids (BCAAs) catabolism, C3 and C5, were shown to decrease after bariatric surgery [17,18,28,30,33,34,43]. A transient increase in longchain ACs levels was observed two-weeks after surgery [28,44], while most studies report a decrease in medium-and long-chain ACs over the long-term in patients submitted to bariatric surgery [17,18,42,43].…”