Metabolic and Endocrine Consequences of Bariatric Surgery

Abstract

Obesity is one of the most serious worldwide epidemics of the twenty-first century according to the World Health Organization. Frequently associated with a number of comorbidities, obesity threatens and compromises individual health and quality of life. Bariatric surgery (BS) has been demonstrated to be an effective treatment to achieve not only sustained weight loss but also significant metabolic improvement that goes beyond mere weight loss. The beneficial effects of BS on metabolic traits are so widely recognized that some authors have proposed BS as metabolic surgery that could be prescribed even for moderate obesity. However, most of the BS procedures imply malabsorption and/or gastric acid reduction which lead to nutrient deficiency and, consequently, further complications could be developed in the long term. In fact, BS not only affects metabolic homeostasis but also has pronounced effects on endocrine systems other than those exclusively involved in metabolic function. The somatotropic, corticotropic, and gonadal axes as well as bone health have also been shown to be affected by the various BS procedures. Accordingly, further consequences and complications of BS in the long term in systems other than metabolic system need to be addressed in large cohorts, taking into account each bariatric procedure before making generalized recommendations for BS. In this review, current data regarding these issues are summarized, paying special attention to the somatotropic, corticotropic, gonadal axes, and bone post-operative health.

Keywords: bariatric surgery; bone metabolism; corticotropic axis; gonadal axis; somatotropic axis.

Copyright © 2019 Cornejo-Pareja, Clemente-Postigo and Tinahones.

Figures

Figure 1

Mechanism for T2DM resolution. Mechanisms and modifications of main gastrointestinal hormones involved in T2DM resolution after bariatric surgery. Several mechanisms have been proposed to explain the metabolic improvement after bariatric surgery. However, due to the fact that each bariatric procedure does not involve the same gastrointestinal tract modifications, it has been suggested that each procedure acts by means of different mechanisms to achieve T2DM resolution, including differential shifts in gastrointestinal hormones levels. It has been proposed that the exclusion of the duodenum and proximal jejunum in bariatric procedures such as RYGB or BPD would inhibit the “anti-incretin” signaling (“foregut hypothesis”). This kind of remodeling would also reduce the time that nutrients take to reach distal jejunum which could imply an early activation of incretin-secreting L-cells in the distal ileum and proximal colon (“hindgut hypothesis”). Incretins such as GLP-1, PYY, or oxyntomodulin improve pancreatic insulin secretion and reduce glucagon release. By contrast, the main gastrointestinal hormonal shift expected after SG is the decrease in the levels of the orexigenic hormone ghrelin due to the removal of the gastric fundus and therefore, of the ghrelin-producing mucosa. However, it has also been described an increase in GLP-1 and PYY levels after SG likely due to a shorter intestinal transit after surgery. Apart from changes in gastrointestinal hormone patterns, alterations in bile acid metabolism, gut microbiota composition, modification in gastrointestinal vagal signaling or changes in adipokines levels described after the different bariatric procedures, could be also involved in the bariatric metabolic improvement and T2DM resolution after surgery. BPD, biliopancreatic diversion; GIP, gastric inhibitory polypeptide; GLP-1, Glucagon-like Peptide 1; PYY, Peptide YY; RYGB, Roux-en-Y gastric bypass; SG, sleeve gastrectomy; T2DM, Type 2 diabetes mellitus.