Bariatric Surgery and Liver Disease: General Considerations and Role of the Gut-Liver Axis

Abstract

Weight loss is a therapeutic solution for many metabolic disorders, such as obesity and its complications. Bariatric surgery aims to achieve lasting weight loss in all patients who have failed after multiple dietary attempts. Among its many benefits, it has been associated with the regression of non-alcoholic fatty liver disease (NAFLD), which is often associated with obesity, with evidence of substantial improvement in tissue inflammation and fibrosis. These benefits are mediated not only by weight loss, but also by favorable changes in systemic inflammation and in the composition of the gut microbiota. Changes in microbial metabolites such as short-chain fatty acids (SCFAs), capable of acting as endocrine mediators, and bile acids (BAs) as well as modifications of the gut-brain axis, are among the involved mechanisms. However, not all bariatric surgeries show beneficial effects on the liver; those leading to malabsorption can cause liver failure or a marked worsening of fibrosis and the development of cirrhosis. Nevertheless, there are still many unclear aspects, including the extent of the benefits and the magnitude of the risks of bariatric surgery in cirrhotic patients. In addition, the usefulness and the safety of these procedures in patients who are candidates to or who have undergone liver transplant need solid supporting evidence. This paper aims to review literature data on the use of bariatric surgery in the setting of chronic liver disease.

Keywords: MAFLD; NAFLD; bariatric surgery; cirrhosis; gut microbiota; liver transplant.

Figure 1

Description of the main types of bariatric surgery procedures. Figure was adapted from https://siceitalia.com/chirurgia-dellobesita accessed on 29 July 2021 (Italian Society of Endocrine Surgery—SICE).

Figure 2

Mechanisms linking the gut microbiota to metabolic derangement in obese patients. Short chain fatty acids (SCFAs) derived from bacteria metabolism also influence lipid metabolism by increasing lipogenesis in the liver and in the adipose tissue, and inhibiting fatty acids oxidation; together with bile acids (BAs), SCFAs can modulate host appetite and insulin release through the secretion of gastrointestinal incretins (i.e., glucagon-like peptide 1 (GLP-1), and gastrointestinal insulinotropic polypeptide (GIP) and peptide YY), as well as the activation of the farnesoid X receptor (FXR). Choline depletion due to bacteria utilization also contributes to liver lipid accumulation, as well as the reduction of fasting-induced adipocyte factor (FIAF). LPS is another important modulator of glucose metabolism and insulin sensitivity. These alterations, associated with the increased intestinal permeability and bacterial overgrowth typical of obesity, as well as endogenous ethanol production by the gut microbiota, contribute to liver inflammation leading to non-alcoholic steatohepatitis (NASH) and fibrosis.