Effect of weight loss induced by laparoscopic sleeve gastrectomy on liver histology and serum adipokine levels

Abstract

Background & Aim: Bariatric surgery is a valid treatment option for persons with non-alcoholic fatty liver disease. This study prospectively examined the impact of laparoscopic sleeve gastrectomy (LSG) on liver histopathology, and blood levels of adiponectin, leptin, resistin, and pre-B cell enhancing factor/Nampt/visfatin. Patients & Methods: In 81 patients with non-alcoholic fatty liver disease who underwent LSG, paired liver biopsies and blood specimens were obtained before and 18 months after LSG. Differences between preoperative and 18 months postoperative data were tested by paired Student's t-test or Wilcoxon rank test as appropriate. Results: At follow up, there was a significant improvement in biochemical markers for glucose homeostasis, including fasting glucose, HbA1c, insulin levels, and homeostatic model assessment index. Postoperative liver function tests, namely serum alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase level, showed a significant improvement compared to before weight loss. The number of patients who had definite, borderline, or no non-alcoholic steatohepatitis was 43 (53%), 27 (33%), and 11 (14%), respectively, at baseline, and 9 (11%), 32 (40%), and 40 (49%) at 18-month postsurgery follow up. A significant reduction in steatosis, liver fibrosis, lobular inflammation, and hepatocyte ballooning was observed in the postoperative biopsies (P < 0.001 each). In addition, at the follow-up assessment, there was a significant increase in serum adiponectin levels and significant decline in serum levels of leptin, resisitin, and pre-B cell enhancing factor/Nampt/visfatin. Conclusion: Weight loss after sleeve gastrectomy was associated with a significant improvement in several metabolic parameters, liver enzyme levels, liver histopathology, and changes in serum adipokine levels towards antidiabetic and anti-inflammatory profiles.

The Metabolic Rearrangements of Bariatric Surgery: Focus on Orexin-A and the Adiponectin System

“…It is well known that obesity induces not only an alteration of many metabolic mediators alerting glucose and lipid profiles, but also induces an imbalance in the expression of pro- and anti-inflammatory adipokines such as Adiponectin. As reported by Salman et al bariatric surgery induces a significant increase in serum Adiponectin levels and a significant decline in serum levels of leptin, resisitin, and pre-B cell enhancing factor/Nampt/visfatin, confirming the role of this technique in hormonal rearrangement [ 55 ].…”

Hepatic Steatosis Is Associated with Elevated Serum Iron in Patients with Obesity and Improves after Laparoscopic Sleeve Gastrectomy

“…Additionally, LSG is useful as a therapeutic option to improve or reverse NAFLD. Patients with NAFLD who underwent LSG showed a significant reduction in liver steatosis and fibrosis 18 months after surgery [6]. The histology and liver function of patients with morbid obesity are significantly improved after LSG via mechanisms that involve the reduction of oxidative stress and inflammatory processes [7].…”

c‐Jun acts downstream of PI3K/AKT signaling to mediate the effect of leptin on methionine adenosyltransferase 2B in hepatic stellate cells in vitro and in vivo

“…It is noteworthy that serum leptin may be related to the rate of fibrosis progression in nondiabetic patients with chronic HBV infection [12]. Recent results showed that weight loss in obese patients with NAFLD was associated with a significant improvement in anti‐inflammatory profiles, which was accompanied with a decline in serum levels of leptin [13] and of liver fibrosis [14]. Direct support for the role of leptin in human liver fibrosis is that leptin‐mediated NADPH oxidase enhances fibrogenesis in experimental and human NASH [15].…”