Effects of weight loss induced by bariatric surgery on hepatic adipocytokine expression☆
Received 3 January 2009; received in revised form 20 May 2009; accepted 2 June 2009. published online 06 July 2009.
Background/Aims
Adipocytokines play a key role in the pathophysiology of non-alcoholic fatty liver diseases (NAFLD). Whereas adiponectin has mainly anti-inflammatory functions, leptin, resistin and pre-B cell enhancing factor (PBEF)/Nampt/visfatin are considered as mainly pro-inflammatory mediators regulating metabolic and immune processes.
Methods
We prospectively examined the effect of weight loss on systemic levels and/or hepatic expression of adiponectin/adiponectin receptors, leptin/leptin receptors, resistin and PBEF/Nampt/visfatin. Severely obese patients underwent laparoscopic adjustable gastric banding (LABG) and serum samples (n=30) were collected before, and after 6 and 12 months. Paired liver biopsies (before and 6 months after LABG) were obtained from 18 patients.
Results
Bariatric surgery improved insulin resistance, abnormal liver function tests and liver histology. Pronounced weight loss after 6 and 12 months was accompanied by a significant increase in serum adiponectin levels whereas both leptin and PBEF/Nampt/visfatin levels decreased. Resistin serum levels increased after 6 months but fell below baseline values after 12 months. Liver mRNA expression of adiponectin increased slightly after 6 months whereas leptin mRNA expression did not change. Interestingly, weight loss resulted in a significant decrease of hepatic mRNA expression of resistin, PBEF/Nampt/visfatin and both leptin receptor isoforms while expression of type 1 and 2 adiponectin receptor was not affected. Liver immunohistochemistry performed on index and follow-up liver biopsies revealed an increase in adiponectin staining, showed no effect on resistin/leptin positivity, and demonstrated a decrease in PBEF/Nampt/visfatin immunoreactivity.
Conclusions
Weight loss after LABG surgery drives the adipocytokine milieu towards a more anti-inflammatory direction both systemically and in the liver.
1Christian Doppler Research Laboratory for Gut Inflammation, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria
2Internal Medicine II (Gastroenterology and Hepatology), Innsbruck Medical University, Innsbruck, Austria
3Internal Medicine I (Metabolic Diseases, Pulmology, Infectious Diseases, Endocrinology, Rheumatology and Angiology), Innsbruck Medical University, Innsbruck, Austria
4Internal Medicine V (Hematology and Oncology), Innsbruck Medical University, Innsbruck, Austria
5Department of General and Transplant Surgery, Innsbruck Medical University, Innsbruck, Austria
6Institute of Pathology, Kantonsspital Baden, Baden, Switzerland
7Institute of Pathology, Innsbruck Medical University, Innsbruck, Austria
☆ The authors who have taken part in this study declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript.
ABSTRACT