Effects of weight loss induced by bariatric surgery on hepatic adipocytokine expression

J Hepatol. 2009 Oct;51(4):765-77. doi: 10.1016/j.jhep.2009.06.016. Epub 2009 Jul 5.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipokines / blood
  • Adipokines / genetics
  • Adipokines / metabolism*
  • Adiponectin / blood
  • Adiponectin / genetics
  • Adiponectin / metabolism
  • Adult
  • Bariatric Surgery*
  • Base Sequence
  • Cytokines / blood
  • Cytokines / genetics
  • Cytokines / metabolism
  • DNA Primers / genetics
  • Fatty Liver / genetics
  • Fatty Liver / metabolism
  • Fatty Liver / surgery
  • Female
  • Gastroplasty
  • Gene Expression
  • Humans
  • Leptin / blood
  • Leptin / genetics
  • Leptin / metabolism
  • Liver / metabolism*
  • Male
  • Middle Aged
  • Nicotinamide Phosphoribosyltransferase / blood
  • Nicotinamide Phosphoribosyltransferase / genetics
  • Nicotinamide Phosphoribosyltransferase / metabolism
  • Obesity, Morbid / genetics
  • Obesity, Morbid / metabolism
  • Obesity, Morbid / pathology
  • Obesity, Morbid / surgery
  • Prospective Studies
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Resistin / blood
  • Resistin / genetics
  • Resistin / metabolism
  • Weight Loss / genetics
  • Weight Loss / physiology*

Substances

  • ADIPOQ protein, human
  • Adipokines
  • Adiponectin
  • Cytokines
  • DNA Primers
  • Leptin
  • RETN protein, human
  • RNA, Messenger
  • Resistin
  • Nicotinamide Phosphoribosyltransferase
  • nicotinamide phosphoribosyltransferase, human