Effects of weight loss induced by bariatric surgery on hepatic adipocytokine expression.
OBJECTIVE
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.
Moschen
Alexander R
AR
Christian Doppler Research Laboratory for Gut Inflammation, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria.
Molnar
Clemens
C
Wolf
Anna Maria
AM
Weiss
Helmut
H
Graziadei
Ivo
I
Kaser
Susanne
S
Ebenbichler
Christoph F
CF
Stadlmann
Sylvia
S
Moser
Patrizia L
PL
Tilg
Herbert
H
D054392:Adipokines / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D052242:Adiponectin / Q000097:blood / Q000235:genetics / Q000378:metabolism; D000328:Adult; D050110:Bariatric Surgery; D001483:Base Sequence; D016207:Cytokines / Q000097:blood / Q000235:genetics / Q000378:metabolism; D017931:DNA Primers / Q000235:genetics; D005234:Fatty Liver / Q000235:genetics / Q000378:metabolism / Q000601:surgery; D005260:Female; D015391:Gastroplasty; D015870:Gene Expression; D006801:Humans; D020738:Leptin / Q000097:blood / Q000235:genetics / Q000378:metabolism; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood / Q000235:genetics / Q000378:metabolism; D009767:Obesity, Morbid / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000601:surgery; D011446:Prospective Studies; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D052243:Resistin / Q000097:blood / Q000235:genetics / Q000378:metabolism; D015431:Weight Loss / Q000235:genetics / Q000502:physiology*
C499918:ADIPOQ protein, human; D054392:Adipokines; D052242:Adiponectin; D016207:Cytokines; D017931:DNA Primers; D020738:Leptin; C499624:RETN protein, human; D012333:RNA, Messenger; D052243:Resistin; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human