liu.seSearch for publications in DiVA
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Rosuvastatin limits the activation of hepatic stellate cells in diet-induced obese mice
University of Estado Rio De Janeiro, Brazil.
University of Estado Rio De Janeiro, Brazil.
Linköping University, Faculty of Medicine and Health Sciences.
University of Estado Rio De Janeiro, Brazil.
Show others and affiliations
2017 (English)In: Hepatology Research, ISSN 1386-6346, E-ISSN 1872-034X, Vol. 47, no 9, 928-940 p.Article in journal (Refereed) Published
Abstract [en]

Aim The aim of this study was to investigate the effects of rosuvastatin in a model of diet-induced obesity and non-alcoholic fatty liver disease, with attention to the activation of hepatic stellate cells (HSCs). Method Male C57BL/6 mice received a control diet (C; 10% energy as lipids) or a high-fat diet (HF; 50% energy as lipids) for 12 weeks, followed by 7 weeks of treatment. Group CR received control diet + rosuvastatin; group HFR received high-fat diet + rosuvastatin. Results The HF group showed higher insulin, total cholesterol, triacylglycerol, and leptin levels than the C group, all of which were significantly diminished by rosuvastatin in the HFR group. The HF group had greater steatosis and activated HSCs than the C group, whereas rosuvastatin diminished the steatosis (less 21%, P amp;lt; 0.001) and significantly inhibited the activation of the HSCs in the HFR group compared to the HF group. The sterol regulatory element-binding protein-1 and the peroxisome proliferator-activated receptor (PPAR)-gamma protein expressions were increased in HF animals and reduced after treatment in the HFR group. By contrast, low PPAR-alpha and carnitine palmitoyltransferase-1 expressions were found in the HF group, and were restored by rosuvastatin treatment in the HFR group. Conclusion Rosuvastatin mitigated hepatic steatosis by modulating PPAR balance, favoring PPAR-alpha over PPAR-gamma downstream effects. The effects were accompanied by a diminishing of insulin resistance, the anti-inflammatory adipokine profile, and HSC activation, avoiding non-alcoholic fatty liver disease progression and non-alcoholic steatohepatitis onset in this model.

Place, publisher, year, edition, pages
WILEY , 2017. Vol. 47, no 9, 928-940 p.
Keyword [en]
beta-oxidation; hepatic stellate cells; lipogenesis; NAFLD; statin; stereology
National Category
Biochemistry and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-139906DOI: 10.1111/hepr.12821ISI: 000406717000010PubMedID: 27653239OAI: oai:DiVA.org:liu-139906DiVA: diva2:1135750
Note

Funding Agencies|Brazilian Council of Science and Technology [302.154/2011-6]; Rio de Janeiro Foundation for Research [E-26/201.186/2014]

Available from: 2017-08-24 Created: 2017-08-24 Last updated: 2017-08-24

Open Access in DiVA

No full text

Other links

Publisher's full textPubMed
By organisation
Faculty of Medicine and Health Sciences
In the same journal
Hepatology Research
Biochemistry and Molecular Biology

Search outside of DiVA

GoogleGoogle Scholar

Altmetric score

Total: 47 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf