The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis

Abstract Dietary palmitic acid (PA) promotes liver fibrosis in patients with nonalcoholic steatohepatitis (NASH). Herein, we clarified the intestinal absorption kinetics of dietary PA and effect of trans-portal PA on the activation of hepatic stellate cells (HSCs) involved in liver fibrosis in NASH....

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Autores principales: Masakazu Hanayama, Yasunori Yamamoto, Hiroki Utsunomiya, Osamu Yoshida, Shuang Liu, Masaki Mogi, Bunzo Matsuura, Eiji Takeshita, Yoshiou Ikeda, Yoichi Hiasa
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Publicado: Nature Portfolio 2021
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spelling oai:doaj.org-article:a9fe924bb8cb41818066b88cd7398b972021-12-02T16:10:35ZThe mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis10.1038/s41598-021-92790-z2045-2322https://doaj.org/article/a9fe924bb8cb41818066b88cd7398b972021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92790-zhttps://doaj.org/toc/2045-2322Abstract Dietary palmitic acid (PA) promotes liver fibrosis in patients with nonalcoholic steatohepatitis (NASH). Herein, we clarified the intestinal absorption kinetics of dietary PA and effect of trans-portal PA on the activation of hepatic stellate cells (HSCs) involved in liver fibrosis in NASH. Blood PA levels after meals were significantly increased in patients with NASH compared to those in the control. Expression of genes associated with fat absorption and chylomicron formation, such as CD36 and MTP, was significantly increased in the intestine of NASH model rats compared with that in the controls. Plasma levels of glucagon-like peptide-2, involved in the upregulation of CD36 expression, were elevated in NASH rats compared with those in the controls. Furthermore, portal PA levels after meals in NASH rats were significantly higher than those in control and nonalcoholic fatty liver rats. Moreover, PA injection into the portal vein to the liver in control rats increased the mRNA levels associated with the activation of HSCs. Increased intestinal absorption of diet-derived PA was observed in NASH. Thus, the rapid increase in PA levels via the portal vein to the liver may activate HSCs and affect the development of liver fibrosis in NASH.Masakazu HanayamaYasunori YamamotoHiroki UtsunomiyaOsamu YoshidaShuang LiuMasaki MogiBunzo MatsuuraEiji TakeshitaYoshiou IkedaYoichi HiasaNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Masakazu Hanayama
Yasunori Yamamoto
Hiroki Utsunomiya
Osamu Yoshida
Shuang Liu
Masaki Mogi
Bunzo Matsuura
Eiji Takeshita
Yoshiou Ikeda
Yoichi Hiasa
The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
description Abstract Dietary palmitic acid (PA) promotes liver fibrosis in patients with nonalcoholic steatohepatitis (NASH). Herein, we clarified the intestinal absorption kinetics of dietary PA and effect of trans-portal PA on the activation of hepatic stellate cells (HSCs) involved in liver fibrosis in NASH. Blood PA levels after meals were significantly increased in patients with NASH compared to those in the control. Expression of genes associated with fat absorption and chylomicron formation, such as CD36 and MTP, was significantly increased in the intestine of NASH model rats compared with that in the controls. Plasma levels of glucagon-like peptide-2, involved in the upregulation of CD36 expression, were elevated in NASH rats compared with those in the controls. Furthermore, portal PA levels after meals in NASH rats were significantly higher than those in control and nonalcoholic fatty liver rats. Moreover, PA injection into the portal vein to the liver in control rats increased the mRNA levels associated with the activation of HSCs. Increased intestinal absorption of diet-derived PA was observed in NASH. Thus, the rapid increase in PA levels via the portal vein to the liver may activate HSCs and affect the development of liver fibrosis in NASH.
format article
author Masakazu Hanayama
Yasunori Yamamoto
Hiroki Utsunomiya
Osamu Yoshida
Shuang Liu
Masaki Mogi
Bunzo Matsuura
Eiji Takeshita
Yoshiou Ikeda
Yoichi Hiasa
author_facet Masakazu Hanayama
Yasunori Yamamoto
Hiroki Utsunomiya
Osamu Yoshida
Shuang Liu
Masaki Mogi
Bunzo Matsuura
Eiji Takeshita
Yoshiou Ikeda
Yoichi Hiasa
author_sort Masakazu Hanayama
title The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
title_short The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
title_full The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
title_fullStr The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
title_full_unstemmed The mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
title_sort mechanism of increased intestinal palmitic acid absorption and its impact on hepatic stellate cell activation in nonalcoholic steatohepatitis
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/a9fe924bb8cb41818066b88cd7398b97
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