Rapid alternative absorption of dietary long-chain fatty acids with upregulation of intestinal glycosylated CD36 in liver cirrhosis  

Oleh:

Yamamoto, Yasunori ; Hiasa, Yoichi ; Murakami, Hidehiro ; Ikeda, Yoshio

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The American Journal of Clinical Nutrition vol. 96 no. 01 (Jul. 2012), page 90-101 .
Topik: LIVER DISEASES; Hepatic Inflammation; Hepatocarcinogenesis

Ketersediaan

Perpustakaan FK Nomor Panggil: A07.K.2012.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background: Dietary long-chain fatty acid (LCFA) intake is an important risk factor for hepatic inflammation and hepatocarcinogenesis. An alternate route of dietary LCFA absorption has been suggested in patients with liver cirrhosis (LC). Objective: We aimed to determine this alternate route and to identify its mechanism. Design: Twenty healthy control subjects and 47 patients with LC—n = 23 with portal hypertension [PH(+)LC] and 24 without portal hypertension [PH(-)LC)]—were enrolled. [13C]Palmitate (an LCFA) and octanoate (a medium-chain fatty acid [MCFA]) were administered by using gastrointestinal endoscopy. Breath 13CO2 was measured to quantify metabolized fatty acids. We also examined intestinal specimens of patients in these groups. Results: A more rapid increase in metabolized palmitate, which showed a pattern similar to that of octanoate metabolism, was observed in patients with LC than in healthy control subjects. The increase in the PH(-)LC group was higher than that in the PH(+)LC group. However, the concentration of metabolized palmitate increased with treatment of the PH(+)LC group with a portal-systemic shunt. Morphologic changes such as expanded lymph and blood vessels were present, and glycosylated CD36 increased in the jejunum of the PH(+)LC group. This group had high serum concentrations of glucagon-like peptide-2. These data suggest that dietary LCFAs, similar to MCFAs, are absorbed via blood vessels in patients with LC. Conclusions: Rapid absorption of LCFAs by an alternative method occurred in patients with LC. This altered LCFA processing is likely related to upregulation of intestinal glycosylated CD36 and could contribute to pathogenesis in patients with LC.

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