Poster Topical Area: Dietary Bioactive Components

Location: Hall D

Poster Board Number: 277

P08-019 - Fatty liver-driven apoptosis due to high-fat diet in SAMP8 ageing model is alleviated by administration of a potato bioactive peptide

Monday, Jun 11
8:00 AM – 3:00 PM

Nonalcoholic Fatty Liver Disease (NAFLD) has become a growing epidemic in westernized-lifestyle population groups. Previous studies revealed a potential lipolysis-stimulating role for oral supplementation of a potato-extracted crude-protein hydrolysate (CPP) to young adult murine model . Given that peptide segments exhibit highly efficacious advantages due to high absorption and low power, compared to parent protein; we hypothesized that intraperitoneal delivery of a purified bioactive peptide from CPP to HFD-fed SAMP8 aging mice would effectively modulate hepatic targets involving in lipolysis-promoting activities and then confer protection against hepatocytes apoptosis triggered by lipotoxicity.

Accordingly, DIKTNKPVIF peptide were purified, synthesized and used alongside with its parent protein (CPP) and the hypolipidaemic drug, probucol. Six-month-old mice were divided into five groups (n=4, each) for a fourteen-week experimental design. The normal control group (CHO) fed a standard chow upon sacrifice. After six weeks of HFD (60% calories from fat), remaining mice groups were treated without (HFco) or simultaneously with: either DIKTNKPVIF peptide (HF-DF; 15 mg/kg b.w. q24h × 8w, i.p.), CPP (HF-CPP; 50 mg/kg b.w. q24h × 8w, via oral gavage) or Probucol (HF-Pr; 500 mg/kg b.w. q24h × 8w, via oral tube) for the final eight weeks.

Compared to CHO, histopathological analyses of liver tissue samples revealed massive hepatic fat accumulation in HFco, but reduced fatty changes in HF-DF. In contrast to HFco, the number of TUNEL-positive hepatic cells were considerably low in HF-DF which showed: (1) reduced macro- and micro- vesicular fatty changes; and, at protein level, (2) upregulation of SIRT1 / PGC-1α axis (p<0,001) and survival markers such as p-Akt (p<0,01) with concomitant inhibition of pro-apoptotic activity promoted by JNK signaling.

The present data indicate that intraperitoneal (i.p.) administration of our synthesized peptide in aging mice effectively attenuated HFD-induced steatosis and hepatocyte apoptosis through enhancing SIRT1 / PGC-1α axis. Therefore, DIKTNKPVIF peptide may be proposed as potential therapeutic strategy capable of ameliorating hepatocellular injury underlining NAFLD in elderly.

Funding Source: This study was financially supported in part by grants from the Ministry of Science and Technology of Taiwan (MOST103-2410-H-029-037 and MOST104-2410-H-029- 033-MY2). We express our gratitude to Taiwan Ministry of Foreign Affairs (MOFA) Scholarship Program for the Republic of Haiti, through which SD (Faculte de Medecine et de Pharmacie, Universite d'Etat d'Haiti - FMP UEH) was supported.

CoAuthors: Stanley DUmeUS, MD – State University of Haiti Faculty of Medicine and Pharmacy; Wei-Wen Kuo, PhD – China Medical University; Chih-Yang Huang, PhD – China Medical University

Stanley DUmeUS

Academic Officer
State University of Haiti Faculty of Medicine and Pharmacy
Taichung, Taichung, Taiwan (Republic of China)