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

Objectives:
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.


Methods:
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.


Results:
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.


Conclusions:
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)