Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin

Yoshikatsu Miwa, Hitoshi Mitsuzumi, Mika Yamada, Norie Arai, Fujimi Tanabe, Katsuhide Okada, Michio Kubota, Hiroto Chaen, Takahiro Sunayama, Masayoshi Kibata

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Our previous study has shown that a soluble hesperidin derivative, glucosyl hesperidin (G-hesperidin), preferentially lowers serum triglyceride (TG) level in hypertriglyceridemic subjects through the improvement of very low-density lipoprotein (VLDL) metabolic abnormality. G-Hesperidin has also been found to decrease an elevated serum apolipoprotein B (apo B) level in the hypertriglyceridemic subjects, suggesting a possibility that this compound suppresses excess VLDL secretion in the liver. In the present study, to gain a better understanding of possible mechanisms by which G-hesperidin lowers serum TG, we examined whether this derivative affects apo B secretion from HepG2 human hepatoma cells, a model of hepatic VLDL secretion. As a result, G-hesperidin significantly reduced apo B secretion from the oleate-stimulated HepG2 cells. Furthermore, G-hesperidin significantly suppressed apo B secretion only in the oleate-stimulated cells and failed to act on the cells incubated without oleate. In the oleate-stimulated cells, G-hesperidin significantly decreased cellular cholesteryl ester (CE), although it had no effect on cellular TG or free cholesterol amounts. Moreover, the oleate-stimulated cells had a decrease in cellular apo B amounts by G-hesperidin exposure. These findings indicate that G-hesperidin downregulates the assembly of apo B-containing lipoproteins via the reduction of CE synthesis augmented with oleate and results in suppressing excess apo B secretion from the cells. This effect is speculated to be associated with the improvement of VLDL metabolic abnormality in hypertriglyceridemic subjects and considered as a mechanism of lowering serum TG.

Original languageEnglish
Pages (from-to)223-231
Number of pages9
JournalJournal of Nutritional Science and Vitaminology
Volume52
Issue number3
DOIs
Publication statusPublished - Jun 2006
Externally publishedYes

Fingerprint

hesperidin
apolipoprotein B
Hep G2 Cells
Apolipoproteins B
Oleic Acid
secretion
VLDL Lipoproteins
oleic acid
very low density lipoprotein
Triglycerides
Hesperidin
cells
triacylglycerols
Cholesterol Esters
Serum
cholesteryl esters
chemical derivatives
Liver
glucosyl hesperidin
liver

Keywords

  • Apolipoprotein B
  • Cholesteryl ester
  • Glucosyl hesperidin
  • HepG2 cells
  • Very low-density lipoprotein

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Miwa, Y., Mitsuzumi, H., Yamada, M., Arai, N., Tanabe, F., Okada, K., ... Kibata, M. (2006). Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin. Journal of Nutritional Science and Vitaminology, 52(3), 223-231. https://doi.org/10.3177/jnsv.52.223

Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin. / Miwa, Yoshikatsu; Mitsuzumi, Hitoshi; Yamada, Mika; Arai, Norie; Tanabe, Fujimi; Okada, Katsuhide; Kubota, Michio; Chaen, Hiroto; Sunayama, Takahiro; Kibata, Masayoshi.

In: Journal of Nutritional Science and Vitaminology, Vol. 52, No. 3, 06.2006, p. 223-231.

Research output: Contribution to journalArticle

Miwa, Y, Mitsuzumi, H, Yamada, M, Arai, N, Tanabe, F, Okada, K, Kubota, M, Chaen, H, Sunayama, T & Kibata, M 2006, 'Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin', Journal of Nutritional Science and Vitaminology, vol. 52, no. 3, pp. 223-231. https://doi.org/10.3177/jnsv.52.223
Miwa, Yoshikatsu ; Mitsuzumi, Hitoshi ; Yamada, Mika ; Arai, Norie ; Tanabe, Fujimi ; Okada, Katsuhide ; Kubota, Michio ; Chaen, Hiroto ; Sunayama, Takahiro ; Kibata, Masayoshi. / Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin. In: Journal of Nutritional Science and Vitaminology. 2006 ; Vol. 52, No. 3. pp. 223-231.
@article{ae0ead42293b43f6a634930dea7b25e2,
title = "Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin",
abstract = "Our previous study has shown that a soluble hesperidin derivative, glucosyl hesperidin (G-hesperidin), preferentially lowers serum triglyceride (TG) level in hypertriglyceridemic subjects through the improvement of very low-density lipoprotein (VLDL) metabolic abnormality. G-Hesperidin has also been found to decrease an elevated serum apolipoprotein B (apo B) level in the hypertriglyceridemic subjects, suggesting a possibility that this compound suppresses excess VLDL secretion in the liver. In the present study, to gain a better understanding of possible mechanisms by which G-hesperidin lowers serum TG, we examined whether this derivative affects apo B secretion from HepG2 human hepatoma cells, a model of hepatic VLDL secretion. As a result, G-hesperidin significantly reduced apo B secretion from the oleate-stimulated HepG2 cells. Furthermore, G-hesperidin significantly suppressed apo B secretion only in the oleate-stimulated cells and failed to act on the cells incubated without oleate. In the oleate-stimulated cells, G-hesperidin significantly decreased cellular cholesteryl ester (CE), although it had no effect on cellular TG or free cholesterol amounts. Moreover, the oleate-stimulated cells had a decrease in cellular apo B amounts by G-hesperidin exposure. These findings indicate that G-hesperidin downregulates the assembly of apo B-containing lipoproteins via the reduction of CE synthesis augmented with oleate and results in suppressing excess apo B secretion from the cells. This effect is speculated to be associated with the improvement of VLDL metabolic abnormality in hypertriglyceridemic subjects and considered as a mechanism of lowering serum TG.",
keywords = "Apolipoprotein B, Cholesteryl ester, Glucosyl hesperidin, HepG2 cells, Very low-density lipoprotein",
author = "Yoshikatsu Miwa and Hitoshi Mitsuzumi and Mika Yamada and Norie Arai and Fujimi Tanabe and Katsuhide Okada and Michio Kubota and Hiroto Chaen and Takahiro Sunayama and Masayoshi Kibata",
year = "2006",
month = "6",
doi = "10.3177/jnsv.52.223",
language = "English",
volume = "52",
pages = "223--231",
journal = "Journal of Nutritional Science and Vitaminology",
issn = "0301-4800",
publisher = "Center for Academic Publications Japan",
number = "3",

}

TY - JOUR

T1 - Suppression of apolipoprotein B secretion from HepG2 cells by glucosyl hesperidin

AU - Miwa, Yoshikatsu

AU - Mitsuzumi, Hitoshi

AU - Yamada, Mika

AU - Arai, Norie

AU - Tanabe, Fujimi

AU - Okada, Katsuhide

AU - Kubota, Michio

AU - Chaen, Hiroto

AU - Sunayama, Takahiro

AU - Kibata, Masayoshi

PY - 2006/6

Y1 - 2006/6

N2 - Our previous study has shown that a soluble hesperidin derivative, glucosyl hesperidin (G-hesperidin), preferentially lowers serum triglyceride (TG) level in hypertriglyceridemic subjects through the improvement of very low-density lipoprotein (VLDL) metabolic abnormality. G-Hesperidin has also been found to decrease an elevated serum apolipoprotein B (apo B) level in the hypertriglyceridemic subjects, suggesting a possibility that this compound suppresses excess VLDL secretion in the liver. In the present study, to gain a better understanding of possible mechanisms by which G-hesperidin lowers serum TG, we examined whether this derivative affects apo B secretion from HepG2 human hepatoma cells, a model of hepatic VLDL secretion. As a result, G-hesperidin significantly reduced apo B secretion from the oleate-stimulated HepG2 cells. Furthermore, G-hesperidin significantly suppressed apo B secretion only in the oleate-stimulated cells and failed to act on the cells incubated without oleate. In the oleate-stimulated cells, G-hesperidin significantly decreased cellular cholesteryl ester (CE), although it had no effect on cellular TG or free cholesterol amounts. Moreover, the oleate-stimulated cells had a decrease in cellular apo B amounts by G-hesperidin exposure. These findings indicate that G-hesperidin downregulates the assembly of apo B-containing lipoproteins via the reduction of CE synthesis augmented with oleate and results in suppressing excess apo B secretion from the cells. This effect is speculated to be associated with the improvement of VLDL metabolic abnormality in hypertriglyceridemic subjects and considered as a mechanism of lowering serum TG.

AB - Our previous study has shown that a soluble hesperidin derivative, glucosyl hesperidin (G-hesperidin), preferentially lowers serum triglyceride (TG) level in hypertriglyceridemic subjects through the improvement of very low-density lipoprotein (VLDL) metabolic abnormality. G-Hesperidin has also been found to decrease an elevated serum apolipoprotein B (apo B) level in the hypertriglyceridemic subjects, suggesting a possibility that this compound suppresses excess VLDL secretion in the liver. In the present study, to gain a better understanding of possible mechanisms by which G-hesperidin lowers serum TG, we examined whether this derivative affects apo B secretion from HepG2 human hepatoma cells, a model of hepatic VLDL secretion. As a result, G-hesperidin significantly reduced apo B secretion from the oleate-stimulated HepG2 cells. Furthermore, G-hesperidin significantly suppressed apo B secretion only in the oleate-stimulated cells and failed to act on the cells incubated without oleate. In the oleate-stimulated cells, G-hesperidin significantly decreased cellular cholesteryl ester (CE), although it had no effect on cellular TG or free cholesterol amounts. Moreover, the oleate-stimulated cells had a decrease in cellular apo B amounts by G-hesperidin exposure. These findings indicate that G-hesperidin downregulates the assembly of apo B-containing lipoproteins via the reduction of CE synthesis augmented with oleate and results in suppressing excess apo B secretion from the cells. This effect is speculated to be associated with the improvement of VLDL metabolic abnormality in hypertriglyceridemic subjects and considered as a mechanism of lowering serum TG.

KW - Apolipoprotein B

KW - Cholesteryl ester

KW - Glucosyl hesperidin

KW - HepG2 cells

KW - Very low-density lipoprotein

UR - http://www.scopus.com/inward/record.url?scp=33746888685&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746888685&partnerID=8YFLogxK

U2 - 10.3177/jnsv.52.223

DO - 10.3177/jnsv.52.223

M3 - Article

C2 - 16967768

AN - SCOPUS:33746888685

VL - 52

SP - 223

EP - 231

JO - Journal of Nutritional Science and Vitaminology

JF - Journal of Nutritional Science and Vitaminology

SN - 0301-4800

IS - 3

ER -