Plasma homocysteine level and hepatic sulfur amino acid metabolism in mice fed a high-fat diet

Yun, Kang Uk; Ryu, Chang Seon; Oh, Jung Min; Kim, Chung Hyun; Lee, Kye Sook; Lee, Chul‐Ho; Lee, Hyun-Sun; Kim, Bong-Hee; Kim, Sang Kyum

doi:10.1007/s00394-011-0294-0

Cited by 32 publications

(18 citation statements)

References 39 publications

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“…Our data showed that HFD significantly increased plasma homocysteine concentration. This is in agreement with previous studies showing that HFD increases plasma homocysteine concentration (Yun et al, 2013). Interestingly, SAM improves vascular dysfunction without decreasing homocysteine concentration.…”

Section: Discussionsupporting

confidence: 93%

“…In addition, SAM treated rats did not exhibit differences in serum total cholesterol, LDL cholesterol, HDL cholesterol, and FFA compared to HFD-fed rats (Table 1). As expected and in accordance with previous studies (Yun et al, 2013), administration of HFD significantly increased plasma homocysteine concentration (Fig. 1C).…”

Section: Sam Improves Endothelial Function In Hfd-fed Ratssupporting

confidence: 93%

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S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Kim

Hong

Kim

et al. 2013

Molecules and Cells

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* S-adenosyl methionine (SAM) is a key intermediate in themetabolism of sulfur amino acids and is a major methyl donor in the cell. Although the low plasma level of SAM has been associated with atherosclerosis, the effect of SAM administration on atherosclerosis is not known. Endothelial dysfunction is an early prerequisite for atherosclerosis. This study was undertaken to investigate the possible preventive effect of SAM on endothelial dysfunction and the molecular mechanism of its action. SAM treatment prevented endothelial dysfunction in high fat diet (HFD)-fed rats. In cultured human aortic endothelial cells, linoleic acid (LA) increased and SAM decreased cell apoptosis and endoplasmic reticulum stress. Both LA and SAM increased heme oxygenase-1 (HO-1) expression in an NF-E2-related factor 2-dependent manner. However, knockdown of HO-1 reversed only the SAM-induced preventive effect of cell apoptosis. The LA-induced HO-1 expression was dependent on PPARα, whereas SAM induced HO-1 in a PPAR-independent manner. These data demonstrate that SAM treatment prevents endothelial dysfunction in HFDfed animals by inducing HO-1 in vascular endothelial cells. In cultured endothelial cells, SAM-induced HO-1 was responsible for the observed prevention of cell apoptosis. We propose that SAM treatment may represent a new therapeutic strategy for atherosclerosis.

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Section: Discussionsupporting

confidence: 93%

Section: Sam Improves Endothelial Function In Hfd-fed Ratssupporting

confidence: 93%

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Kim

Hong

Kim

et al. 2013

Molecules and Cells

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“…Previous studies have suggested that increased circulating homocysteine level is probably due to reduced CBS activity [11][12][13]. Activation of CBS activity by salvianolic acid A markedly reduced the plasma level of homocysteine in rats fed with HFD [12].…”

Section: Discussionmentioning

confidence: 99%

“…The elevation of homocysteine level in NAFLD/NASH may result from inhibition of CBS activity [11][12][13] or protein expression [15]. However, the underlying molecular mechanism remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Exendin-4 regulates redox homeostasis in rats fed with high-fat diet

Niu

Wang

et al. 2015

ABBS

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Non-alcoholic fatty liver disease (NAFLD) is associated with increased plasma homocysteine level, which is caused by down-regulation of hepatic cystathionine beta-synthase (CBS) activity. CBS catalyzes the first step in the transsulfuration of homocysteine to cysteine, which contributes ∼50% of the cysteine required for hepatic biosynthesis of glutathione (GSH), the most abundant antioxidant in cells. As the glucagon-like peptide-1 (GLP-1) receptor agonists (e.g. exendin-4) effectively reverse hepatic steatosis, the effect of exendin-4 on both homocysteine and redox status was investigated in the livers of rats fed with high-fat diet (HFD). It was found that HFD down-regulated CBS protein expression, which was probably due to induction of rno-miR-376c expression in the liver. The level of GSH was markedly reduced, whereas the level of malonydialdehyde, an indicator of lipid peroxidation, was significantly increased in the livers of rats fed with HFD. Exendin-4 treatment increased hepatic CBS protein and GSH levels, and reduced malonydialdehyde level in hyperlipidemic rats. Our findings suggest that GLP-1 receptor agonists have beneficial effects on redox homeostasis in NAFLD.

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“…Our previous studies showed that changes in plasma homocysteine level in obese or diabetic conditions were dependent on the type of experimental animal model used [6][7][8]. Plasma total homocysteine concentration increased by 1.6-fold in obese mice fed a high-fat diet for 12 weeks [7], but was 40% lower in db/ db mice, obese type 2 diabetic animals with a G-to-T point mutation of the leptin receptor [6]. In contrast, plasma homocysteine levels were similar between control rats and non-obese type diabetic Goto-Kakizaki rats [8].…”

Section: Introductionmentioning

confidence: 99%

Sulfur amino acid metabolism in Zucker diabetic fatty rats

Kwak

Kim

et al. 2015

Biochemical Pharmacology

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Plasma homocysteine level and hepatic sulfur amino acid metabolism in mice fed a high-fat diet

Abstract: This study suggests that plasma homocysteine level is increased in obesity-associated hepatic steatosis, possibly as a result of increased hepatic homocysteine efflux along with an altered sulfur amino acid metabolism.

Cited by 32 publications

References 39 publications

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

S-Adenosyl Methionine Prevents Endothelial Dysfunction by Inducing Heme Oxygenase-1 in Vascular Endothelial Cells

Exendin-4 regulates redox homeostasis in rats fed with high-fat diet

Sulfur amino acid metabolism in Zucker diabetic fatty rats

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