Serum homocysteine levels in patients with nonalcoholic fatty liver disease

Polyzos, Stergios A.; Patsiaoura, Kalliopi; Katsiki, Evangelia; Zafeiriadou, Efthimia; Deretzi, Georgia; Zavos, Christos; Gavalas, Emmanuel; Katsinelos, Panagiotis; Mane, Vasileia; Slavakis, Aristidis

doi:10.1016/s1665-2681(19)31488-7

Cited by 53 publications

(64 citation statements)

References 32 publications

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“…itive association with NASH severity (Gulsen et al 2005), another reported that homocysteine levels were inversely related to increasing grades of portal inflammation, fibrosis, and the distribution of steatosis in NASH (Polyzos et al 2012a). The underlying cause for such discrepancies may be multifactorial, since systemic homocysteine levels are regulated by hepatic efflux (Stead et al 2000;Jensen et al 2011) and renal clearance rates (Finkelstein 1998).…”

Section: Clinical Evidence Of a Disordered Cbs/cse System In Nafldmentioning

confidence: 99%

“…Perturbations in circulating homocysteine and H 2 S levels have been reported in NAFLD patients and in NAFLD associated co-morbidities. It has been suggested that homocysteine could be a non-invasive marker of NAFLD (Polyzos et al 2012a) and also a predictor of NASH (Gulsen et al 2005). However, a thorough review of the literature yields conflicting findings regarding the relative change in homocysteine levels across the various NAFLD spectrums ( For instance, while one study found homocysteine to have a pos- Fig.…”

Section: Clinical Evidence Of a Disordered Cbs/cse System In Nafldmentioning

confidence: 99%

“…1). However, homocysteine levels in NAFLD patients are not always related to changes in these B vitamins (Bosy-Westphal et al 2001;Hirsch et al 2005;Polyzos et al 2012a). Impairment of the CBS/CSE system could be partly to blame, since increased homocysteine levels have been ascribed to a deficiency in CBS expression in cirrhotic patients (Garcia-Tevijano et al 2001).…”

Section: Clinical Evidence Of a Disordered Cbs/cse System In Nafldmentioning

confidence: 99%

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The CBS/CSE system: a potential therapeutic target in NAFLD?

Siow

2015

Can. J. Physiol. Pharmacol.

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Non-alcoholic fatty liver disease (NAFLD) is a broad spectrum liver disorder diagnosed in patients without a history of alcohol abuse. NAFLD is growing at alarming rates worldwide. Its pathogenesis is complex and incompletely understood. The cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) system regulates homocysteine and cysteine metabolism and contributes to endogenous hydrogen sulfide (H2S) biosynthesis. This review summarizes our current understanding of the hepatic CBS/CSE system, and for the first time, positions this system as a potential therapeutic target in NAFLD. As will be discussed, the CBS/CSE system is highly expressed and active in the liver. Its dysregulation, presenting as alterations in circulating homocysteine and (or) H2S levels, has been reported in NAFLD patients and in NAFLD-associated co-morbidities such as obesity and type 2 diabetes. Intricate links between the CBS/CSE system and a number of metabolic and stress related molecular mediators have also emerged. Various dysfunctions in the hepatic CBS/CSE system have been reported in animal models representative of each NAFLD spectrum. It is anticipated that a newfound appreciation for the hepatic CBS/CSE system will emerge that will improve our understanding of NAFLD pathogenesis, and give rise to new prospective targets for management of this disorder.

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Section: Clinical Evidence Of a Disordered Cbs/cse System In Nafldmentioning

confidence: 99%

Section: Clinical Evidence Of a Disordered Cbs/cse System In Nafldmentioning

confidence: 99%

Section: Clinical Evidence Of a Disordered Cbs/cse System In Nafldmentioning

confidence: 99%

See 1 more Smart Citation

The CBS/CSE system: a potential therapeutic target in NAFLD?

Siow

2015

Can. J. Physiol. Pharmacol.

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“…However, these potential explanations can not explain the incidence in controlled animal experiments. The major organs responsible for excretion and metabolism of homocysteine are kidney and liver, respectively (Polyzos et al, 2012;Matthews and Elmore, 2007). However, there were no significant differences in plasma concentration of creatinine and blood urea nitrogen (BUN), or activities of AST and ALT among treatment groups (data not shown), suggesting that the defect in excretion or hepatotoxicity may not be related to observed elevation of homocysteine.…”

Section: Discussionmentioning

confidence: 98%

The Impact of Intratracheally Instilled Carbon Black on the Cardiovascular System of Rats: Elevation of Blood Homocysteine and Hyperactivity of Platelets

Kim

Kwak

et al. 2012

Journal of Toxicology and Environmental Health, Part A

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Carbon black (CB) is an industrial chemical with high potential for human exposure. Although the relationship between exposure to particulate matter (PM) and cardiovascular disease is well documented, the risk of adverse cardiovascular effects attributed to CB particles has not been clearly characterized. This study was performed to (1) investigate the effects of CB on cardiovascular system and (2) identify the target tissue or potential biomarkers. Carbon black with a distinct particle size, N330 (ultrafine particle) and N990 (fine particle), was intratracheally instilled into rats at a doses of 1, 3, or 10 mg/kg. Measurements of thrombotic activity and determination of plasma homocysteine levels, cardiac functionality, and inflammatory responses were conducted at 24-h and 1-wk time points. Exposure to N330 accelerated platelet-dependent blood clotting at 10 mg/kg, the highest exposure tested. Unexpectedly, both N330 and N990 led to prolongation of activated partial thromboplastin time (aPTT), whereas these CB particles failed to affect prothrombin time (PT). N990 produced a significant elevation in the level of plasma homocysteine, a well-established etiological factor in cardiovascular diseases. Both N330 and N990 induced apparent inflammation in the lungs; however, both particles failed to initiate systemic inflammation. Neither CB particle produced observable cardiac symptoms as detected by electrocardiography. Taken together, data show CB exposure enhanced the cardiovascular risk by inducing hyperhomocysteinemia and platelet hyperactivity, although these effects may be variable depending on particle size and exposure duration. Homocysteine may be a potential biomarker for cardiovascular toxicity following CB exposure.

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“…Polyzos et al [1,4] have reported that Hcy levels were similar in NAFLD patients and controls, in subjects with NASH being lower than in subjects with non-alcoholic simple steatosis (SS). They speculated, without statements to be supported by assessment of methionine and glutathione, that lower Hcy in NASH than SS could be a counterbalancing effect; Hcy is depleted in NASH because of the amplification of both Hcy transsulfuration and remethylation.…”

Section: Dear Editormentioning

confidence: 99%