Comparative study of the effects of short- and long-term ethanol treatment and alcohol withdrawal on phospholipid biosynthesis in rat hepatocytes

Carrasco, Marı́a P.; Jiménez-López, José M.; Segovia, J.L.; Marco, Carmen

doi:10.1016/s1096-4959(02)00006-4

Cited by 36 publications

(24 citation statements)

References 20 publications

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“…PON is known as an antioxidant enzyme which can detoxify Hcy metabolite [19]. Also, ethanol in acute and chronic exposure amounts causes a significant rise in S-adenosyl methionine and that activates methylation pathway in the hepatocytes, converting Hcy to methionine [11] .…”

Section: Discussionmentioning

confidence: 99%

“…Each of these lifestyle factors, therefore, has the ability to alter adipose tissue mass, possibly via leptin [9]. On the other hand, short-term and chronic ethanol intake influences Hcy concentration by changes in the methylation pathway, folate and cofactors concentration [11]. Ethanol-induced increase in serum Hcy levels has been observed in active alcoholics.…”

Section: Introductionmentioning

confidence: 99%

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Exposure to Acute and Chronic Ethanol in Developmental Stage of Chick can Change the Brain Homocysteine and Leptin

Farahani¹,

Taherianfard²,

Nazifi³

2013

Biochem Physiol

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Aim: Ethanol intake decreases food intake in rat, and one of the possible mediators of this alcohol effect is leptin. On the other hand, the concentration of total plasma homocysteine is a well-established indicator for the risk of cardiovascular disease, and seems to be related to ethanol consumption. So, the aim of the present study was to investigate the effect of exposure to acute (70%) and chronic (10%) evaporated ethanol on 1) brain leptin and homocysteine concentration on the 15 th day of embryonic development of chick; 2) brain leptin and homocysteine concentration immediately after hatch of chick; 3) serum leptin concentration immediately after hatch of chick.Methods: 60 fertilized eggs were used. Eggs were divided into 3 groups, 1) Control; 2) acute exposure to ethanol 3) chronic exposure to ethanol. Homocysteine was measured by using enzyme-linked assay, and leptin was measured with the chick leptin radioimmunoassay kit.Results: Data showed that exposure to acute and chronic ethanol significantly (P<0.05) decreased brain homocysteine concentration on the 15 th day of embryonic stage of chicken, but did not have any effect on brain homocysteine concentration immediately after hatch Exposure to acute and chronic ethanol significantly (P<0.05) increased brain leptin on the 15 th day of embryonic stage, brain leptin immediately after hatch of chick and plasma leptin immediately after hatch of chick. Conclusion:Present results indicated that exposure to acute and chronic ethanol by evaporation in embryonic stage of chicken can change the brain homocysteine, brain leptin and serum leptin.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Exposure to Acute and Chronic Ethanol in Developmental Stage of Chick can Change the Brain Homocysteine and Leptin

Farahani¹,

Taherianfard²,

Nazifi³

2013

Biochem Physiol

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“…Hepatic fatty acid and triglycerides are increased after acute and chronic ethanol consumption [57]. Utilizing cell-based model, increased lipogenesis has been shown to occur due to higher expression and activation of lipogenic enzymes [58,59] [60,61]. SREBP-1c level is increased transcriptionally and by decreased proteasomal degradation of protein in acute and chronic alcohol exposure [62].…”

Section: Activation Of Transcription Factorsmentioning

confidence: 99%

Role of Angiotensin Peptides Precursor in Ethanol Mediated Hepato toxicity: Perspective on Angiotensinogen

Ansari¹

2012

TOGASJ

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Alcohol usage poses serious social and economical challenges. Its overuse is responsible for loss of billions of dollars due to fatal accidents and causes multiple diseases. Chronic alcoholism leads to liver disorders, including steatosis, hepatitis, fibrosis and cirrhosis. Both binge and chronic alcohol drinking result in blood pressure elevation and hypertension. As a significant mechanism, changes in the levels of angiotensinogen-released peptides play an important role in advanced alcohol liver disease. This review summarizes some of the studies that have demonstrated their role in liver fibrosis, cirrhosis and hypertension. Further, the individual variants and polymorphic sites may play a role in alcoholmediated regulation of angiotensinogen. Possible role of human angiotensinogen on alcohol hepatotoxicity is also discussed.

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“…Alcohol induced hepatic steatosis is mediated by increased de novo lipogenesis and impaired fatty acid beta-oxidation [51]. Several studies have identified the genes involved in alcohol induced dysregulation of lipid metabolism leading to steatosis [52,53];…”

Section: Alcoholic Fatty Liver Diseasementioning

confidence: 99%

“…Hepatic lipid synthesis is accelerated after ethanol consumption and is associated with higher expression of lipogenic genes/enzymes, including fatty acid synthase (FASN), acetyl-CoA carboxylase (ACC), ATP citrate lyase (ACL), stearoyl CoA desaturase (SCD), and malic enzyme (ME) [52,53]. Sterol regulatory element binding protein-1c (SREBP-1c) is a transcription factor that plays an important role in regulating the expression of all alcohol induced lipogenic genes (e.g.…”

Section: Alcohol Mediated De Novo Lipogenesis In the Livermentioning

confidence: 99%

Role of phosphodiesterase-4 in alcohol-induced organ injury.

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Comparative study of the effects of short- and long-term ethanol treatment and alcohol withdrawal on phospholipid biosynthesis in rat hepatocytes

Cited by 36 publications

References 20 publications

Exposure to Acute and Chronic Ethanol in Developmental Stage of Chick can Change the Brain Homocysteine and Leptin

Exposure to Acute and Chronic Ethanol in Developmental Stage of Chick can Change the Brain Homocysteine and Leptin

Role of Angiotensin Peptides Precursor in Ethanol Mediated Hepato toxicity: Perspective on Angiotensinogen

Role of phosphodiesterase-4 in alcohol-induced organ injury.

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