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Impact of chronic low to moderate alcohol consumption on blood lipid and heart energy profile in acetaldehyde dehydrogenase 2-deficient mice.

Fan F, Cao Q, Wang C, Ma X, Shen C, Liu XW, Bu LP, Zou YZ, Hu K, Sun AJ, Ge JB - Acta Pharmacol. Sin. (2014)

Bottom Line: Serum ethanol and acetaldehyde levels and blood lipids were measured.Metabolomics was used to characterize the heart and serum metabolism profiles.Thus, preserved ALDH2 function is essential for the protective effect of low to moderate alcohol on the cardiovascular system.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

ABSTRACT

Aim: To investigate the roles of acetaldehyde dehydrogenase 2 (ALDH2), the key enzyme of ethanol metabolism, in chronic low to moderate alcohol consumption-induced heart protective effects in mice.

Methods: Twenty-one male wild-type (WT) or ALDH2-knockout (KO) mice were used in this study. In each genotype, 14 animals received alcohol (2.5%, 5% and 10% in week 1-3, respectively, and 18% in week 4-7), and 7 received water for 7 weeks. After the treatments, survival rate and general characteristics of the animals were evaluated. Serum ethanol and acetaldehyde levels and blood lipids were measured. Metabolomics was used to characterize the heart and serum metabolism profiles.

Results: Chronic alcohol intake decreased the survival rate of KO mice by 50%, and significantly decreased their body weight, but did not affect those of WT mice. Chronic alcohol intake significantly increased the serum ethanol levels in both WT and KO mice, but KO mice had significantly higher serum acetaldehyde levels than WT mice. Chronic alcohol intake significantly increased the serum HDL cholesterol levels in WT mice, and did not change the serum HDL cholesterol levels in KO mice. After chronic alcohol intake, WT and KO mice showed differential heart and serum metabolism profiles, including the 3 main energy substrate types (lipids, glucose and amino acids) and three carboxylic acid cycles.

Conclusion: Low to moderate alcohol consumption increases HDL cholesterol levels and improves heart energy metabolism profile in WT mice but not in ALDH2-KO mice. Thus, preserved ALDH2 function is essential for the protective effect of low to moderate alcohol on the cardiovascular system.

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Related in: MedlinePlus

Effect of ALDH2 deficiency on blood lipid post-alcohol consumption. All mice were fasted overnight, and serum after 4 weeks of 18% alcohol consumption was collected. (A, B, and C) The serum TC, TG, and HDL-C levels were measured as described in the methods. (D) The LDL levels were calculated using the Friedwald formula. n=7 for each group. Mean±SEM. bP<0.05 vs WT. eP<0.05 vs WT+Alcohol. hP<0.05 vs KO.
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fig3: Effect of ALDH2 deficiency on blood lipid post-alcohol consumption. All mice were fasted overnight, and serum after 4 weeks of 18% alcohol consumption was collected. (A, B, and C) The serum TC, TG, and HDL-C levels were measured as described in the methods. (D) The LDL levels were calculated using the Friedwald formula. n=7 for each group. Mean±SEM. bP<0.05 vs WT. eP<0.05 vs WT+Alcohol. hP<0.05 vs KO.

Mentions: Ethanol has been recognized as an effective blood lipid regulator, and blood lipids are one of the most important risk factors for heart disease6. The baseline lipid levels, including TC, TG, HDL-C, and LDL-C, showed no difference between the WT and KO mice. After alcohol consumption, both TC and HDL-C were increased in the WT mice compared with their non-drinking counterparts (TC: 62.2±26.4 vs 104.0±16.8 mg/dL, P<0.05; HDL-C: 47.6±15.0 vs 79.3±12.4 mg/dL, P<0.05, Figure 3A, 3C). However, in the alcohol drinking KO mice, only TC was increased (63.3±9.2 vs 92.7±22.1 mg/dL, P<0.05, Figure 3A), and HDL-C remained unchanged compared with the non-drinking KO mice (45.9±8.9 vs 58.7±15.9 mg/dL, P=0.1353, Figure 3C). The levels of TG and LDL-C showed no differences in all four groups (Figure 3B, 3D). These results imply that alcohol consumption induced a positive elevation of HDL-C that can be repressed by ALDH2 deficiency.


Impact of chronic low to moderate alcohol consumption on blood lipid and heart energy profile in acetaldehyde dehydrogenase 2-deficient mice.

Fan F, Cao Q, Wang C, Ma X, Shen C, Liu XW, Bu LP, Zou YZ, Hu K, Sun AJ, Ge JB - Acta Pharmacol. Sin. (2014)

Effect of ALDH2 deficiency on blood lipid post-alcohol consumption. All mice were fasted overnight, and serum after 4 weeks of 18% alcohol consumption was collected. (A, B, and C) The serum TC, TG, and HDL-C levels were measured as described in the methods. (D) The LDL levels were calculated using the Friedwald formula. n=7 for each group. Mean±SEM. bP<0.05 vs WT. eP<0.05 vs WT+Alcohol. hP<0.05 vs KO.
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Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4125715&req=5

fig3: Effect of ALDH2 deficiency on blood lipid post-alcohol consumption. All mice were fasted overnight, and serum after 4 weeks of 18% alcohol consumption was collected. (A, B, and C) The serum TC, TG, and HDL-C levels were measured as described in the methods. (D) The LDL levels were calculated using the Friedwald formula. n=7 for each group. Mean±SEM. bP<0.05 vs WT. eP<0.05 vs WT+Alcohol. hP<0.05 vs KO.
Mentions: Ethanol has been recognized as an effective blood lipid regulator, and blood lipids are one of the most important risk factors for heart disease6. The baseline lipid levels, including TC, TG, HDL-C, and LDL-C, showed no difference between the WT and KO mice. After alcohol consumption, both TC and HDL-C were increased in the WT mice compared with their non-drinking counterparts (TC: 62.2±26.4 vs 104.0±16.8 mg/dL, P<0.05; HDL-C: 47.6±15.0 vs 79.3±12.4 mg/dL, P<0.05, Figure 3A, 3C). However, in the alcohol drinking KO mice, only TC was increased (63.3±9.2 vs 92.7±22.1 mg/dL, P<0.05, Figure 3A), and HDL-C remained unchanged compared with the non-drinking KO mice (45.9±8.9 vs 58.7±15.9 mg/dL, P=0.1353, Figure 3C). The levels of TG and LDL-C showed no differences in all four groups (Figure 3B, 3D). These results imply that alcohol consumption induced a positive elevation of HDL-C that can be repressed by ALDH2 deficiency.

Bottom Line: Serum ethanol and acetaldehyde levels and blood lipids were measured.Metabolomics was used to characterize the heart and serum metabolism profiles.Thus, preserved ALDH2 function is essential for the protective effect of low to moderate alcohol on the cardiovascular system.

View Article: PubMed Central - PubMed

Affiliation: Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai 200032, China.

ABSTRACT

Aim: To investigate the roles of acetaldehyde dehydrogenase 2 (ALDH2), the key enzyme of ethanol metabolism, in chronic low to moderate alcohol consumption-induced heart protective effects in mice.

Methods: Twenty-one male wild-type (WT) or ALDH2-knockout (KO) mice were used in this study. In each genotype, 14 animals received alcohol (2.5%, 5% and 10% in week 1-3, respectively, and 18% in week 4-7), and 7 received water for 7 weeks. After the treatments, survival rate and general characteristics of the animals were evaluated. Serum ethanol and acetaldehyde levels and blood lipids were measured. Metabolomics was used to characterize the heart and serum metabolism profiles.

Results: Chronic alcohol intake decreased the survival rate of KO mice by 50%, and significantly decreased their body weight, but did not affect those of WT mice. Chronic alcohol intake significantly increased the serum ethanol levels in both WT and KO mice, but KO mice had significantly higher serum acetaldehyde levels than WT mice. Chronic alcohol intake significantly increased the serum HDL cholesterol levels in WT mice, and did not change the serum HDL cholesterol levels in KO mice. After chronic alcohol intake, WT and KO mice showed differential heart and serum metabolism profiles, including the 3 main energy substrate types (lipids, glucose and amino acids) and three carboxylic acid cycles.

Conclusion: Low to moderate alcohol consumption increases HDL cholesterol levels and improves heart energy metabolism profile in WT mice but not in ALDH2-KO mice. Thus, preserved ALDH2 function is essential for the protective effect of low to moderate alcohol on the cardiovascular system.

Show MeSH
Related in: MedlinePlus