Neurotrophin levels at admission did not change significantly upon alcohol deprivation and were positively correlated with the BMI and LDL levels.

Journal of molecular psychiatry Pub Date : 2013-12-02 eCollection Date: 2013-01-01 DOI:10.1186/2049-9256-1-20
Aurel Popa-Wagner, Karolina Furczyk, Joerg Richter, Gisela Irmisch, Johannes Thome
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引用次数: 4

Abstract

Background: The neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophic factor 3 (NT3) could play a role in addictive behavior. Interactions between BDNF and dopamine transmission influence the alcohol intake. It has been hypothesized that extensive alcohol consumption leads to diminished circulating BDNF levels and impaired BDNF-mediated protective mechanisms. What is more, alcohol dependency causes changes in lipid metabolism which in turn may influence the neurotrophin system.

Methods: In this study, we tested the hypothesis that alcohol withdrawal increases the serum levels of BDNF in alcoholic patients and investigated correlations between serum BDNF and NT3 and alcohol in breath as well as with the body-mass-index (BMI), lipoprotein profiles and lifestyle factors in 110 male in-patients diagnosed with alcohol addiction on the first day after admission and at discharge.

Results: The intoxication level (alcohol in breath at admission) was significantly correlated with liver enzymes and BDNF concentrations (R = .28; p = .004). Patients with positive breath-alcohol test at admission had about 9 times higher NT3 levels and higher liver enzyme concentration levels than nonintoxicated subjects. Alcohol intoxicated patients with pathological aspartate aminase (ASAT) levels had even higher NT3 level (F = 5.41; p = .022). The concentration of NT3 was positively associated with the (BMI) (admission R = .36; p = .004; discharge R = .33; p = .001), and the obese patients had 3 to 5 times higher NT3 concentration than the others. Low-density lipoprotein (LDL) concentration levels were found to positively correlate with NT3 concentration levels (admission R = .025; p = .015 discharge R = .24; p = .23).

Conclusion: Other than expected, the levels of NT3 and to a lesser extent BDNF levels, were found to be significantly increased in acute alcohol abuse. Alcohol deprivation did not significantly change the serum neurotrophin levels at admission. NT3 levels were positively correlated with the BMI and LDL levels. Because of expected difference between genders, we recommend investigating these correlations further in patients of both genders.

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入院时的神经营养因子水平在酒精剥夺后没有显著变化,并且与BMI和LDL水平呈正相关。
背景:神经营养因子脑源性神经营养因子(BDNF)和神经营养因子3 (NT3)可能在成瘾行为中起作用。BDNF和多巴胺传递之间的相互作用影响酒精摄入量。据推测,大量饮酒会导致循环BDNF水平降低和BDNF介导的保护机制受损。更重要的是,酒精依赖引起脂质代谢的改变,从而可能影响神经营养系统。方法:在本研究中,我们验证了酒精戒断增加酒精患者血清BDNF水平的假设,并研究了110名男性酒精成瘾患者入院和出院后第一天的血清BDNF、NT3和呼吸中的酒精以及与身体质量指数(BMI)、脂蛋白谱和生活方式因素的相关性。结果:中毒水平(入院时呼吸中的酒精)与肝酶和BDNF浓度显著相关(R = 0.28;p = .004)。入院时呼吸酒精测试阳性的患者NT3水平和肝酶浓度水平比未醉酒的患者高约9倍。病理性天冬氨酸氨基酶(ASAT)水平的酒精中毒患者NT3水平更高(F = 5.41;p = .022)。NT3浓度与BMI呈正相关(入院R = 0.36;p = .004;放电R = 0.33;p = .001),肥胖患者的NT3浓度比其他患者高3 ~ 5倍。低密度脂蛋白(LDL)浓度水平与NT3浓度水平呈正相关(入院R = 0.025;p =。015放电R = 0.24;p = .23)。结论:与预期不同的是,急性酒精滥用患者的NT3水平和BDNF水平显著升高。酒精剥夺未显著改变入院时血清神经营养因子水平。NT3水平与BMI、LDL水平呈正相关。由于性别之间的预期差异,我们建议在两性患者中进一步调查这些相关性。
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