PubMed · 14849813
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E DEUTSCH. 1951. [Foresight comes from experience].. https://pubmed.ncbi.nlm.nih.gov/14849813/
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A method for the determination of ethyl glucuronide (EtG) in hair samples, using liquid chromatography/electrospray tandem mass spectrometry (LC/ESI-MS/MS), was developed and validated. The treatment of hair samples was as follows: to 100 mg of washed (dichloromethane followed by methanol, 1 ml each) and cut (1-2 mm) material, 700 microl of water, 20 microl of internal standard solution (pentadeuterated EtG, D(5)-EtG, 500 microg/l) and 20 microl of methanol were added. Samples were incubated at 25 degrees C overnight and then ultrasonicated for 2 h. Finally, 8 microl of the centrifuged solution (13,000 rpm) were analyzed by LC/ESI-MS/MS in negative ion mode. The surviving ions of EtG and D(5)-EtG were monitored together with the following MRM transitions: m/z 221 --> 75, m/z 221 --> 85 (EtG) and m/z 226 --> 75, m/z 226 --> 85 (D(5)-EtG). The method exhibited a mean correlation coefficient better than 0.9998 over the dynamic range (3-2000 pg/mg). The lower limit of quantification (LLOQ) and the limit of detection (LOD) were 3 and 2 pg/mg respectively. The intra- and interday precision and accuracy were studied at four different concentration levels (3, 5, 56 and 160 pg/mg) and were always better than 7% (n = 5). Matrix effects did not exceed 20%. The method was applied to several hair samples taken from autopsies of known alcoholics, from patients in withdrawal treatment, from social drinkers, from adult teetotalers and from children not exposed to ethanol, with EtG concentrations globally ranging from < or =2 to 4180 pg/mg.
The neuropeptide galanin (GAL) is widely expressed in the central nervous system. Animal studies have implicated GAL in alcohol abuse and anxiety: chronic ethanol intake increases hypothalamic GAL mRNA; high levels of stress increase GAL release in the central amygdala. The coding sequence of the galanin gene, GAL, is highly conserved and a functional polymorphism has not yet been found. The aim of our study was, for the first time, to identify GAL haplotypes and investigate associations with alcoholism and anxiety. Seven single-nucleotide polymorphisms (SNPs) spanning GAL were genotyped in 65 controls from five populations: US and Finnish Caucasians, African Americans, Plains and Southwestern Indians. A single haplotype block with little evidence of historical recombination was observed for each population. Four tag SNPs were then genotyped in DSM-III-R lifetime alcoholics and nonalcoholics from two population isolates: 514 Finnish Caucasian men and 331 Plains Indian men and women. Tridimensional Personality Questionnaire harm avoidance (HA) scores, a dimensional measure of anxiety, were obtained. There was a haplotype association with alcoholism in both the Finnish (P=0.001) and Plains Indian (P=0.004) men. The SNPs were also significantly associated. Alcoholics were divided into high and low HA groups (>or= and <mean HA of population). In the Finns, haplotype (P<0.0001) and diplotype (P<0.0001) distributions differed between high HA alcoholics, low HA alcoholics and nonalcoholics. Our results from two independent populations suggest that GAL may contribute to vulnerability to alcoholism, perhaps mediated by dimensional anxiety.
Ethanol has been considered as a lifestyle factor that may influence the risk of type 2 diabetes mellitus. In healthy adults, acute ethanol consumption results in insulin resistance. Acute ethanol consumption causes insulin resistance selectively in skeletal muscle by an indirect mechanism. Possible mediators include triglycerides (TGs), catecholamines, acetaldehyde, alterations in insulin binding, and hepatic insulin sensitizing substance (HISS). Recent studies in rats showed that acute administration of ethanol causes insulin resistance in a dose-dependent manner that is secondary to the blockade of insulin-induced HISS release. Chronic ethanol consumption may improve insulin sensitivity, but the results from the randomized controlled trials are mixed. Differences in ethanol dose, consumption period, and abstention period may account for the discrepant results. Epidemiological studies have suggested that the relationship between ethanol and insulin sensitivity is either an inverted U-shape or a positive linear relationship. Future randomized controlled trials should consider the dose of ethanol and the duration of ethanol consumption and abstention in the experimental design. Chronic prenatal and postnatal (nursing) ethanol exposure results in insulin resistance that is secondary to the absence of HISS release/action with the HISS-independent insulin action and insulin-like growth factor-1 (IGF-1)-mediated glucose disposal action remaining unimpaired. The impaired HISS release may be related to a reduction in hepatic glutathione (GSH) levels. The effect of chronic ethanol consumption on HISS has not been evaluated.