PubMed · 6134023
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J T Wright, K D MacRae. 1983-05-28. Drinking during pregnancy.. https://doi.org/10.1016/s0140-6736(83)92506-0
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Excessive alcohol consumption is a major health and social issue in our society. Pharmacologic administration of the endocrine hormone fibroblast growth factor 21 (FGF21) suppresses alcohol consumption through actions in the brain in rodents, and genome-wide association studies have identified single nucleotide polymorphisms in genes involved with FGF21 signaling as being associated with increased alcohol consumption in humans. However, the neural circuit(s) through which FGF21 signals to suppress alcohol consumption are unknown, as are its effects on alcohol consumption in higher organisms. Here, we demonstrate that administration of an FGF21 analog to alcohol-preferring non-human primates reduces alcohol intake by 50%. Further, we reveal that FGF21 suppresses alcohol consumption through a projection-specific subpopulation of KLB-expressing neurons in the basolateral amygdala. Our results illustrate how FGF21 suppresses alcohol consumption through a specific population of neurons in the brain and demonstrate its therapeutic potential in non-human primate models of excessive alcohol consumption.
Variation in serum high density lipoprotein cholesterol (HDL-C) concentrations is believed to be largely explained by triglycerides, but this has been mainly explored in cross-sectional analyses. Eight hundred and eighty one white male participants in a health screening program attended on a total of 2158 occasions for measurements that included fasting HDL-C, low density lipoprotein cholesterol (LDL-C) and homeostasis model assessment insulin resistance (HOMA-R). Baseline, change between-visit and repeated-measures regression models were used to analyse predictors of between- and within-individual variation in HDL-C. Independent predictors of between-individual variation included serum triglycerides (20.3 or 19.6% of the variance explained, depending on the model used), body mass index (BMI: 4.7 and 4.3%), cigarette smoking (3.3 and 1.5%) and alcohol consumption (0.4 and 1.1%). Within-individual variation in HDL-C was explained by changes in serum triglycerides (4.7 and 7.5%) and BMI (5.3 and 2.9%). In multivariate models, 24.3 and 24.9% of between-individual variation in HDL-C, and 7.9 and 8.8% of within-individual variation could be explained, depending on the model used. Sixty percent of the variation in HDL-C was due to unobserved factors. The majority of variation in HDL-C remains to be explained by influences other than the conventional variables: triglyceride and LDL cholesterol concentrations, insulin resistance, smoking and alcohol.
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