Short-term effects of moderate alcohol consumption on lipid metabolism and energy balance in normal men
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Prenatal fat exposure and hypothalamic PPAR β/δ: Possible relationship to increased neurogenesis of orexigenic peptide neurons
2016, PeptidesCitation Excerpt :These prenatal fat-induced neurochemical changes are accompanied by changes in behavior, such as increased fat preference and anxiety [19,80,84], which may promote further drug use, consistent with a report in mice showing early fat exposure to increase ethanol intake in the adult offspring [15]. While the physiological and molecular mechanisms that mediate the effects of prenatal fat on these behaviors are not known, one signal possibly serving this function may come from circulating lipids, particularly fatty acids (FAs), which are elevated along with triglycerides (TG) by consumption of a fat-rich diet as well as nicotine or ethanol [28,78] and are known to be biologically active [43]. In adult rats, these lipids have been linked to an increase in food intake [3,39], expression of ENK and OX mRNA [20,19,84], and release of accumbens DA [69,84].
Alcohol drinking patterns and biomarkers of coronary risk in the Spanish population
2014, Nutrition, Metabolism and Cardiovascular DiseasesCitation Excerpt :As regards irregular heavy drinking, it has been associated with a 45% increase in CHD risk after adjustment for the volume of alcohol consumed; thus, it seems that any cardioprotective effect of moderate alcohol consumption may be negated by irregular heavy drinking occasions [4]. The mechanisms of the cardiovascular effect of heavy drinking are poorly understood; while a few clinical trials suggest that heavy drinking increases HDL-cholesterol [5–7], it may also exert a detrimental effect on thrombosis, blood pressure and atrial fibrillation [8,9]. Short-term trials may not be appropriate to characterize the effect of long-term drinking patterns.
Cardiovascular risk, lipidemic phenotype and steatosis. A comparative analysis of cirrhotic and non-cirrhotic liver disease due to varying etiology
2014, AtherosclerosisCitation Excerpt :At variance with what observed in the general population, patients with liver disease fail to display the strict and proportional association between increasing (total and LDL-) CH and TG levels and cardiovascular morbidity, suggesting that other factors, such as steatosis and IR, further to lipid profile, may be important. Three common steatogenic liver diseases (NAFLD, AFL and HCV-related disease) are associated with premature atherosclerosis despite varying or even opposite lipid phenotypes, whereas PBC and chronic HBV infection are protected from both steatosis and CVR (Table 2) [10,12–36,40,41,45–48,52–54,65–68,72–74,88–94,97,105–107,111,115,116,119–124,129–138,149,150,158–179,182–184,190,191,198–201]. These findings support the paradigm that steatosis per se, almost invariably associated with IR, pro-thrombotic and pro-inflammatory liver and systemic milieu, sets the stage for increased CVR (Fig. 1).
- 1
Supported by grants from the University of Helsinki and the Sigrid Juselius Foundation (M.R.T.), Helsinki, Finland.
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Deceased September 1986.