Effect of Acute and Chronic Moderate Red or White Wine Consumption on Fasted and Postprandial Lipemia in the Rat

Abstract

The effects of acute and chronic (10 wk) red or white wine consumption on fasted and postprandial lipemia in the rat model are reported. Fasted rats, in the acute study, were loaded intragastrically with 5 ml of an olive oil emulsion (30% w/v) in the presence or absence of wine (8% v/v ethanol), and either mesenteric lymph or blood was collected 3 h postprandially. Animals in the chronic study received either red or white wine in drinking water for a period of 10 wk (3% v/v ethanol). Blood samples were collected from animals in either the fasted state or after fat-wine loading. Postprandially, wine delayed gastric emptying, reduced lymph triacylglycerol (TAG) secretion concomitantly with increased number and decreased chylomicron (CM) size, and increased plasma TAG and CM concentrations. Phospholipid and cholesterol contents of CM, but not very-low-density lipoprotein (VLDL), were increased, indicating enhanced liver bile secretion; however, a significant increase in plasma VLDL concentration was observed. In the chronic study, a wine-fat load resulted in increased high-density lipoprotein (HDL) cholesterol concentration and less pronounced postprandial hypertriglyceridemia and hyperchylomicronemia. In the fasted state, plasma TAG and total apolipoprotein B concentrations were not modified in these animals, and an increase in HDL and a decrease in low-density lipoprotein (LDL)/HDL cholesterol ratios were observed. No liver function or intestinal lipid absorption impairment was observed. In conclusion, unlike binge drinking, chronic moderate wine consumption appears to have a cardioprotective effect in the fasted state, an effect attenuated by the observed temporary postprandial hyperchylomicronemia and hypertriglyceridemia resulting from a direct effect of alcohol on CM size and number.

Effects of Chronic Red Wine Consumption on the Expression of Vascular Endothelial Growth Factor, Angiopoietin 1, Angiopoietin 2, and Its Receptors in Rat Erectile Tissue

“…The results of biochemical assays depicted in Table 2 demonstrated that in RW‐treated rats, the plasma levels of triglycerides, total cholesterol, and HDL were increased but without statistical significance, when compared to C group. Interestingly, both EtOH and C rats presented a similar lipid profile, which contrasts with other reports showing an increase in serum triglycerides (TG) and LDL, but not cholesterol, in adult rats treated during 4 wk with a 20% EtOH solution (Ojeda and others 2008) or 10 wk with a RW solution with 8% EtOH (Daher and others 2006). On the other hand, there seems to exist a general view that moderate wine consumption has a global cardioprotective effect in what concerns the metabolism of lipids.…”

The Effect of Alcohol on Postprandial and Fasting Triglycerides

“…This HT results from an increased production of large VLDL particles by the liver, while the splanchnic extraction of TG from chylomicron- and VLDL-remnants is secondarily enhanced. In another rat experiment, Daher et al confirmed a rise in plasma triacylglycerol and chylomicron concentrations after ethanol ingestion but also found a decreased chylomicron size with a change in cholesterol and phospholipid content indicating enhanced liver bile secretion [8]. In case the animals were put on a moderate alcohol diet for a period of ten weeks, their postprandial HT and hyperchylomicronemia were less pronounced.…”

Downregulation of Platelet Responsiveness Upon Contact With LDL by the Protein-Tyrosine Phosphatases SHP-1 and SHP-2

“…Under preprandial conditions, high levels of apoB-containing lipoproteins like LDL make individuals prone to CVD. Under postprandial conditions, levels of apoB-containing lipoproteins increase, [42][43][44] and variations in subclasses of these lipoproteins are even greater when lipoprotein lipase is associated to apoB. 45 The rapid postprandial increase in triglyceride-rich lipoproteins (containing apoB100 and apoE) of normal individuals is increased in diseases related to arterial disease eg, diabetes mellitus, 46 and myocardial infarction.…”