Introduction. Effects of white wine and the role of wine polyphenols on weight gain in rats of different age were examined in the 4‐week‐voluntary‐consumption trial. Methods and Materials. Biochemically characterized standard (low polyphenols, W) and macerated (high polyphenolic content, PW) white wines were compared. One‐ and three‐month‐old Sprague‐Dawley male rats (n = 78) were used. Each age group was subdivided into water‐only‐drinking controls (C), W, and PW‐drinking animals. Daily wine and total liquid consumption, food intake, and body weight were measured, and energy intake and feed efficiency index were calculated. Results. In both age categories, wine‐drinking animals consumed less food and gained less weight in comparison to C (181 ± 2, 179 ± 6, and 201 ± 5 in younger animals and 32 ± 5, 28 ± 6, and 47 ± 4 grams in older animals, resp.), regardless of wine type. Total energy intake was the lowest in PW‐drinking animals. Conclusion. Wine‐drinking animals gained less weight in comparison to C, regardless of the wines’ polyphenol content. Although our results are indicative of the major role of nonphenolic constituents of the wines (probably ethanol), the modifying role of wine phenolics on weight gain cannot be excluded as the group consuming PW had lower total energy intake than other groups.

Effects of white wine (WW) consumption on the expression of inflammatory markers/mediators (MMP-2, MMP-9, NF-ĸB p65 and TGF-β1) in myocardial tissue after experimentally induced permanent myocardial ischemia was investigated. Male Sprague-Dawley rats were given either a combination of WW and water or only water, for 28 days. After coronary ligation, animals were left to survive for 24 hours. Three representative areas: infarct/ischemic, peri-infarct/border zone, and control/non-ischemic zones were analyzed for expression of immunoreactivity by measuring the threshold area % of signal density. For MMP-9, significantly smaller expression was found in all 3 zones of wine drinking animals (P < 0.001). There was no difference in MMP-2 immunoreactivity between the 2 groups, except in peri-infarct zones, where the signal was significantly decreased (P < 0.001). The same pattern of expression was found for the NF-κB p65 signal, although no differences between experimental groups were observed for TGF-β1. White wine consumption decreases the expression of the 3 investigated inflammatory markers/mediators in the peri-infarct zone, suggesting its significant modulatory effect. For MMP-9 and MMP-2, expression was similar to the effect of postischemic reperfusion. No effect on TGF-β1 was observed, highlighting its role in being the master-switch, changing from the inflammatory to the proliferative stage of infarct healing.

Neutrophils and monocytes through their CD15s, CD11b and CD44 adhesion molecules are implicated in the initiation and resolution of cardiac inflammation as well as in healing processes after the myocardial infarction (MI). The aim of this study was to determine the effect of white wine consumption on granulocyte and monocyte CD15s, CD11b, and CD44 expression 24h after the surgically inflicted MI. Granulocytes and monocytes were analyzed by flow cytometry, using whole blood of male Sprague–Dawley rats that consumed white wine for 4 weeks. This group was compared with water only drinking controls, sham animals (subject to surgery without myocardial infarction) and baseline group (intact animals that received no intervention prior to being sacrificed). Sham animals did not differ from baseline animals in CD11b+CD44+ percentage and CD44+ median fluorescence intensity. Wine drinking was associated with striking increase in CD44 expression on monocyte subpopulations. Its expression was three and fourfold increased on monocytes and large monocytes, respectively, relative to the water only drinking controls. Because of known role of CD44 on suppression of post-infarction inflammation, its upregulation on granulocytes and monocytes may significantly contribute to the microenvironment favourable for the cardiac regeneration.

Iron overload is often associated with type 2 diabetes (T2D), indicating that hepcidin, the master regulator of iron homeostasis, might be involved in diabetes pathogenesis. Alcohol consumption may also result in increased body iron stores. However, the moderate consumption of wine with meals might be beneficial in T2D. This effect has been mainly attributed to both the ethanol and the polyphenolic compounds in wine. Therefore, we examined the effects of red wine on hepcidin in T2D patients and non-diabetic controls. The diabetic patients (n = 18) and age- and BMI-matched apparently healthy controls (n = 13) were men, aged 40–65 years, non-smoking, with BMI < 35 kg/m². Following a 2-week alcohol-free period, both groups consumed 300 mL of red wine for 3 weeks. The blood samples for the iron status analysis were taken at the end of each period. The red wine intake resulted in a decrease in serum hepcidin in both the diabetic subjects (p = 0.045) and controls (p = 0.001). The levels of serum ferritin also decreased after wine in both groups, reaching statistical significance only in the control subjects (p = 0.017). No significant alterations in serum iron, transferrin saturation, or soluble transferrin receptors were found. The suppression of hepcidin, a crucial iron-regulatory hormone and acute-phase protein, in T2D patients and healthy controls, is a novel biological effect of red wine. This may deepen our understanding of the mechanisms of the cardiometabolic effects of wine in T2D.

How moderate white wine consumption modulates inflammatory cells infiltration of the ischemic myocardium following permanent coronary ligation was the key question addressed in this study. Male Sprague–Dawley rats were given either a combination of different white wines or water only for 28 days. Three peri-infarct/border zones and a control/nonischemic zone were analysed to determine the expression of myeloperoxidase (MPO) and cluster of differentiation 68 (CD68). Smaller expressions for both MPO and CD68 were found in all three peri-infarct zones of wine drinking animals (p < 0.001). There was no difference in the expression of leukocyte markers between animals drinking standard and polyphenol-rich white wine, although for CD68, a nonsignificant attenuation was noticed. In sham animals, a subepicardial MPO/CD68 immunoreactive “inflammatory ring” is described. Standard white wine consumption caused attenuation of the expression of MPO but not of CD68 in these animals. We conclude that white wine consumption positively modulates peri-infarct inflammatory infiltration.