Excessive alcohol consumption is a risk factor associated with colorectal cancer; however, some epidemiological studies have reported that moderate alcohol consumption may not contribute additional risk for developing colorectal cancer while others suggest that moderate alcohol consumption may provide a protective effect that reduces colorectal cancer risk. Prior experimental data have indicated the importance of proliferation, differentiation, and apoptosis as parameters to consider when evaluating colonic cell growth and tumorigenesis. Chemopreventative agents are reported to decrease cell proliferation and to increase differentiation and apoptosis. The present study examined whether chronic low‐to‐moderate ethanol consumption had an effect on these parameters of colonic cell growth. Twenty‐four nondeprived young adult (109 days old) Wistar rats (n=12/group) and twenty‐four nondeprived middle‐aged (420 days old) Wistar rats (n=12/group) were allowed to voluntarily consume a 20% v/v ethanol solution on alternate days for 13 weeks (45 ethanol drinking sessions total) or were given access only to water (non ethanol‐exposed control). The intermittent access 20% ethanol drinking paradigm utilized results in mean blood alcohol levels of ~30–50 mg/dl in the outbred Wistar strain when measured 30–120 min into a standard drinking session. Following the final experimental session, colon tissues were collected for quantitative immunohistochemical analyses of cell proliferation, differentiation and apoptosis using Ki‐67, goblet cell and TUNEL (Terminal deoxynucleotidyl transferase dUTP nick end labeling), respectively. Ethanol treatment resulted in a lower cell proliferation index in both young (P = 0.05) and older (P < 0.001) rats, as well as a lower proliferative zone (P < 0.01 for both ages). Older rats had a shorter colon, but there was no significant difference for proliferation index between young and old rats. Cell differentiation between ethanol‐treated animals and controls was not significant for young rats, but older rats had a lower level of differentiation in the ethanol group. For apoptosis, there was no significant effect of ethanol treatment for either young or old rats. Younger rats had higher values than older rats for both differentiation and apoptosis (P < 0.05). These findings suggest that moderate consumption of ethanol improves at least one notable parameter (cell proliferation) in colonic tumorigenesis regardless of age, however, reduced cell differentiation among older animals. Support or Funding Information Support Contributed By: NIH AA023291
Excessive alcohol intake is known to elevate risk for cardiovascular diseases (CVD); however, several studies have reported that moderate alcohol consumption may not contribute additional risk or may provide a protective effect against CVD. It is critical to understand how moderate ethanol exposure interacts with other essential dietary components such as n‐3 fatty acids to influence inflammation underlying CVD pathogenesis. The purpose of this study was to examine the effects of moderate ethanol consumption as a function of dietary n‐6:n‐3 fatty acid composition on markers associated with inflammation and total antioxidant capacity (TAC) in mice. Twenty‐three mice (12 male, 11 female) consumed an 18% ethanol solution or 26.9% maltose dextrin solution (non‐ethanol isocaloric control) for 12 weeks. In each group, half of the mice were fed either a high n‐6 (n‐6:n‐3 = 50:1) diet or a balanced n‐3 (n‐6:n‐3 = 1:1) diet ad libitum. There were no differences in initial body weight between the two groups; however, the control group gained significantly more weight than the ethanol group (P = 0.020) associated with higher maltose dextrin fluid intake (P < 0.001). C‐reactive protein and high mobility group box 1 protein were significantly lower in the ethanol group compared to the control group (P < 0.001 and P = 0.029, respectively). There was a significant main effect of n‐3 diet on total antioxidant capacity (TAC; P < 0.001) and no significant effect of ethanol on TAC. These findings indicate that moderate consumption of alcohol may improve inflammatory markers associated with CVD in mice; however, the results should be interpreted with caution due to the differences in weight gain between groups.
Several studies have found a non‐linear relationship between alcohol consumption and cardiovascular disease (CVD) risk, suggesting that low or moderate consumption of alcohol may provide cardioprotective effects, while excessive alcohol consumption increases the risk of CVD. Studies also suggest that increased dietary consumption of n‐3 fatty acids may reduce CVD risk. The purpose of this study is to examine the effects of moderate ethanol consumption as a function of dietary n‐6:n‐3 fatty acid composition on markers associated with cardiovascular disease and liver dysfunction in mice. Twenty‐three mice (12 male, 11 female) consumed an 18% ethanol solution or 26.9% maltose dextrin solution (non‐ethanol isocaloric control) for 12 weeks. In each group, half of the mice were fed either a high n‐6 (n‐6:n‐3 = 50:1) diet or a balanced n‐3 (n‐6:n‐3 = 1:1) diet ad libitum. There were no differences in initial body weight between the two groups; however, the control group gained significantly more weight than the ethanol group (P = 0.020) associated with higher maltose dextrin fluid intake (P < 0.001). In the control group, the balanced n‐3 diet resulted in significantly lower aspartate aminotransferase (AST) levels (P = 0.010) compared to the high n‐6 diet. In the ethanol group, the balanced n‐3 diet resulted in lower levels of serum triglycerides (P = 0.086), total cholesterol (P= 0.096), and low‐density lipoprotein (LDL) levels (P = 0.053) that were approaching significance. These findings indicate that a diet with a balanced n‐6 to n‐3 ratio may improve several lipid profile markers associated with CVD in mice who concurrently consume moderate amounts of alcohol. Support or Funding Information NIH AA023291
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