Effects of chronic ethanol consumption on levels of adipokines in visceral adipose tissues and sera of rats

Abstract

Aim: To investigate the effects of ethanol on adipokines (leptin, adiponectin, resistin, visfatin and cartonectin) levels in visceral adipose tissue (VAT) and sera, and explore the correlation between VAT and serum adipokine levels.

Methods: Forty-eight Wistar rats were randomly divided into control, low, middle and high ethanol treatment groups that received 0, 0.5, 2.5, or 5.0 g of ethanol x kg(-1) x d(-1), respectively, via gastric tubes for 22 weeks. The levels of fasting blood glucose (FBG) and fasting serum insulin (FINS) were measured and homeostasis model assessment of insulin resistance (HOMA-IR) values were calculated. Adipokines in perirenal and epididymal VAT and sera were measured by enzyme-linked immunosorbent assays (ELISAs).

Results: High-dose treatments of ethanol (vs control group) significantly increased FINS (eg 37.86%) and HOMA-IR values (eg 40.63%). In VAT, levels of leptin, resistin and visfatin in the middle- and high-dose groups were significantly elevated, whereas adiponectin and cartonectin levels decreased. In sera, changes in adipokine levels were similar to that observed in VAT, with the exception of cartonectin. These ethanol-induced effects were dose-dependent. A positive correlation existed between VAT and serum adipokine levels, except for cartonectin.

Conclusion: Chronic ethanol consumption affects adipokine levels in VAT and sera in a dose-dependent manner, with the exception of serum cartonectin. The altered levels of adipokines in VAT and sera are positively correlated.

Figure 1

Effects of chronic ethanol treatments on leptin levels in VAT (A) and sera (B) of rats. Wistar rats were fed with edible ethanol at doses of 0, 0.5, 2.5, and 5.0 g·kg^-1·d^-1for 22 weeks. VAT was obtained from epididymal and perirenal fat pads and blood samples were collected. Leptin levels in both VAT and sera were measured by ELISA. Values are given as mean±SD (n=12 in the 0 and 0.5 g·kg^-1·d^-1groups; n=11 in the 2.5 g·kg^-1·d^-1group; n = 10 in the 5.0 g·kg^-1·d^-1group).^bP<0.05, ^cP<0.01 vs 0 g·kg^-1·d^-1 group; ^fP<0.01 vs 5 g·kg^-1·d^-1 group.

Figure 2

Effects of chronic ethanol treatment on adiponectin levels in VAT (A) and sera (B) of rats. Wistar rats were fed with edible ethanol at doses of 0, 0.5, 2.5, and 5.0 g·kg^-1·d^-1for 22 weeks. VAT was obtained from epididymal and perirenal fat pads and blood samples were collected. Adiponectin levels in both VAT and sera were measured by ELISA. Values are given as mean±SD (n=12 in the 0 and 0.5 g·kg^-1·d^-1groups; n=11 in the 2.5 g·kg^-1·d^-1group; n=10 in the 5.0 g·kg^-1·d^-1group). ^bP<0.05, ^cP<0.01 vs 0 g·kg^-1·d^-1 group; ^eP<0.05 vs 5 g·kg^-1·d^-1 group.

Figure 3

Effects of chronic ethanol treatment on resistin levels in VAT (A) and sera (B) of rats. Wistar rats were fed with edible ethanol at doses of 0, 0.5, 2.5, and 5.0 g·kg^-1·d^-1for 22 weeks. VAT was obtained from epididymal and perirenal fat pads and blood samples were collected. Resistin levels in both VAT and sera were measured by ELISA. Values are given as mean±SD (n=12 in the 0 and 0.5 g·kg^-1·d^-1groups; n=11 in the 2.5 g·kg^-1·d^-1group; n=10 in the 5.0 g·kg^-1·d^-1group). ^bP<0.05, ^cP<0.01 vs 0 g·kg^-1·d^-1 group; ^eP<0.05 vs 5 g·kg^-1·d^-1 group.

Figure 4

Effects of chronic ethanol treatment on visfatin levels in VAT (A) and sera (B) of rats. Wistar rats were fed with edible ethanol at doses of 0, 0.5, 2.5, and 5.0 g·kg^-1·d^-1for 22 weeks. VAT was obtained from epididymal and perirenal fat pads and blood samples were collected. Visfatin levels in both VAT and sera were measured by ELISA. Values are given as mean±SD (n=12 in the 0 and 0.5 g·kg^-1·d^-1groups; n=11 in the 2.5 g·kg^-1·d^-1group; n=10 in the 5.0 g·kg^-1·d^-1group). ^cP<0.01 vs 0 g·kg^-1·d^-1 group; ^fP<0.01 vs 5 g·kg^-1·d^-1 group; ^hP<0.05, ⁱP<0.01 vs 0.5 g·kg^-1·d^-1 group.

Figure 5

Effects of chronic ethanol treatment on cartonectin levels in VAT (A) and sera (B) of rats. Wistar rats were fed with edible ethanol at doses of 0, 0.5, 2.5, and 5.0 g·kg^-1·d^-1 for 22 weeks. VAT was obtained from epididymal and perirenal fat pads and blood samples were collected. Cartonectin levels in both VAT and sera were measured by ELISA. Values are given as mean±SD (n=12 in the 0 and 0.5 g·kg^-1·d^-1 groups; n=11 in the 2.5 g·kg^-1·d^-1group; n=10 in the 5.0 g·kg^-1·d^-1 group). ^cP<0.01 vs 0 g·kg^-1·d^-1 control group;^eP<0.05 vs 5 g·kg^-1·d^-1 group.

Figure 6

Effects of chronic ethanol treatment on serum TNF-α levels. Wistar rats were fed with edible ethanol at doses of 0, 0.5, 2.5, and 5.0 g·kg^-1·d^-1for 22 weeks. Serum TNF-α levels were quantified by ELISA. Values are given as mean±SD (n=12 in the 0 and 0.5 g·kg^-1·d^-1 groups; n=11 in the 2.5 g·kg^-1·d^-1group; n=10 in the 5.0 g·kg^-1·d^-1group). ^cP<0.01 vs 0 g·kg^-1·d^-1 group.

Figure 7

Correlation between VAT and serum adipokine levels of rats. A correlation analysis was applied to test for significant correlations as follows: (A) correlations between VAT and serum leptin levels; (B) correlations between VAT and serum adiponectin levels; (C) correlations between VAT and serum resistin levels; (D) correlations between VAT and serum visfatin levels.

Figure 8

Comparison of the increasing ratio of respective adipokine levels in both VAT and serum of rats. Wistar rats were fed with edible ethanol at 5.0 g·kg^-1·d^-1 for 22 weeks. VAT was obtained from epididymal and perirenal fat pads and blood samples were collected. Adipokine levels in both VAT and serum were measured by ELISA. The increasing ratio of adipokine levels (vs 0 g·kg^-1·d^-1 group) in both VAT and serum of rats is indicated in the bar graph.