Effects of guanidinoacetic acid supplementation on liver and breast muscle fat deposition, lipid levels, and lipid metabolism-related gene expression in ducks

Abstract

Exogenous supplementation of guanidinoacetic acid can mechanistically regulate the energy distribution in muscle cells. This study aimed to investigate the effects of guanidinoacetic acid supplementation on liver and breast muscle fat deposition, lipid levels, and lipid metabolism-related gene expression in ducks. We randomly divided 480 42 days-old female Jiaji ducks into four groups with six replicates and 20 ducks for each replicate. The control group was fed the basal diet, and the experimental groups were fed the basal diet with 400, 600, and 800 mg/kg (GA400, GA600, and GA800) guanidinoacetic acid, respectively. Compared with the control group, (1) the total cholesterol (p = 0.0262), triglycerides (p = 0.0357), malondialdehyde (p = 0.0452) contents were lower in GA400, GA600 and GA800 in the liver; (2) the total cholesterol (p = 0.0365), triglycerides (p = 0.0459), and malondialdehyde (p = 0.0326) contents in breast muscle were decreased in GA400, GA600 and GA800; (3) the high density lipoprotein (p = 0.0356) and apolipoprotein-A1 (p = 0.0125) contents were increased in GA600 in the liver; (4) the apolipoprotein-A1 contents (p = 0.0489) in breast muscle were higher in GA600 and GA800; (5) the lipoprotein lipase contents (p = 0.0325) in the liver were higher in GA600 and GA800; (6) the malate dehydrogenase contents (p = 0.0269) in breast muscle were lower in GA400, GA600, and GA800; (7) the insulin induced gene 1 (p = 0.0326), fatty acid transport protein 1 (p = 0.0412), and lipoprotein lipase (p = 0.0235) relative expression were higher in GA400, GA600, and GA800 in the liver; (8) the insulin induced gene 1 (p = 0.0269), fatty acid transport protein 1 (p = 0.0234), and lipoprotein lipase (p = 0.0425) relative expression were increased in GA400, GA600, and GA800 in breast muscle. In this study, the optimum dosage of 600 mg/kg guanidinoacetic acid improved the liver and breast muscle fat deposition, lipid levels, and lipid metabolism-related gene expression in ducks.

Keywords: fat deposition; fatty acid composition; guanidinoacetic acid; lipase activity; lipid metabolism genes.

Figure 1

Effects of guanidinoacetic acid on lipid levels in ducks. The data in CG, GA400, GA600 and GA800 were (A) total cholesterol (mmol/L) in the liver 5.49 ± 0.34^a, 4.70 ± 0.46^b, 3.71 ± 0.24^c, 3.68 ± 0.23^c, respectively, p = 0.0262; and in breast muscle 4.92 ± 0.20^a, 4.51 ± 0.12^b, 3.81 ± 0.25^c, 3.40 ± 0.12^d, respectively, p = 0.0365; (B) triglycerides (mmol/L) in the liver 1.67 ± 0.05^a, 1.48 ± 0.04^b, 1.39 ± 0.02^c, 1.36 ± 0.05^c, respectively, p = 0.0357; and in breast muscle 1.93 ± 0.03^a, 1.70 ± 0.05^b, 1.40 ± 0.04^c, 1.39 ± 0.02^c, respectively, p = 0.0459; (C) phospholipid (mg/g) in the liver 0.92 ± 0.02^c, 1.15 ± 0.03^b, 1.30 ± 0.10^a, 1.14 ± 0.04^b, respectively, P = 0.0456; and in breast 1.09 ± 0.03^d, 1.15 ± 0.02^c, 1.36 ± 0.11^a, 1.20 ± 0.01^b, respectively, p = 0.0431; (D) malondialdehyde (mmol/L) in the liver 4.91 ± 0.10^a, 4.55 ± 0.18^b, 4.13 ± 0.21^c, 4.12 ± 0.22^c, respectively, p = 0.0452; in breast muscle 4.90 ± 0.32^a, 4.30 ± 0.21^b, 4.25 ± 0.23^b, 3.83 ± 0.09^c, respectively, p = 0.0326; (E) intramuscular fat (%) in breast muscle 3.15 ± 0.15^b, 3.49 ± 0.06^a, 3.49 ± 0.04^a, 3.49 ± 0.09^a, respectively, p = 0.0235; (F) abdominal fat percentage (%) of ducks 3.77 ± 0.11^a, 3.44 ± 0.06^b, 3.21 ± 0.04^c, 3.23 ± 0.05^c, respectively, p = 0.0249; (G) creatine contents in breast muscle 3,920 ± 30.59^c, 4,127 ± 26.85^b, 4,689 ± 30.24^a, 4,691 ± 38.67^a, respectively, p = 0.0358.

Figure 2

Effects of guanidinoacetic acid on lipid metabolism-related gene expression in ducks. The data in CG, GA400, GA600, and GA800 were (A) SCD (stearoyl CoA desaturase) in the liver 1.00 ± 0.01, 0.99 ± 0.01; 0.99 ± 0.01, 1.01 ± 0.01, respectively, p = 0.3236; and in breast muscle 1.00 ± 0.01, 1.01 ± 0.01, 1.01 ± 0.01, 0.99 ± 0.01, respectively, p = 0.6328; (B) INSIG1 (insulin induced gene 1) in the liver 1.00 ± 0.01^c, 1.23 ± 0.02^b, 1.31 ± 0.02^a, 1.3 ± 0.03^a, respectively, p = 0.0326; and in breast muscle 1 ± 0.01^c, 1.34 ± 0.02^b, 1.42 ± 0.03^a, 1.42 ± 0.02^a, respectively, p = 0.0269; (C) FATP1 (fatty acid transport protein 1) in the liver 1 ± 0.01^b, 1.62 ± 0.03^a, 1.63 ± 0.02^a, 1.64 ± 0.03^a, respectively, p = 0.0412; and in breast muscle 1.00 ± 0.01^b, 1.53 ± 0.02^a, 1.52 ± 0.03^a, 1.54 ± 0.02^a, respectively, p = 0.0234; (D) LPL (lipoprotein lipase) in the liver 1.00 ± 0.01^c, 1.23 ± 0.01^b, 1.45 ± 0.03^a, 1.46 ± 0.03^a, respectively, p = 0.0235; and in breast muscle 1 ± 0.01^c, 1.29 ± 0.03^b, 1.52 ± 0.02^a, 1.54 ± 0.04^a, respectively, p = 0.0425; (E) FAS (fatty acid synthetase) in the liver 1.00 ± 0.01^a, 0.86 ± 0.02^b, 0.73 ± 0.02^c, 0.71 ± 0.03^c, respectively, p = 0.0235; and in breast muscle 1.00 ± 0.01^a, 0.76 ± 0.01^b, 0.65 ± 0.02^c, 0.63 ± 0.03^c, respectively, p = 0.0349; (F) FFAR4 (free fatty acid receptor 4) in the liver 1 ± 0.01, 0.99 ± 0.02, 1.01 ± 0.02, 1.01 ± 0.03, respectively, p = 0.5236; and in 1.00 ± 0.01, 0.99 ± 0.01, 1.02 ± 0.03, 1.01 ± 0.02, respectively, p = 0.4571.