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Dietary copper supplementation enhances lipolysis in Rex rabbits.
Journal of Trace Elements in Medicine and Biology 2021 December
BACKGROUND: Copper is an important regulator of lipid metabolism in mammals, as a cofactor of many enzymes and is involved in the lipolysis. Copper deficiency has been considered as a significant factor in human diseases related to abnormal lipid metabolism, while adding copper to the diet seems to be the simplest and most effective way to prevent copper deficiency.
AIMS: The aim of this study was to investigate the effects of dietary copper level on lipid metabolism in Rex Rabbits.
METHODS: A total of 120 90-d-old Rex Rabbits were randomly allotted into three treatments, with 40 replicates (20 males, 20 females) in each treatment (1 rabbit per replicate). The diets included 1) control (8.4 mg/kg), normal-copper diet (39.1 mg/kg), 3) high-copper diet (67.5 mg/kg). The trial including a one-week adaptation period and a five-week experimental period.
RESULT: The results showed that copper (39.1 mg/kg) diet increased average daily feed intake (ADFI) (P<0.05, N = 34), and tended to increase the final body weight (FBW) (P = 0.0556, N = 34). Moreover, dietary copper addition (39.1 and 67.5 mg/kg) significantly increased the foreleg and hindleg weight (P<0.05, N = 8), and decreased the weight of Perirenal fat and the concentration of triglycerides (TG) in the liver (P<0.05, N = 8). The concentration of triglycerides (TG), epinephrine (EPI), and glucagon (GC) in serum were obviously higher than that in control group (P<0.05, N = 8), and the concentration of insulin (INS), and very low-density lipoprotein (VLDL) in serum were significantly decreased (P<0.05, N = 8). The copper group (39.1 mg/kg) showed up-regulated gene expression levels of carnitine palmitoyl transferases (CPT-1 and CPT-2) and peroxisome proliferator-activated receptor (PPAR-α) in liver (P < 0.05, N = 8) and down-regulated gene expression levels of fatty acid synthase (FAS) and Acetyl-CoA carboxylase (ACC) (P < 0.05, N = 8). In skeletal muscle, CPT-1, CPT-2, PPAR-α, fatty acid transport protein (FATP), fatty acid-binding protein (FABP) and lipoprotein lipase (LPL) levels were significantly up-regulated by copper treatment (P < 0.05, N = 8). Rex Rabbits receiving copper addition had higher CPT-1, CPT-2, PPAR-a and hormone-sensitive lipase (HSL) mRNA levels in adipose tissue (P < 0.05, N = 8).
CONCLUSION: Copper diets promoted skeletal muscle growth and reduced fat accumulation by enhancing fatty acid oxidation, at the same time, dietary copper inhibited De novo lipogenesis in the liver. PPAR-α signaling in liver, skeletal muscle and adipose tissues were involved in the regulation of lipid metabolism by copper.
AIMS: The aim of this study was to investigate the effects of dietary copper level on lipid metabolism in Rex Rabbits.
METHODS: A total of 120 90-d-old Rex Rabbits were randomly allotted into three treatments, with 40 replicates (20 males, 20 females) in each treatment (1 rabbit per replicate). The diets included 1) control (8.4 mg/kg), normal-copper diet (39.1 mg/kg), 3) high-copper diet (67.5 mg/kg). The trial including a one-week adaptation period and a five-week experimental period.
RESULT: The results showed that copper (39.1 mg/kg) diet increased average daily feed intake (ADFI) (P<0.05, N = 34), and tended to increase the final body weight (FBW) (P = 0.0556, N = 34). Moreover, dietary copper addition (39.1 and 67.5 mg/kg) significantly increased the foreleg and hindleg weight (P<0.05, N = 8), and decreased the weight of Perirenal fat and the concentration of triglycerides (TG) in the liver (P<0.05, N = 8). The concentration of triglycerides (TG), epinephrine (EPI), and glucagon (GC) in serum were obviously higher than that in control group (P<0.05, N = 8), and the concentration of insulin (INS), and very low-density lipoprotein (VLDL) in serum were significantly decreased (P<0.05, N = 8). The copper group (39.1 mg/kg) showed up-regulated gene expression levels of carnitine palmitoyl transferases (CPT-1 and CPT-2) and peroxisome proliferator-activated receptor (PPAR-α) in liver (P < 0.05, N = 8) and down-regulated gene expression levels of fatty acid synthase (FAS) and Acetyl-CoA carboxylase (ACC) (P < 0.05, N = 8). In skeletal muscle, CPT-1, CPT-2, PPAR-α, fatty acid transport protein (FATP), fatty acid-binding protein (FABP) and lipoprotein lipase (LPL) levels were significantly up-regulated by copper treatment (P < 0.05, N = 8). Rex Rabbits receiving copper addition had higher CPT-1, CPT-2, PPAR-a and hormone-sensitive lipase (HSL) mRNA levels in adipose tissue (P < 0.05, N = 8).
CONCLUSION: Copper diets promoted skeletal muscle growth and reduced fat accumulation by enhancing fatty acid oxidation, at the same time, dietary copper inhibited De novo lipogenesis in the liver. PPAR-α signaling in liver, skeletal muscle and adipose tissues were involved in the regulation of lipid metabolism by copper.
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