scholarly journals Supplementing conjugated linoleic acid (CLA) in breeder hens diet increased CLA incorporation in liver and alters hepatic lipid metabolism in chick offspring

2021 ◽  
pp. 1-41
Author(s):  
Chun-Yan Fu ◽  
Yan Zhang ◽  
Wen-Bin Wang ◽  
Xiang-Fa Wei ◽  
Pei-Pei Yan ◽  
...  

Abstract This experiment was designed to investigate the effect of supplementing conjugated linoleic acid (CLA) in breeder hens diet on development and hepatic lipid metabolism of chick offspring. Hy-Line Brown breeder hens were allocated into two groups, supplemented with 0 (CT) or 0.5% CLA for 8 weeks. Offspring chicks were grouped according to the mother generation and fed for 7 days. CLA treatment had no significant influence on development, egg quality, and fertility of breeder hens, but darkened the egg yolks in shade and increased yolk sac mass compared to CT group. Addition of CLA resulted in increased body mass and liver mass, and decreased deposition of subcutaneous adipose tissue in chick offspring. The serum triglyceride (TG) and cholesterol (TC) levels of chick offspring were decreased in CLA group. CLA treatment increased the incorporation of both CLA isomers (c9t11 and t10c12) in liver of chick offspring, accompanied by the decreased hepatic TG levels, related to the significant reduction of fatty acid synthase (FAS) and acetyl-CoA carboxylase (ACC) enzyme activities and the increased of carnitine palmitoyltransferase-1 (CPT1) enzyme activity. Meanwhile, CLA treatment reduced the mRNA expression of genes related to fatty acid biosynthesis (FAS, ACC, and sterol regulatory element-binding protein-1c), and induced the expression of genes related to β-oxidative (CPT1, AMP-activated protein kinase, and peroxisome proliferator-activated receptor α) in chick offspring liver. In summary, the addition of CLA in breeder hens diet significantly increased incorporation of CLA in liver of chick offspring, which further regulate hepatic lipid metabolism.

2020 ◽  
Vol 99 (1) ◽  
pp. 224-234
Author(s):  
Chunyan Fu ◽  
Yan Zhang ◽  
Qimeng Yao ◽  
Xiangfa Wei ◽  
Tianhong Shi ◽  
...  

2014 ◽  
Vol 111 (12) ◽  
pp. 2112-2122 ◽  
Author(s):  
R. O. Benatti ◽  
A. M. Melo ◽  
F. O. Borges ◽  
L. M. Ignacio-Souza ◽  
L. A. P. Simino ◽  
...  

Maternal consumption of a high-fat diet (HFD) during pregnancy and lactation is closely related to hepatic lipid accumulation, insulin resistance and increased serum cytokine levels in offspring and into their adulthood. MicroRNA (miRNA) have been implicated in cholesterol biosynthesis and fatty acid metabolism. We evaluated the modulation of hepatic fatty acid synthesis (de novo), β-oxidation pathways, and miRNA-122 (miR-122) and miRNA-370 (miR-370) expression in recently weaned offspring (day 28) of mouse dams fed a HFD (HFD-O) or a standard chow (SC-O) during pregnancy and lactation. Compared with SC-O mice, HFD-O mice weighed more, had a larger adipose tissue mass and were more intolerant to glucose and insulin (P< 0·05). HFD-O mice also presented more levels of serum cholesterol, TAG, NEFA and hepatic IκB kinase and c-Jun N-terminal kinase phosphorylation compared with SC-O mice (P< 0·05). Protein levels of fatty acid synthase, acetyl-CoA carboxylase and 3-hydroxy-3-methylglutaryl-CoA reductase were similar in HFD-O and SC-O mice, whereas expression levels of SCD1 mRNA and protein were more abundant in HFD-O mice than in SC-O mice (P< 0·05). Interestingly, mRNA expression levels of the β-oxidation-related genes ACADVL and CPT1 were decreased in HFD-O mice (P< 0·05). Furthermore, the expression of miR-122 was reduced but that of miR-370 was increased in HFD-O mice compared with that in SC-O mice (P< 0·05). Changes in hepatic lipid metabolism were accompanied by increased mRNA content of AGPAT1 and TAG deposition in HFD-O mice (P< 0·05). Taken together, the present results strongly suggest that maternal consumption of a HFD affects the early lipid metabolism of offspring by modulating the expression of hepatic β-oxidation-related genes and miRNA that can contribute to metabolic disturbances in adult life.


2019 ◽  
Vol 59 (4) ◽  
pp. 673 ◽  
Author(s):  
Y. Jiang ◽  
X. D. Liao ◽  
M. Xie ◽  
J. Tang ◽  
S. Y. Qiao ◽  
...  

The present study was conducted to evaluate the regulatory role of threonine (Thr) on hepatic lipid metabolism by determining the effects of dietary Thr concentration on lipid deposition and on genes related to lipid expression in the liver of Pekin duck. In total, 240 1-day-old ducklings were randomly allocated according to the average bodyweight to one of five dietary treatments with six replicate cages of eight birds per cage for each treatment. Birds were fed diets with 0.52%, 0.59%, 0.66%, 0.73% and 0.80% Thr (as-fed basis) from 1 to 21 days of age respectively. The results showed that dietary Thr supplementation increased average daily gain (P &lt; 0.0001), average daily feed intake (P &lt; 0.0001) and abdominal fat percentage (P &lt; 0.04), while it decreased feed to gain ratio (P &lt; 0.0001), the hepatic contents of total lipid (P &lt; 0.003) and triglycerides (P &lt; 0.003) of Pekin ducks. However, dietary Thr supplementation had no influence (P &gt; 0.05) on the concentration of hepatic cholesterol, and plasma amino acids and biochemical parameters of Pekin ducks. Moreover, Thr-unsupplemented control diet upregulated (P &lt; 0.05) hepatic gene expression related to lipid uptake (fatty acid-binding protein, apolipoprotein A4, lipoprotein lipase), fatty acid synthesis (sterol regulatory element-binding protein 1c, malic enzyme), fatty acid β-oxidation (peroxisome proliferator-activated receptor α, fatty acyl– coenzyme A (CoA) oxidase), ketogenesis (hydroxymethylglutaryl–CoA synthase 1, and acetyl–CoA synthetase1), responsive genes to amino acid deficiency (general control non-derepressible 2 (GCN2), GCN1, eukaryotic initiation factor 2α, impact RWD domain protein (IMPACT)), and triglyceride transport (apolipoprotein B) of Pekin ducks. In addition, dietary Thr deficiency had no effect on the expression of stearoyl CoA desaturase, fatty acid synthase, and ATP–citrate lyase in the liver of Pekin ducks. It is suggested that dietary Thr supplementation improved hepatic lipid metabolism of Pekin ducks by regulating lipid synthesis, transport and oxidation.


Lipids ◽  
2013 ◽  
Vol 49 (1) ◽  
pp. 15-24 ◽  
Author(s):  
Seong Ho Choi ◽  
David T. Silvey ◽  
Bradley J. Johnson ◽  
Matthew E. Doumit ◽  
Ki Yong Chung ◽  
...  

2017 ◽  
Vol 96 (8) ◽  
pp. 2965-2974 ◽  
Author(s):  
S. Li ◽  
A. Schiller Vestergren ◽  
H. Wall ◽  
S. Trattner ◽  
J. Pickova ◽  
...  

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 4015
Author(s):  
Hong Qin ◽  
Ziyu Song ◽  
Horia Shaukat ◽  
Wenya Zheng

Genistein (GEN) has been shown to significantly inhibit hepatic triglyceride accretion triggered by estrogen deficiency. The main purpose of this in vitro study was to investigate the function and molecular mechanism of estrogen receptor β (ERβ) in regulating hepatic lipid metabolism induced by GEN. Different doses of GEN or GEN with an ERβ antagonist were treated with HepG2 cells. Results showed that 25 μM GEN significantly diminished triglyceride levels. Meanwhile, GEN downregulated the levels of genes and proteins involved in lipogenesis, such as sterol-regulatory element-binding protein-1c (SREBP-1c), fatty acid synthase (FASN), and stearoyl-coenzyme A desaturase 1 (SCD1), and upregulated the gene and protein levels of the regulation factors responsible for fatty acid β-oxidation, such as carnitine palmitoyltransferase 1α (CPT-1α) and peroxisome proliferator-activated receptor α (PPARα). Furthermore, 25 μM GEN reduced the levels of phosphorylation of protein kinase B (Akt) and mechanistic target of rapamycin (mTOR). Moreover, most of these effects from GEN were reverted by pretreatment with the antagonist of ERβ. In conclusion, GEN improved hepatic lipid metabolism by activating ERβ and further modulation of Akt/mTOR signals. The results provide novel aspects of the regulatory mechanism of ERβ on hepatic lipid metabolism and might help to profoundly understand the functions of food-derived phytoestrogens in preventing and treating hepatic steatosis in postmenopausal women.


1995 ◽  
Vol 49 (7) ◽  
pp. 1013-1022 ◽  
Author(s):  
Daniel K. Asiedu ◽  
Abraham Demoz ◽  
Jon Skorve ◽  
Hans J. Grav ◽  
Rolf K. Berge

Sign in / Sign up

Export Citation Format

Share Document