scholarly journals Acanthopanax senticosus Promotes Survival of Tilapia Infected With Streptococcus iniae by Regulating the PI3K/AKT and Fatty Acid Metabolism Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Hong Xia Li ◽  
Jun Qiang ◽  
Chang You Song ◽  
Pao Xu

Streptococcus has greatly restricted the development of healthy tilapia aquaculture. As a green and efficient feed addition, Acanthopanax senticosus (APS) has been increasingly used in culture, but it is unclear whether it represents a disease-resistant feed. Genetically improved farmed tilapia (GIFT, Oreochromis niloticus) was fed with a feed supplemented with 0 (control), 0.5, 1, 2, 4, and 8‰ APS for 56 days, after which fish were injected with 5.9 × 106 CFU/ml Streptococcus iniae into the abdominal cavity. At 96 h after infection, the cumulative survival of GIFT in control and 0.5‰ APS treatments was significantly lower than in other treatments; at APS supplementation rates of 1 and 2‰, serum glucose, triglycerides, and cholesterol contents were all significantly lower than in control treatment fish. Hepatic glycogen and triglyceride contents of 1‰ APS treatment fish were significantly higher than those in fish in control treatment. Transcription levels of peroxisome proliferator activated receptor α (PPAR), fatty acid synthase (FAS), and lipoprotein Lipase (LPL) genes were upregulated, and their expression levels in fish in 1, 2, and 4‰ treatments were significantly higher than those in fish in control treatment at 96 h after S. iniae infection. After 96 h of infection, the red blood cells, hemoglobin, hematocrit, and white blood cells of fish in 1‰ APS treatment were significantly lower than those of fish in 4 and 8‰ treatments; hepatic catalase activity was activated at 48 h, superoxide dismutase activity was also significantly upregulated at 96 h, and the malondialdehyde content significantly decreased. It is noted that 0.5–2‰ APS treatments significantly activated the expression of PI3K and AKT in the liver, while inhibiting the expression of Caspase-9. Therefore, feed with 1‰ APS can promote hepatic glycogen and lipid metabolism in GIFT after infection with S. iniae, which is beneficial to alleviating oxidative stress damage and cell apoptosis in liver tissue.

2005 ◽  
Vol 21 (3) ◽  
pp. 154-162 ◽  
Author(s):  
A. A. ZALATA ◽  
A. B. CHRISTOPHE ◽  
C. E. DEPUYDT ◽  
F. SCHOONJANS ◽  
F. H. COMHAIRE

2002 ◽  
Vol 364 (2) ◽  
pp. 361-368 ◽  
Author(s):  
Mary C. SUGDEN ◽  
Karen BULMER ◽  
Geoffrey F. GIBBONS ◽  
Brian L. KNIGHT ◽  
Mark J. HOLNESS

The aim of the present study was to determine whether peroxisome-proliferator-activated receptor-α (PPARα) deficiency disrupts the normal regulation of triacylglycerol (TAG) accumulation, hepatic lipogenesis and glycogenesis by fatty acids and insulin using PPARα-null mice. In wild-type mice, hepatic TAG concentrations increased (P<0.01) with fasting (24h), with substantial reversal after refeeding (6h). Hepatic TAG levels in fed PPARα-null mice were 2.4-fold higher than in the wild-type (P<0.05), increased with fasting, but remained elevated after refeeding. PPARα deficiency also impaired hepatic glycogen repletion (P<0.001), despite normal insulin and glucose levels after refeeding. Higher levels of plasma insulin were required to support similar levels of hepatic lipogenesis de novo (3H2O incorporation) in the PPARα-null mice compared with the wild-type. This difference was reflected by corresponding changes in the relationship between plasma insulin and the mRNA expression of the lipogenic transcription factor sterol-regulatory-element-binding protein-1c, and that of one of its known targets, fatty acid synthase. In wild-type mice, hepatic pyruvate dehydrogenase kinase (PDK) 4 protein expression (a downstream marker of altered fatty acid catabolism) increased (P<0.01) in response to fasting, with suppression (P<0.001) by refeeding. Although PDK4 up-regulation after fasting was halved by PPARα deficiency, PDK4 suppression after refeeding was attenuated. In summary, PPARα deficiency leads to accumulation of hepatic TAG and elicits dysregulation of hepatic lipid and carbohydrate metabolism, emphasizing the importance of precise control of lipid oxidation for hepatic fuel homoeostasis.


FEBS Letters ◽  
1994 ◽  
Vol 356 (1) ◽  
pp. 122-124 ◽  
Author(s):  
Kiyoto Motojima ◽  
Masanori Isaka ◽  
Yasuko Takino ◽  
Sataro Goto

2020 ◽  
Vol 21 (2) ◽  
pp. 460 ◽  
Author(s):  
Yong-Un Jeong ◽  
Young-Jin Park

Ergosterol peroxide is a natural compound of the steroid family found in many fungi, and it possesses antioxidant, anti-inflammatory, anticancer and antiviral activities. The anti-obesity activity of several edible and medicinal mushrooms has been reported, but the effect of mushroom-derived ergosterol peroxide on obesity has not been studied. Therefore, we analyzed the effect of ergosterol peroxide on the inhibition of triglyceride synthesis at protein and mRNA levels and differentiation of 3T3-L1 adipocytes. Ergosterol peroxide inhibited lipid droplet synthesis of differentiated 3T3-L1 cells, expression of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAT/enhancer-binding protein alpha (C/EBPα), the major transcription factors of differentiation, and also the expression of sterol regulatory element-binding protein-1c (SREBP-1c), which promotes the activity of PPARγ, resulting in inhibition of differentiation. It further inhibited the expression of fatty acid synthase (FAS), fatty acid translocase (FAT), and acetyl-coenzyme A carboxylase (ACC), which are lipogenic factors. In addition, it inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs) involved in cell proliferation and activation of early differentiation transcription factors in the mitotic clonal expansion (MCE) stage. As a result, ergosterol peroxide significantly inhibited the synthesis of triglycerides and differentiation of 3T3-L1 cells, and is, therefore, a possibile prophylactic and therapeutic agent for obesity and related metabolic diseases.


2011 ◽  
Vol 51 (10) ◽  
pp. 952 ◽  
Author(s):  
G. Liste ◽  
G. C. Miranda-de la Lama ◽  
M. M. Campo ◽  
M. Villarroel ◽  
E. Muela ◽  
...  

The study analysed the effect of lairage on some indicators of welfare and meat quality in lambs. Forty-eight lambs were divided into two treatments: T1 without lairage and T2 with 12 h of lairage. Blood samples were collected at slaughter to analyse cortisol, lactate, glucose, creatinine kinase, non-esterified fatty acid, white blood cells, red blood cells, haematocrit and ratio of neutrophil : lymphocytes. Meat from the M. longissimus was analysed in terms of pH 24 h post-mortem, water-holding capacity, texture and colour. Sensory analyses were performed by a trained panel. Lairage had a significant effect on stress response, but had no effect on haematological variables. The lambs with a lairage period before slaughter (T2) had significantly (P ≤ 0.001) lower values of cortisol at the time of slaughter. A similar result was observed for lactate and glucose, with T1 lambs showing significantly (P ≤ 0.05) higher values than T2 lambs. The creatinine kinase activity and non-esterified fatty acid concentrations were highest in T2 lambs (P ≤ 0.05). Instrumental and sensory meat quality were not affected, with the exception of water-holding capacity and some meat colour indicators. The water-holding capacity was significantly higher for T2 (P ≤ 0.05), while T1 lambs had a higher yellow index (P ≤ 0.05) and hue (P ≤ 0.05). The results obtained in this study suggest that animals will be less stressed at the time of slaughter with an overnight lairage compared with slaughter on arrival at the abattoir. While stress at the time of slaughter can influence meat quality, these changes were small and always within the normal commercial range.


Molecules ◽  
2020 ◽  
Vol 25 (9) ◽  
pp. 2042 ◽  
Author(s):  
Yae Rim Choi ◽  
Jaewon Shim ◽  
Min Jung Kim

Soy isoflavones are popular ingredients with anti-adipogenic and anti-lipogenic properties. The anti-adipogenic and anti-lipogenic properties of genistein are well-known, but those of genistin and glycitein remain unknown, and those of daidzein are characterized by contrasting data. Therefore, the purpose of our study was to investigate the effects of daidzein, glycitein, genistein, and genistin on adipogenesis and lipogenesis in 3T3-L1 cells. Proliferation of 3T3-L1 preadipocytes was unaffected by genistin and glycitein, but it was affected by 50 and 100 µM genistein and 100 µM daidzein for 48 h. Among the four isoflavones, only 50 and 100 µM genistin and genistein markedly suppressed lipid accumulation during adipogenesis in 3T3-L1 cells through a similar signaling pathway in a dose-dependent manner. Genistin and genistein suppress adipocyte-specific proteins and genes, such as peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer-binding protein α (C/EBPα), and adipocyte binding protein 2 (aP2)/fatty acid-binding protein 4 (FABP4), and lipogenic enzymes such as ATP citrate lyase (ACL), acetyl-CoA carboxylase 1 (ACC1), and fatty acid synthase (FAS). Both isoflavones also activate AMP-activated protein kinase α (AMPKα), an essential factor in adipocyte differentiation, and inhibited sterol regulatory element-binding transcription factor 1c (SREBP-1c). These results indicate that genistin is a potent anti-adipogenic and anti-lipogenic agent.


2019 ◽  
Vol 22 (6) ◽  
pp. 500-505
Author(s):  
Chiara Valtolina ◽  
Joris H Robben ◽  
Monique E van Wolferen ◽  
Hedwig S Kruitwagen ◽  
Ronald J Corbee ◽  
...  

Objectives The aim of this study was to evaluate if de novo hepatic lipid synthesis contributes to fatty acid overload in the liver of cats with feline hepatic lipidosis (FHL). Methods Lipogenic gene expression of peroxisome proliferator-activated receptor-alpha ( PPAR-α), peroxisome proliferator-activated receptor-gamma ( PPAR-γ), fatty acid synthase ( FASN) and sterol regulatory element-binding factor ( SREBF1) were evaluated using quantitative RT-PCR in liver tissue of six cats with FHL and compared with the liver tissue of eight healthy cats. Results In liver tissue, PPAR-α, PPAR-γ and FASN mRNA expression levels were not significantly different ( P >0.12, P >0.89 and P >0.5, respectively) in the FHL group compared with the control group. SREBF1 gene expression was downregulated around 10-fold in the FHL group vs the control group ( P = 0.039). Conclusions and relevance The downregulation of SREBF1 in the liver tissue of cats with FHL does not support the hypothesis that de novo lipogenesis in the liver is an important pathway of fatty acid accumulation in FHL.


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