Developmental changes in the activities of peroxisomal and mitochondrial β-oxidation in chicken liver

Ishii, Hidemi; Ishii, Satoshi; Suga, Tetsuya; Kazama, Mutsuyoshi

doi:10.1016/0003-9861(85)90264-4

Cited by 10 publications

(4 citation statements)

References 31 publications

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“…Similarly to the results for PPARa, an increased tendency toward mRNA expression was also indicated for the ACOX1 gene in both male and female broilers, which is the first-step enzyme in peroxisomal b-oxidation [36]. Although its peak expression in females was shown at the treatment level of 5 mg DHEA/kg, the results are in accordance with a study conducted with turkeys, whereby the ACOX1 mRNA was highly expressed in the abdominal fat pad and in the liver [37], suggesting a strong peroxisomal FA b-oxidation capacity.…”

Section: Discussionsupporting

confidence: 72%

Effects of Dehydroepiandrosterone (DHEA) on Hepatic Lipid Metabolism Parameters and Lipogenic Gene mRNA Expression in Broiler Chickens

Tang

Zou

2007

Lipids

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The aim of the present study was to identify the effects of dehydroepiandrosterone (DHEA) on hepatic lipid metabolism parameters and lipogenic gene mRNA expression in broiler chickens. A total of 72 1-day-old broiler chicks received a common basal diet with DHEA added at either 0 (control), 5 or 20 mg/kg feed. In the present study, the hepatic triglyceride (TG) concentration was significantly lower in male and female broilers that had bed administered DHEA than in control birds. In contrast, DHEA administration caused a marked rise in the hepatic non-esterified fatty acid (NEFA) concentration in both male and female broilers and also increased lipase (HL) activity in male broilers, while in female birds, no significant differences were observed in HL activity. The expression of peroxisome proliferators-activated receptor alpha (PPARalpha) and carnitine palmitoyl transferase I (CPTI) mRNA was decidedly enhanced following treatment with DHEA, and a similar tendency was also observed in the expression of acyl-Coenzyme A oxidase 1 (ACOX1). However, no significant differences were observed in the expression of either sterol regulatory element binding protein-1c (SREBP-1c) or acetyl CoA carboxylase (ACC) mRNA, except for a decline in the expression of ACC in females treated with 5 mg DHEA/kg. Numerous peroxisomes without a core and an increased number of peroxisomes were evident during morphological observations of broiler livers, in animals that had been treated with DHEA. Overall, the results of the present study indicated that DHEA accelerated lipid catabolism by direct regulation of hepatic lipid metabolism and by induction of relevant gene expression.

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Section: Discussionsupporting

confidence: 72%

Effects of Dehydroepiandrosterone (DHEA) on Hepatic Lipid Metabolism Parameters and Lipogenic Gene mRNA Expression in Broiler Chickens

Tang

Zou

2007

Lipids

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“…Based on the above data, one possible explanation for fat deposition decrease after long-term DHEA administration was a dramatical down regulation of transcriptional regulator of SREBP-1 expression, which altered FAS expression that was involved in the fatty acid, inhibiting the synthesis of endogenous TGs. As shown in Figure 4, a significant decrease of ACO mRNA level was observed in 50 and 100 mg/kg DHEA treatment groups as compared to the highfat diet group, which is the first-step enzyme in peroxisomal β-oxidation (Ishii et al 1985). Our observation showed that LCPT-1 mRNA level was decreased in 50 and 100 mg/kg DHEA treatment groups, which was accompanied by decreased expression of ACO.…”

Section: Discussionsupporting

confidence: 51%

Long-term administration of DHEA prevents fat deposition in rats fed a high-fat diet

Chen¹,

Kang²,

Li³

et al. 2016

CZECH J ANIM SCI

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ABSTRACT:The effects of dehydroepiandrosterone (DHEA) on lipid metabolism and lipogenic gene mRNA expression in rats subjected to a high-fat diet were determined. Totally 75 rats were randomly divided into 5 groups: control group 1 fed a normal diet (NCG), and groups 2-5 fed a high-fat diet with 0 (HCG), 25 (HLG), 50 (HMG), 100 (HHG) mg DHEA per kg body weight via gavage once a day for 8 weeks, respectively. DHEA significantly decreased body weight in HMG group as compared with HCG group (P < 0.05). Hepatic triglyceride and total cholesterol contents were decreased in HMG and HHG groups (P < 0.05), and hepatic lipase activity in HMG group was higher (P < 0.01) than in HCG group. Fatty acid synthesis (FAS) mRNA level was decreased in HLG and HHG groups (P < 0.01), and sterol response element binding protein-1 (SREBP-1) mRNA level was decreased in HMG and HHG groups when compared with HCG group (P < 0.01). Acyl-CoA oxidase (ACO) and liver carnitine palmitoyl transferase-1 (LCPT-1) mRNA abundance was decreased in HLG and HHG groups (P < 0.01), whereas hormone sensitive lipase (HSL) mRNA level was increased in HMG group as compared with HCG group (P < 0.05). These results indicated that long-term administration of DHEA reduced the synthesis of endogenous triglycerides by inhibiting SREBP-1 and FAS expression, and augmented the lipolysis of exogenous triglycerides through enhancing HSL expression, which eventually led to reduced fat deposition in rats fed a high-fat diet.

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“…However, the extent of anti-oxidant effects of l -carnitine in those hatchlings seems to be somewhat decreased, as the ROS level in the co-treatment group did not statistically differ from the level in the PFOA treated group. This might be explained by the extensive labor required for the hatching process [33], in which β-oxidation serves as an important resource of energy [34]. An abundant oxygen supply post hatch might be another reason for this result.…”

Section: Discussionmentioning

confidence: 99%

The Roles of Reactive Oxygen Species and Nitric Oxide in Perfluorooctanoic Acid-Induced Developmental Cardiotoxicity and l-Carnitine Mediated Protection

Zhao

Jiang

Wang

et al. 2017

IJMS

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Perfluorooctanoic acid (PFOA) is an environmental contaminant that could induce developmental cardiotoxicity in a chicken embryo, which may be alleviated by l-carnitine. To explore the roles of reactive oxygen species (ROS) and nitric oxide (NO) in such changes and the potential effects of l-carnitine, fertile chicken eggs were exposed to PFOA via an air cell injection, with or without l-carnitine co-treatment. The ROS and NO levels in chicken embryo hearts were determined with electron spin resonance (ESR), and the protein levels of the nuclear factor κ-light chain-enhancer of activated B cells (NF-κB) p65 and inducible nitric oxide synthase (iNOS) in chicken embryo hearts were assessed with western blotting. The results of ESR indicated that PFOA exposure induced an elevation in the ROS levels in ED19 chicken embryo hearts and hatchling chicken hearts, while l-carnitine could alleviate such changes. Meanwhile, increased NO levels were observed in ED19 embryo hearts and hatchling hearts following PFOA exposure, while l-carnitine co-treatment exerted modulatory effects. Western blotting revealed that p65 translocation in ED19 embryo hearts and hatchling hearts was enhanced by PFOA, while l-carnitine co-treatment alleviated such changes. iNOS expression levels in ED19 embryo hearts followed the same pattern as NO levels, while a suppression of expression was observed in hatchling hearts exposed to PFOA. ROS/NF-κB p65 and iNOS/NO seem to be involved in the late stage (ED19 and post hatch) of PFOA-induced developmental cardiotoxicity in a chicken embryo. l-carnitine could exert anti-oxidant and NO modulatory effects in the developing chicken embryo hearts, which likely contribute to its cardioprotective effects.

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Developmental changes in the activities of peroxisomal and mitochondrial β-oxidation in chicken liver

Cited by 10 publications

References 31 publications

Effects of Dehydroepiandrosterone (DHEA) on Hepatic Lipid Metabolism Parameters and Lipogenic Gene mRNA Expression in Broiler Chickens

Effects of Dehydroepiandrosterone (DHEA) on Hepatic Lipid Metabolism Parameters and Lipogenic Gene mRNA Expression in Broiler Chickens

Long-term administration of DHEA prevents fat deposition in rats fed a high-fat diet

The Roles of Reactive Oxygen Species and Nitric Oxide in Perfluorooctanoic Acid-Induced Developmental Cardiotoxicity and l-Carnitine Mediated Protection

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