Dietary Lipid Source Modulates in Vivo Fatty Acid Metabolism in the Freshwater Fish, Murray Cod (Maccullochella peelii peelii)

2007 ◽  
Vol 55 (4) ◽  
pp. 1582-1591 ◽  
Author(s):  
David S. Francis ◽  
Giovanni M. Turchini ◽  
Paul L. Jones ◽  
Sena S. De Silva
Keyword(s):  
Fatty Acid ◽  
Freshwater Fish ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Dietary Lipid ◽  
Lipid Source ◽  
Dietary Lipid Source ◽  
Murray Cod

scholarly journals Increased Excretion of C4-Carnitine Species after a Therapeutic Acetylsalicylic Acid Dose: Evidence for an Inhibitory Effect on Short-Chain Fatty Acid Metabolism

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Catharina M. C. Mels ◽  
Peet Jansen van Rensburg ◽  
Francois H. van der Westhuizen ◽  
Pieter J. Pretorius ◽  
Elardus Erasmus
Keyword(s):  
Fatty Acid ◽  
Acetylsalicylic Acid ◽  
Fatty Acid Metabolism ◽  
Short Chain Fatty Acid ◽  
Acid Metabolism ◽  
Human Subjects ◽  
Inhibitory Effect ◽  
Chain Fatty Acid ◽  
Short Chain

Acetylsalicylic acid and/or its metabolites are implicated to have various effects on metabolism and, especially, on mitochondrial function. These effects include both inhibitory and stimulatory effects. We investigated the effect of both combined and separate oral acetylsalicylic acid and acetaminophen administration at therapeutic doses on the urinary metabolite profile of human subjects. In this paper, we provided in vivo evidence, in human subjects, of a statistically significant increase in isobutyrylcarnitine after the administration of a therapeutic dose of acetylsalicylic acid. We, therefore, propose an inhibitory effect of acetylsalicylic acid on the short-chain fatty acid metabolism, possibly at the level of isobutyryl-CoA dehydrogenase.

Free fatty acid metabolism and obesity in man: In vivo in vitro comparisons

Metabolism ◽  
1986 ◽  
Vol 35 (6) ◽  
pp. 505-514 ◽  
Author(s):  
S. Lillioja ◽  
J. Foley ◽  
C. Bogardus ◽  
D. Mott ◽  
B.V. Howard
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Free Fatty Acid Metabolism

scholarly journals The Mutual Inhibition of FoxO1 and SREBP-1c Regulated the Progression of Hepatoblastoma by Regulating Fatty Acid Metabolism

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Yu Hu ◽  
Hongyan Zai ◽  
Wei Jiang ◽  
Zhenglin Ou ◽  
Yuanbing Yao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Tumor Tissue ◽  
Acid Metabolism ◽  
Migration And Invasion ◽  
Mouse Tumor ◽  
Liver Malignancy ◽  
Foxo1 Gene

Background. Hepatoblastoma (HB) is the most common liver malignancy in pediatrics, but the treatment for this disease is minimal. This study is aimed at exploring the effect of FoxO1 and SREBP-1c on HB and their mechanism. Methods. FoxO1, SREBP-1c, FASN, ACLY, ACC, and MAGL expressions in tissue samples were detected by RT-qPCR and WB. IHC was utilized to measure FASN content. Overexpression and knockdown of FoxO1 and sSREBP-1c were performed on Huh-6 cells. Cell proliferation, migration, and invasion were examined by CCK8, scratch, and transwell assay. ELISA was performed to test the ATP, FAO, NEFA, and Acetyl-CoA contents. ChIP was used to detect the interaction between SREBP-1c protein and the FoxO1 gene. In vivo tumorigenesis was conducted on mice. The morphology of tumor tissue sections was observed by HE staining. Results. FoxO1 expression was downregulated in HB tissue, while the expressions of SREBP-1c, FASN, ACLY, ACC, and MAGL were upregulated. In Huh-6 cells and mouse tumor tissues, FoxO1 knockdown resulted in increased cell proliferation, migration, and invasion and active fatty acid metabolism. On the contrary, after the knockdown of SREBP-1c, cell proliferation, migration, and invasion were weakened, and fatty acid metabolism was significantly reduced. SREBP-1c interacted with the promoter of the FoxO1 gene. When FoxO1 was knocked down, the tumor tissue was more closely packed. After the knockdown of the SREBP-1c gene, the structure of tumor cells was deformed. Conclusion. FoxO1 and SREBP-1c inhibited each other in HB, leading to the increase of intracellular fatty acid metabolism, and ultimately facilitated the development of HB.

scholarly journals Anti-influenza A Virus Effects and Mechanisms of Emodin and Its Analogs via Regulating PPARα/γ-AMPK-SIRT1 Pathway and Fatty Acid Metabolism

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Yufei Bei ◽  
Boyu Tia ◽  
Yuze Li ◽  
Yingzhu Guo ◽  
Shufei Deng ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Influenza A Virus ◽  
Fatty Acid Metabolism ◽  
Influenza A ◽  
Acid Metabolism ◽  
Fatty Acid Biosynthesis ◽  
Sirtuin 1 ◽  
Peroxisome Proliferator ◽  
In Vivo Test

The peroxisome proliferator-activated receptor (PPAR) α/γ-adenosine 5 ′ -monophosphate- (AMP-) activated protein kinase- (AMPK-) sirtuin-1 (SIRT1) pathway and fatty acid metabolism are reported to be involved in influenza A virus (IAV) replication and IAV-pneumonia. Through a cell-based peroxisome proliferator responsive element- (PPRE-) driven luciferase bioassay, we have investigated 145 examples of traditional Chinese medicines (TCMs). Several TCMs, such as Polygonum cuspidatum, Rheum officinale Baillon, and Aloe vera var. Chinensis (Haw.) Berg., were found to possess high activity. We have further detected the anti-IAV activities of emodin (EMO) and its analogs, a group of common important compounds of these TCMs. The results showed that emodin and its several analogs possess excellent anti-IAV activities. The pharmacological tests showed that emodin significantly activated PPARα/γ and AMPK, decreased fatty acid biosynthesis, and increased intracellular ATP levels. Pharmaceutical inhibitors, siRNAs for PPARα/γ and AMPKα1, and exogenous palmitate impaired the inhibition of emodin. The in vivo test also showed that emodin significantly protected mice from IAV infection and pneumonia. Pharmacological inhibitors for PPARα/γ and AMPK signal and exogenous palmitate could partially counteract the effects of emodin in vivo. In conclusion, emodin and its analogs are a group of promising anti-IAV drug precursors, and the pharmacological mechanism of emodin is linked to its ability to regulate the PPARα/γ-AMPK pathway and fatty acid metabolism.

100th Anniversary of the discovery of insulin Perspective: Insulin and Adipose Tissue Fatty Acid Metabolism

2021 ◽  
Author(s):  
André C. Carpentier
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Dietary Fatty Acids ◽  
Nonesterified Fatty Acid ◽  
Adipose Tissue Fatty Acid ◽  
Tissue Fatty Acid

Insulin inhibits systemic nonesterified fatty acid (NEFA) flux to a greater degree than glucose or any other metabolite. This remarkable effect is mainly due to insulin-mediated inhibition of intracellular triglyceride (TG) lipolysis in adipose tissues and is essential to prevent diabetic ketoacidosis, but also to limit the potential lipotoxic effects of NEFA in lean tissues that contributes to the development of diabetes complications. Insulin also regulates adipose tissue fatty acid esterification, glycerol and TG synthesis, lipogenesis and possibly oxidation, contributing to the trapping of dietary fatty acids in the postprandial state. Excess NEFA flux at a given insulin level has been used to define in vivo adipose tissue insulin resistance. Adipose tissue insulin resistance defined in this fashion has been associated with several dysmetabolic features and complications of diabetes, but the mechanistic significance of this concept is not fully understood. This review focusses on the in vivo regulation of adipose tissue fatty acid metabolism by insulin and the mechanistic significance of the current definition of adipose tissue insulin resistance. One hundred years after the discovery of insulin and despite decades of investigations, much is still to be understood about the multifaceted in vivo actions of this hormone on adipose tissue fatty acid metabolism.

Sign in / Sign up

Export Citation Format

Share Document