scholarly journals Gene Expression Associated with Apple Aroma Biosynthesis

HortScience ◽  
2006 ◽  
Vol 41 (4) ◽  
pp. 977C-977
Author(s):  
Nobuko Sugimoto ◽  
Steve van Nocker ◽  
Schuyler Korban ◽  
Randy Beaudry

A microarray containing over 10,000 gene fragments was used to link changes in gene expression with changes in aroma biosynthesis in ripening apple (Malus ×domestica Borkh). The microarray was probed with fluorescent-tagged cDNA derived from RNA extracted from `Jonagold' apple skin and cortex tissue representing eight distinct physiological stages spanning 70 days during ripening and senescence. The ripening stages, in chronological order, were: 1) early preclimacteric; 2) late preclimacteric and onset of trace ester biosynthesis; 3) onset of the autocatalytic ethylene and rapidly increasing ester biosynthesis; 4) half-maximal ester biosynthesis and engagement of the respiratory climacteric; 5) near maximal ester biosynthesis, peak in respiratory activity, and the onset of rapid tissue softening; 6) maximal ester biosynthesis prior to its decline, the conclusion of the respiratory climacteric, and the completion of tissue softening; 7) midpoint in the decline in ester biosynthesis and maximal ethylene biosynthesis; and 8) postclimacteric minimum in ester production. Patterns in gene expression reflecting the rise and fall in ester formation were found in some putative genes for beta-oxidation (acyl-CoA oxidase, enoyl-CoA hydratase, and acetyl-CoA acetyl transferase), ester formation (aminotransferase, alcohol dehydrogenase, and alcohol acyl transferase), and fatty acid oxidation (lipoxygenase), but not fatty acid biosynthetic genes. A marked decline coinciding with the onset of ester production was detected in several putative genes for ADH.

2013 ◽  
Vol 110 (7) ◽  
pp. 1220-1232 ◽  
Author(s):  
Rantao Zuo ◽  
Qinghui Ai ◽  
Kangsen Mai ◽  
Wei Xu

The effects of conjugated linoleic acid (CLA) on growth performance, non-specific immunity, antioxidant capacity, lipid deposition and related gene expression were investigated in the large yellow croaker (Larmichthys crocea). Fish (7·56 (sem 0·60) g) were fed soyabean oil-based diets with graded levels of CLA (0, 0·42, 0·83, 1·70 %) for 70 d. Quantitative PCR was used to assess the effects of CLA on the transcription of inflammation- and fatty acid oxidation-related genes. Growth in fish fed the diet with 0·42 % CLA was significantly higher. Also, phagocytic index and respiratory burst activity were significantly higher in fish fed the diets containing 0·42 and 0·83 % CLA, respectively. Hepatic total antioxidative capacity and catalase activities increased significantly when CLA increased from 0 to 0·83 %, and then decreased with further increase of CLA. However, hepatic malondialdehyde content decreased significantly as dietary CLA increased. Lipid concentration in the whole body and muscle increased significantly with increasing dietary CLA. Transcription of genes related to inflammation (cyclo-oxygenase-2 and IL-β) in the liver and kidney and fatty acid oxidation (carnitine palmitoyl transferase I and acyl CoA oxidase) in the kidney decreased significantly as dietary CLA increased. PPARα and acyl CoA oxidase expression in the liver decreased significantly as CLA increased from 0·42 to 1·70 %. These results strongly suggest that dietary CLA could significantly affect growth performance, non-specific immunity, antioxidant capacity, lipid deposition and transcription of inflammation- and fatty acid oxidation-related genes of the large yellow croaker. This may contribute to our understanding of the mechanisms related to the physiological effects of dietary CLA in fish.


Author(s):  
Ch. Shiva Prasad ◽  
R. Vinoo ◽  
R.N. Chatterjee ◽  
M. Muralidhar ◽  
D. Narendranath ◽  
...  

Background: Acetyl-CoA Carboxylase Beta (ACACB) plays a key role in fatty acid oxidation and was known to be involved in production of very-long-chain fatty acid and other compounds needed for proper development. This gene is mainly expressed in the tissues of heart, muscle, liver and colon. It chiefly involved in the production of malonyl-coA, a potent inhibitor of carnitine palmitoyl transferase I (CPT-I) enzyme needed in transport of long-chain fatty acyl-coAs to the mitochondria for β-oxidation.Methods: The present study was conducted to explore the expression pattern of the ACACB gene in breast muscle tissue during pre-hatch embryonic day (ED) 5th to 18th and post-hatch (18th, 22nd and 40th week of age) periods of White leghorn (IWI line) by using Quantitative real-time PCR (qPCR). Then, fold change of ACACB gene expression was calculated.Result: Our study showed that the ACACB gene expression was down-regulated during embryonic stages from ED6 to ED18. The gene expression was also down-regulated during adult stages i.e. on 22nd and 40th week of age. This result indicated that the initial expression of the ACACB gene is required for embryo development and during adult periods, low gene expression leads to the less fat deposition in muscle of layer chicken. Finally, it can be concluded that there was a differential expression pattern of the ACACB gene during the pre-hatch embryonic and post-hatch adult periods to mitigate varied requirements of lipids during different physiological stages in layer chicken.


2001 ◽  
Vol 281 (4) ◽  
pp. G865-G869 ◽  
Author(s):  
Steven D. Clarke

This review addresses the hypothesis that polyunsaturated fatty acids (PUFA), particularly those of the n-3 family, play pivotal roles as “fuel partitioners” in that they direct fatty acids away from triglyceride storage and toward oxidation and they enhance glucose flux to glycogen. In doing this, PUFA may reduce the risk of enhanced cellular apoptosis associated with excessive cellular lipid accumulation. PUFA exert their beneficial effects by upregulating the expression of genes encoding proteins involved in fatty acid oxidation while simultaneously downregulating genes encoding proteins of lipid synthesis. PUFA govern oxidative gene expression by activating the transcription factor peroxisome proliferator-activated receptor-α. PUFA suppress lipogenic gene expression by reducing the nuclear abundance and DNA binding affinity of transcription factors responsible for imparting insulin and carbohydrate control to lipogenic and glycolytic genes. In particular, PUFA suppress the nuclear abundance and expression of sterol regulatory element binding protein-1 and reduce the DNA binding activities of nuclear factor Y, stimulatory protein 1, and possibly hepatic nuclear factor-4. Collectively, the studies discussed suggest that the fuel “repartitioning” and gene expression actions of PUFA should be considered among the criteria used in defining the dietary needs of n-6 and n-3 fatty acids and in establishing the dietary ratio of n-6 to n-3 fatty acids needed for optimum health benefit.


PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0122024 ◽  
Author(s):  
Linyi Li ◽  
Hisae Yoshitomi ◽  
Ying Wei ◽  
Lingling Qin ◽  
Jingxin Zhou ◽  
...  

Nutrients ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 2037 ◽  
Author(s):  
Petra Kroupova ◽  
Evert M. van Schothorst ◽  
Jaap Keijer ◽  
Annelies Bunschoten ◽  
Martin Vodicka ◽  
...  

Antisteatotic effects of omega-3 fatty acids (Omega-3) in obese rodents seem to vary depending on the lipid form of their administration. Whether these effects could reflect changes in intestinal metabolism is unknown. Here, we compare Omega-3-containing phospholipids (krill oil; ω3PL-H) and triacylglycerols (ω3TG) in terms of their effects on morphology, gene expression and fatty acid (FA) oxidation in the small intestine. Male C57BL/6N mice were fed for 8 weeks with a high-fat diet (HFD) alone or supplemented with 30 mg/g diet of ω3TG or ω3PL-H. Omega-3 index, reflecting the bioavailability of Omega-3, reached 12.5% and 7.5% in the ω3PL-H and ω3TG groups, respectively. Compared to HFD mice, ω3PL-H but not ω3TG animals had lower body weight gain (−40%), mesenteric adipose tissue (−43%), and hepatic lipid content (−64%). The highest number and expression level of regulated intestinal genes was observed in ω3PL-H mice. The expression of FA ω-oxidation genes was enhanced in both Omega-3-supplemented groups, but gene expression within the FA β-oxidation pathway and functional palmitate oxidation in the proximal ileum was significantly increased only in ω3PL-H mice. In conclusion, enhanced intestinal FA oxidation could contribute to the strong antisteatotic effects of Omega-3 when administered as phospholipids to dietary obese mice.


1981 ◽  
Vol 196 (3) ◽  
pp. 803-809 ◽  
Author(s):  
F Bauché ◽  
D Sabourault ◽  
Y Giudicelli ◽  
J Nordmann ◽  
R Nordmann

To elucidate the mechanisms through which 2-mercaptoacetate administration inhibits fatty acid oxidation in the liver, the respiration rates induced by different substrates were studied polarographically in rat hepatic mitochondria isolated 3 h after 2-mercaptoacetate administration. Palmitoyl-L-carnitine oxidation was almost completely inhibited in either the absence or presence of malonate. Octanoate oxidation was also inhibited, and the intramitochondrial acyl-CoA content was markedly increased. The oxidation rate of pyruvate and 2-oxoglutarate on the one hand and of 3-hydroxybutyrate, succinate and glutamate on the other was either normal or only slightly decreased. In the presence of 2,4-dinitrophenol, the extent of the inhibition of palmitoyl-L-carnitine oxidation was unchanged. All these results are consistent with the hypothesis that the 2-mercaptoacetate inhibition of fatty acid oxidation is due to an inhibition of the beta-oxidation pathway itself. Finally, the mitochondrial defect responsible for this inhibition was shown to be an inhibition of palmitoyl-CoA dehydrogenase activity (EC 1.3.99.3).


1980 ◽  
Vol 238 (3) ◽  
pp. G255-G262
Author(s):  
J. Chacin ◽  
G. Martinez ◽  
E. Severin

The role of beta-oxidation in the mechanism of stimulation of acid secretion was examined in toad gastric mucosa in vitro. The incubation with 4-pentenoate selectively inhibited in a dose-dependent manner the rate of 14CO2 formation from [1-14C]octanoate. Pretreatment with 20 mM 4-pentenoate sharply reduced the respiratory and secretory responses to theophylline and histamine. Tracer studies showed a major utilization of exogenous octanoate over glucose and pyruvate by the in vitro toad gastric mucosa. Theophylline and histamine stimulated by 69% the rate of octanoate oxidation. Over 60% of the increments in oxygen uptake produced by theophylline and histamine accounted for the increments in octanoate oxidation, whereas glucose and pyruvate together accounted for less than 25%. Octanoate-dependent respiration was shown to correlate with octanoate oxidation under both inhibition with 4-pentenoate and stimulation with theophylline. Theophylline stimulated by 25% the rate of octanoate oxidation in Cl--free glucuronate-nutrient solutions. The present work provides further evidence for the primary role of fatty acid oxidation in the mechanism of acid secretion in amphibian.


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