Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.3.99.3 (
acyl-CoA dehydrogenase
)
1,425
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Castration induces the accumulation of body fat and deposition of intramuscular fat in Korean cattle, resulting in improved beef quality. However, little is known about the metabolic adaptations in the liver following castration. To understand changes in lipid metabolism following castration, hepatic expression levels of lipid metabolism genes were compared between Korean bulls and steers. Steers had higher (p<0.001) hepatic lipids contents and higher (p<0.01) mRNA levels of lipogenic acetyl-CoA carboxylase. This differential gene expression may, in part, contribute to increased hepatic lipid content following the castration of bulls. However, we found no differences in the hepatic expression levels of genes related to triglyceride synthesis (mitochondrial glycerol-3-phosphate acyltransferase, diacylglycerol O-acyltransferase 1 and 2) and fatty acid (FA) oxidation (carnitine palmitoyltransferase 1A, C-4 to C-12 straight chain
acyl-CoA dehydrogenase
, very
long chain acyl-CoA dehydrogenase
) between bulls and steers. No differences in gene expression for very-low-density lipoprotein (VLDL) secretion, including apolipoprotein B mRNA and microsomal triglyceride transfer protein (MTTP) protein, were observed in the liver although MTTP mRNA levels were higher in steers compared to bulls. In conclusion, FA synthesis may contribute to increased hepatic lipid deposition in steers following castration. However, hepatic lipid metabolism, including triglyceride synthesis, FA oxidation, and VLDL secretion, was not significantly altered by castration. Our results suggest that hepatic lipid metabolism does not significantly contribute to increased body fat deposition in steers following castration.
...
PMID:Effects of castration on expression of lipid metabolism genes in the liver of korean cattle. 2555 84
Some success in identifying
acyl-CoA dehydrogenase
(
ACAD
) deficiencies before they are symptomatic has been achieved through tandem mass spectrometry. However, there has been several challenges that need to be confronted, including excess false positives, the occasional false negatives and indicators selection. To select ideal indicators and evaluate their performance for identifying
ACAD
deficiencies, data from 352,119 newborn babies, containing 20 cases, were used in this retrospective study. A total of three new ratios, C4/C5DC+C6-OH, C8/C14:1, and C14:1/C16-OH, were selected from 43 metabolites. Around 903 ratios derived from pairwise combinations of all metabolites
via
multivariate logistic regression analysis were used. In the current study, the regression analysis was performed to identify short chain acyl-CoA dehydrogenase (SCAD) deficiency, medium chain
acyl-CoA dehydrogenase
(MCAD) deficiency, and very
long chain acyl-CoA dehydrogenase
(VLCAD) deficiency. In both model-building and testing data, the C4/C5DC+C6-OH, C8/C14:1 and C14:1/C16-OH were found to be better indicators for SCAD, MCAD and VLCAD deficiencies, respectively, compared to [C4, (C4, C4/C2)], [C8, (C6, C8, C8/C2, C4DC+C5-OH/C8:1)], and [C14:1, (C14:1, C14:1/C16, C14:1/C2)], respectively. In addition, 22 mutations, including 5 novel mutations and 17 reported mutations, in
ACADS
,
ACADM
, and
ACADL
genes were detected in 20 infants with
ACAD
deficiency by using high-thorough sequencing based on target capture. The pathogenic mutations of c.1031A > G in
ACADS
, c.449_452delCTGA in
ACADM
and c.1349G > A in
ACADL
were found to be hot spots in Suzhou patients with SCAD, MCAD, and VLCAD, respectively. In conclusion, we had identified three new ratios that could improve the performance for
ACAD
deficiencies compared to the used indicators. We considered to utilize C4/C5DC+C6-OH, C8/C14:1, and C14:1/C16-OH as primary indicators for SCAD, MCAD, and VLCAD deficiency, respectively, in further expanded newborn screening practice. In addition, the spectrum of mutations in Suzhou population enriches genetic data of Chinese patients with one of
ACAD
deficiencies.
...
PMID:New Ratios for Performance Improvement for Identifying Acyl-CoA Dehydrogenase Deficiencies in Expanded Newborn Screening: A Retrospective Study. 3162 Jan 61
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