Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:6.4.1.2 (acetyl-CoA carboxylase)
 2,876 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six midlactation Holstein cows were fed a total mixed ration supplemented with either 4.8% canola meal, 3.3% unprotected canola seeds plus 1.5% canola meal, or 4.8% formaldehyde-protected canola seeds, according to a double 3 x 3 Latin square design. Each period lasted 3 wk; experimental analyses were restricted to the last week of each period. Mammary biopsies were taken the last day of each period for gene expression measurements. Milk production and milk protein percentage were reduced by canola seeds, whether protected or unprotected. Protected canola seeds also decreased dry matter intake. Feeding canola seeds reduced the content of C8 to C16 fatty acids in milk and increased the content of oleic acid (C18:1c9). Unprotected canola seeds elevated the concentrations of C18:0. Protected canola seeds increased the C18:2 and C18:3 content, and reduced the C18d:0/C18:1c9 ratio. Similar results were obtained for plasma fatty acids, with some specific features, such as an increased C16:0/C16:1 ratio with protected canola seeds. Canola seeds had no significant effects on insulin, triglycerides, or cholesterol present in serum, but increased the concentration of nonesterified fatty acids; a greater increase was obtained with protected canola seeds. Expression levels of acetyl-CoA carboxylase and delta 9-stearoyl-CoA desaturase genes measured in the mammary gland did not differ significantly between diets. Therefore, the reduced C18s:0/C18:1c9 ratio observed in milk with protected canola seeds was not due to an enhanced expression of the delta-9 desaturase in the mammary gland.
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PMID:Milk fatty acid composition and mammary lipid metabolism in Holstein cows fed protected or unprotected canola seeds. 1141 95

Carbohydrate response element (ChRE)-binding protein (ChREBP) is a recently discovered transcription factor that is activated in response to high glucose concentrations in liver independently of insulin. ChREBP was first identified by its ability to bind the ChRE of the liver pyruvate kinase (LPK) gene. We recently reported that the increase in expression of multiple liver lipogenic enzyme mRNAs elicited by feeding a high-carbohydrate diet as well as that of LPK mRNA is markedly reduced in mice lacking ChREBP gene expression (ChREBP(-/-)) in comparison to WT mice. The present study provides evidence for a direct and dominant role of ChREBP in the glucose regulation of two key liver lipogenic enzymes, acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS). ACC, FAS, and LPK mRNA levels were higher in WT hepatocytes cultured with high (25 mM) rather than low (5.5 mM) glucose medium, but there was no effect of glucose concentration on these mRNA levels in ChREBP(-/-) hepatocytes. Similarly, reporter constructs containing ACC, FAS, or LPK gene ChREs were responsive to glucose when transfected into WT but not ChREBP(-/-) hepatocytes, and glucose transactivation of the constructs in ChREBP(-/-) hepatocytes was restored by cotransfection with a ChREBP expression plasmid. ChREBP binding to ACC, FAS, and LPK ChRE sequences in vitro was demonstrated by electrophoretic mobility super shift assays. In vivo binding of ChREBP to ACC, FAS, and LPK gene promoters in intact liver nuclei from rats fed a high-carbohydrate diet was demonstrated by using a formaldehyde crosslinking and chromatin immunoprecipitation procedure.
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PMID:Carbohydrate response element binding protein directly promotes lipogenic enzyme gene transcription. 1549 71

Fourteen Alpine goats at midlactation were fed a diet of hay and concentrate (55:45), without (control) or with formaldehyde-treated linseed (FLS) or oleic sunflower oil (OSO) at 11.2 or 3.5% of dry matter intake, respectively, in a 3 x 3 Latin Square design with three 3-wk periods. Milk yield was lower in goats fed FLS than control or OSO (2.13 vs. 2.32 kg/d). Milk fat content was higher with FLS or OSO than control (40.8 vs. 33.8 g/kg). Formaldehyde-treated linseed and OSO caused a significant decrease (23 and 18%, respectively) of C10 to C17 fatty acids secretion compared with control. The secretion of cis-9 C18:1 and cis-9, trans-11 C18:2 were increased 1.44- and 1.54-fold for FLS and 1.78- and 1.36-fold for OSO, compared with control. The C18:3 (n-3) secretion was increased 2.61-fold with FLS compared with control. Milk cis-9 C14:1/C14:0, cis-9 C16:1/C16:0, and cis-9 C18:1/C18:0 ratios decreased with the supplemented diets compared with control. Mammary stearoyl-CoA desaturase mRNA and activity were decreased by the lipid supplements, whereas no significant change was observed for acetyl-CoA carboxylase and fatty acid synthase. The activities of glucose-6-phosphate dehydrogenase, malic enzyme, and glycerol-3-phosphate dehydrogenase were not affected by the lipid supplements. Mammary lipoprotein lipase mRNA increased with OSO, whereas lipoprotein lipase activity tended to decrease with FLS compared with control. Milk lipoprotein lipase activity sharply decreased with lipid supplement (by 59 and 71%, for FLS and OSO, respectively). The changes in milk fatty acid profile due to FLS and OSO supplements were partly related to changes in the levels of mammary enzyme activities or mRNA.
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PMID:Mammary lipid metabolism and milk fatty acid secretion in alpine goats fed vegetable lipids. 1577 17