Regulation of Mitochondrial 3-Hydroxy-3-methylglutaryl-coenzyme A Synthase Protein by Starvation, Fat Feeding, and Diabetes

Serra, Dolors; Casals, Núria; Asins, Guillermina; Royo, Teresa; Ciudad, Carlos J.; Hegardt, Fausto G.

doi:10.1006/abbi.1993.1557

Cited by 53 publications

(48 citation statements)

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“…In suckling rats no fasting-induced changes in mRNA levels have been observed [46] ; thus the significant fasting-induced rise in mitochondrial HMG-CoA synthase mRNA in the liver of piglets ( Figure 5) resembled that observed in fasted adult rats [7,8]. In an attempt to compare transcript amount in the two models, RNA from liver of fasted animals was probed with pig, rat and human mitochondrial HMG-CoA synthase probe (human probe ; PCR-produced with PIG1 and PIG2 primers by using the human cDNA clone of mitochondrial HMG-CoA synthase as a target [32] ; this 365 bp human probe was 89.9 % or…”

Section: Mrna and Activity Levels Of Mitochondrial Hmg-coa Synthase Dmentioning

confidence: 71%

“…In rats, hepatic ketogenic capacity increases rapidly during postnatal development [4] or fasting [5], when the liver mRNA, protein and activity of mitochondrial HMG-CoA synthase increase [6][7][8][9][10][11]. Ketogenesis is also associated with increased substrate availability and changes in the activities of enzymes central to β-oxidation.…”

Section: Gene Expression Of Mitochondrial 3-hydroxy-3-methylglutaryl-mentioning

confidence: 99%

“…Administration of dexamethasone or dibutyryl-cAMP to adult rats elicits increased liver mRNA, protein and enzymic activity [7,8,16], whereas opposite results are observed with insulin [7]. In addition, the rat mitochondrial HMG-CoA synthase gene contains elements that mediate its multihormonal regulation and tissue specificity [17].…”

Section: Gene Expression Of Mitochondrial 3-hydroxy-3-methylglutaryl-mentioning

confidence: 99%

“…Circulating hormones and fatty acids could affect the expression of mitochondrial HMG-CoA synthase [7,8,17,18]. To gain an insight into their roles in the fasting-induced rise in mitochondrial HMG-CoA expression ( Figure 5), insulin, glucagon and NEFA concentrations were determined in suckled (n l 7) and fasted (n l 5) piglets.…”

Section: Figure 6 Species Comparison Of Liver Mitochondrial Hmg-coa Smentioning

confidence: 99%

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Gene expression of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in a poorly ketogenic mammal: effect of starvation during the neonatal period of the piglet

Adams

Alho

Asins

et al. 1997

Biochemical Journal

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The low ketogenic capacity of pigs correlates with a low activity of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase. To identify the molecular mechanism controlling such activity, we isolated the pig cDNA encoding this enzyme and analysed changes in mRNA levels and mitochondrial specific activity induced during development and starvation. Pig mitochondrial synthase showed a tissue-specific expression pattern. As with rat and human, the gene is expressed in liver and large intestine; however, the pig differs in that mRNA was not detected in testis, kidney or small intestine. During development, pig mitochondrial HMG-CoA synthase gene expression showed interesting differences from that in the rat: (1) there was a 2–3 week lag in the postnatal induction; (2) the mRNA levels remained relatively abundant through the suckling–weaning transition and at maturity, in contrast with the fall observed in rats at similar stages of development; and (3) the gene expression was highly induced by fasting during the suckling, whereas no such change in mitochondrial HMG-CoA synthase mRNA levels has been observed in rat. The enzyme activity of mitochondrial HMG-CoA synthase increased 27-fold during starvation in piglets, but remained one order of magnitude lower than rats. These results indicate that post-transcriptional mechanism(s) and/or intrinsic differences in the encoded enzyme are responsible for the low activity of pig HMG-CoA synthase observed throughout development or after fasting.

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Section: Mrna and Activity Levels Of Mitochondrial Hmg-coa Synthase Dmentioning

confidence: 71%

Section: Gene Expression Of Mitochondrial 3-hydroxy-3-methylglutaryl-mentioning

confidence: 99%

Section: Gene Expression Of Mitochondrial 3-hydroxy-3-methylglutaryl-mentioning

confidence: 99%

Section: Figure 6 Species Comparison Of Liver Mitochondrial Hmg-coa Smentioning

confidence: 99%

See 2 more Smart Citations

Gene expression of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in a poorly ketogenic mammal: effect of starvation during the neonatal period of the piglet

Adams

Alho

Asins

et al. 1997

Biochemical Journal

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show abstract

“…It has been suggested that intramitochondrial 3-hydroxy-3-methylglutaryl-CoA (mHMG-CoA) synthase becomes an important locus of control under these conditions [71,72]. Insulin treatment of starved or diabetic rats results in the rapid decline in the hepatic concentration of mHMG-CoA synthase mRNA and protein [72,73].…”

Section: Enzymes Involved In the Partitioning Of Fatty Acids Between mentioning

confidence: 99%

Role of insulin in hepatic fatty acid partitioning: emerging concepts

Zammit

1996

Biochemical Journal

114

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Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes

Laffel

1999

Diabetes Metab. Res. Rev.

1,152

1,047

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Regulation of Mitochondrial 3-Hydroxy-3-methylglutaryl-coenzyme A Synthase Protein by Starvation, Fat Feeding, and Diabetes

Cited by 53 publications

References 0 publications

Gene expression of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in a poorly ketogenic mammal: effect of starvation during the neonatal period of the piglet

Gene expression of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase in a poorly ketogenic mammal: effect of starvation during the neonatal period of the piglet

Role of insulin in hepatic fatty acid partitioning: emerging concepts

Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes

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