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The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism.
  • R. Veech
  • Biology, Medicine
  • Prostaglandins, leukotrienes, and essential fatty…
  • 1 March 2004
TLDR
The effects of ketone body metabolism suggests that mild ketosis may offer therapeutic potential in a variety of different common and rare disease states, and current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupled mitochondrial uncoupling proteins. Expand
Cytosolic phosphorylation potential.
TLDR
Agreement between two highly active enzyme systems in the same compartment is taken as evidence of the existence of near-equilibrium in both these systems and suggests that free cytosolic [sigma ADP] is probably 20-fold lower than measured cell ADP content in mitochondrial-containing tissues. Expand
Sir2 regulates skeletal muscle differentiation as a potential sensor of the redox state.
TLDR
Results indicate that Sir2 regulates muscle gene expression and differentiation by possibly functioning as a redox sensor in response to exercise, food intake, and starvation, Sir2 may sense modifications of the redox state and promptly modulate gene expression. Expand
Nutritional Ketosis Alters Fuel Preference and Thereby Endurance Performance in Athletes.
TLDR
This work studied the biochemical advantages of ketosis in humans using a ketone ester-based form of nutrition without the unwanted milieu of endogenous ketone body production by caloric or carbohydrate restriction. Expand
Effects of pH and free Mg2+ on the Keq of the creatine kinase reaction and other phosphate hydrolyses and phosphate transfer reactions.
  • J. Lawson, R. Veech
  • Chemistry, Medicine
  • The Journal of biological chemistry
  • 25 July 1979
TLDR
The observed equilibrium constants (Kobs) of the creatine kinase, myokinase, glucose-6-phosphatase, and fructose-1,6-diph phosphatase reactions have been determined at 38 degrees C, pH 7.0, ionic strength 0.25, and varying free magnesium concentrations. Expand
The redox state of free nicotinamide-adenine dinucleotide phosphate in the cytoplasm of rat liver.
TLDR
The application of the method of calculation to data published by Kraupp, Adler-Kastner, Niessner & Plank (1967), Goldberg, Passonneau & Lowry (1966) and Kauffman, Brown,passonneau and Lowry (1968) shows that the redox states of the NAD and NADP couples in cardiac-muscle cytoplasm and in mouse-brain cytop lasm are of the same order as those in rat liver. Expand
Insulin, ketone bodies, and mitochondrial energy transduction
TLDR
The moderate ketosis characteristic of prolonged fasting or type II diabetes appears to be an elegant compensation for the defects in mitochondrial energy transduction associated with acute insulin deficiency or mitochondrial senescence. Expand
Kinetics, safety and tolerability of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate in healthy adult subjects.
TLDR
Induction of mild states of hyperketonemia may improve physical and cognitive performance and ingestion of (R)-3-hydroxybutyrate is a safe and simple method to elevate blood ketone levels, compared with the inconvenience of preparing and consuming a ketogenic diet. Expand
Control of glucose utilization in working perfused rat heart.
TLDR
The results illustrate that the control of the metabolic flux in glucose metabolism of rat heart is not exerted by a single enzyme but variably distributed among enzymes depending upon substrate availability, hormonal stimulation, or other changes of conditions. Expand
D-beta-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease.
TLDR
It is shown that addition of 4 mM d-beta-hydroxybutyrate protected cultured mesencephalic neurons from MPP(+) toxicity and hippocampal neurons from Abeta(1-42) toxicity, suggesting that ketone bodies may play a therapeutic role in these most common forms of human neurodegeneration. Expand
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