Peter W. Stacpoole

ORCID: 0000-0003-0680-5881
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About
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Research Areas
  • Metabolism and Genetic Disorders
  • Mitochondrial Function and Pathology
  • Glutathione Transferases and Polymorphisms
  • Biochemical Acid Research Studies
  • Folate and B Vitamins Research
  • Amino Acid Enzymes and Metabolism
  • Diet and metabolism studies
  • Renal function and acid-base balance
  • Metabolomics and Mass Spectrometry Studies
  • Pharmacogenetics and Drug Metabolism
  • Genomics, phytochemicals, and oxidative stress
  • Lipoproteins and Cardiovascular Health
  • Diabetes, Cardiovascular Risks, and Lipoproteins
  • Plant biochemistry and biosynthesis
  • Biochemical and Molecular Research
  • Alcoholism and Thiamine Deficiency
  • ATP Synthase and ATPases Research
  • Ion Transport and Channel Regulation
  • Pancreatic function and diabetes
  • Malaria Research and Control
  • Cancer, Hypoxia, and Metabolism
  • Adipose Tissue and Metabolism
  • Metabolism, Diabetes, and Cancer
  • Cancer, Lipids, and Metabolism
  • Sulfur Compounds in Biology

University of Florida
2015-2024

Florida College
2013-2024

Columbia University Irving Medical Center
2020

Radboud University Nijmegen
2020

Radboud University Medical Center
2020

University of Florida Health
2020

Medical College of Wisconsin
2011-2018

Columbus Oncology and Hematology Associates
2018

Children's Hospital of Wisconsin
2011

University of California, San Diego
2007-2010

OBJECTIVE—To determine the effects of exercise, without weight loss, on insulin sensitivity (SI), postheparin plasma lipase activity (PHPL), intravenous fat clearance rate (K2), and fasting lipids in sedentary adults. RESEARCH DESIGN AND METHODS—At baseline after 6 months walk training (intensity 45–55 or 65–75% heart reserve, frequency 3–4 5–7 days/week, duration 30 min/session), anthropometric indexes, SI, PHPL, K2, were measured 18 adults (12 women, men; 51.9 ± 5.8 years age, BMI 28.9 4.6...

10.2337/diacare.26.3.557 article EN Diabetes Care 2003-03-01

<b>Objective: </b> To evaluate the efficacy of dichloroacetate (DCA) in treatment mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). <b>Background: High levels ventricular lactate, brain spectroscopic signature MELAS, correlate with more severe neurologic impairment. The authors hypothesized that chronic cerebral exacerbates neuronal injury MELAS therefore, investigated DCA, a potent lactate-lowering agent, as potential for MELAS. <b>Methods: conducted...

10.1212/01.wnl.0000196641.05913.27 article EN Neurology 2006-02-13

Mortality is very high in lactic acidosis, and there no satisfactory treatment other than of the underlying cause. Uncontrolled studies have suggested that dichloroacetate, which stimulates oxidation lactate to acetyl-coenzyme A carbon dioxide, might reduce morbidity improve survival among patients with this condition.We conducted a placebo-controlled, randomized trial intravenous sodium dichloroacetate therapy 252 acidosis; 126 were assigned receive placebo. The entry criteria included an...

10.1056/nejm199211263272204 article EN New England Journal of Medicine 1992-11-26

OBJECTIVE. Open-label studies indicate that oral dichloroacetate (DCA) may be effective in treating patients with congenital lactic acidosis. We tested this hypothesis by conducting the first double-blind, randomized, control trial of DCA disease. METHODS. Forty-three who ranged age from 0.9 to 19 years were enrolled. All had persistent or intermittent hyperlactatemia, and most severe psychomotor delay. Eleven pyruvate dehydrogenase deficiency, 25 1 more defects enzymes respiratory chain, 7...

10.1542/peds.2005-1226 article EN PEDIATRICS 2006-05-01

We administered dichloroacetate, which prevents or reverses hyperlactatemia in animals and lowers plasma lactate levels human beings, to 13 patients with lactic acidosis of various causes. All had hypotension, their acidemia resisted treatment sodium bicarbonate. The metabolic effects dichloroacetate were evaluated 11 patients. In seven significantly reduced the level arterial blood (P less than 0.005) from base-line value raised bicarbonate 0.02) pH 0.005). six these seven, resolved...

10.1056/nejm198308183090702 article EN New England Journal of Medicine 1983-08-18

Dichloroacetate is known to reduce plasma glucose and triglycerides in diabetic starved animals lower lactate under various experimental conditions. To investigate its metabolic effects man, we administered oral doses (3 4 g) of dichloroacetate as the sodium salt patients with diabetes mellitus or hyperlipoproteinemia both for six seven days. significantly reduced fasting hyperglycemia an average 24 per cent (P<0.01) from base line produced marked, concomitant falls (73 cent; P<0.05 <0.01)...

10.1056/nejm197803092981002 article EN New England Journal of Medicine 1978-03-09

Metabolic reprogramming between resistance and tolerance occurs within the immune system in response to sepsis. While metabolic tissues such as liver are subjected damage during sepsis, how their energy ensures survival is unclear. Employing comprehensive metabolomic, lipidomic, transcriptional profiling a mouse model of we show that hepatocyte lipid metabolism, mitochondrial tricarboxylic acid (TCA) energetics, redox balance significantly reprogrammed after cecal ligation puncture (CLP). We...

10.7554/elife.64611 article EN public-domain eLife 2021-02-22

Dichloroacetate (DCA) decreases blood, cerebral spinal fluid, and intracellular lactate concentrations by activating the mitochondrial pyruvate dehydrogenase enzyme complex. The authors reviewed efficacy of this investigational drug in treatment acquired or congenital forms lactic acidosis from data 40 English-language publications. hypolactatemic effect DCA occurs over a broad range pretreatment is directly related to baseline level. maximum lactate-lowering dependent on its dose but...

10.1177/0091270003254637 article EN The Journal of Clinical Pharmacology 2003-07-01

Hyperhomocysteinemia in humans is associated with genetic variants of several enzymes folate and one-carbon metabolism deficiencies vitamins B 12 6 . In each case, hyperhomocysteinemia might be caused by diminished folate-dependent homocysteine remethylation, but this has not been confirmed vivo. Because published stable isotopic tracer approaches cannot distinguish from folate-independent we developed a dual-tracer procedure which [U- 13 C 5 ]-methionine used conjunction [3- C]serine to...

10.1152/ajpendo.00351.2003 article EN AJP Endocrinology and Metabolism 2004-01-31

Editorials1 August 1986Lactic Acidosis: The Case Against Bicarbonate TherapyPETER W. STACPOOLE, Ph.D, M.D.PETER M.D.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-105-2-276 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptLactic acidosis is perhaps the commonest most poorly treated acid-base disorder. If a blood lactate concentration of at least 5 meq/L (5 mmol/L) an arterial pH 7.2...

10.7326/0003-4819-105-2-276 article EN Annals of Internal Medicine 1986-08-01

Dichloroacetate (DCA) is a xenobiotic of interest to both environmental toxicologists and clinicians. The chemical product water chlorination the metabolism various drugs industrial chemicals. Its accumulation in groundwater at certain Superfund sites considered potential health hazard. However, concern about DCA toxicity predicated mainly on data obtained inbred rodent strains administered doses thousands times higher than those which humans are usually exposed. In these animals, chronic...

10.1289/ehp.98106s4989 article EN public-domain Environmental Health Perspectives 1998-08-01
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