Beneficial effects of creatine, CoQ10, and lipoic acid in mitochondrial disorders
Rodriguez MC, MacDonald JR, Mahoney DJ, Parise G, Beal MF, Tarnopolsky MA
Muscle & nerve · 192 citas
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Financiación no declaradaDatos neutrales que nuestra revisión registró sobre cómo se hizo este estudio. Describen el método, nunca si nos gusta el resultado.
Cómo se estudió
- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Marcadores de salud y funcionamiento
Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2006-11-01 · Muscle Nerve · vol. 35 · número 2 · págs. 235–242
- Editorial
- Wiley
- Citado
- 256 citas · más que el 95% de estudios similares · 4.3× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 39 trabajos
- Acceso
- De pago
- Áreas de investigación
- Mitochondrial Function and Pathology · Coenzyme Q10 studies and effects · Metabolism and Genetic Disorders
- Palabras clave
- mitochondrial disease, creatine monohydrate, coenzyme Q10, alpha-lipoic acid, combination therapy, MELAS, mitochondrial DNA deletions, chronic progressive external ophthalmoplegia, Kearns-Sayre syndrome, plasma lactate, reactive oxygen species, anaerobic metabolism, fat-free mass, ankle dorsiflexion strength, ATP production
- MeSH
- humans, mitochondrial diseases, creatine, ubiquinone, creatinine, coenzymes, thioctic acid, dinoprost, deoxyguanosine, antioxidants, analysis of variance, cross-over studies, double-blind method, body composition, adolescent, adult, middle aged, child, female, male, 8-hydroxy-2'-deoxyguanosine
6 autores
- M. Christine Rodriguez🇨🇦McMaster University
- Jay R. MacDonald🇨🇦McMaster University
- Douglas J. Mahoney🇨🇦McMaster University
- Gianni Parise🇨🇦McMaster University
- M. Flint Beal🇺🇸Cornell University; Weill Cornell Medicine
- Mark Andrew Tarnopolsky🇨🇦 · autor de correspondenciaMcMaster University
Resumen
El texto original del estudio, en el idioma en que se publicó.
Mitochondrial disorders share common cellular consequences: (1) decreased ATP production; (2) increased reliance on alternative anaerobic energy sources; and (3) increased production of reactive oxygen species. The purpose of the present study was to determine the effect of a combination therapy (creatine monohydrate, coenzyme Q(10), and lipoic acid to target the above-mentioned cellular consequences) on several outcome variables using a randomized, double-blind, placebo-controlled, crossover study design in patients with mitochondrial cytopathies. Three patients had mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), four had mitochondrial DNA deletions (three patients with chronic progressive external ophthalmoplegia and one with Kearns-Sayre syndrome), and nine had a variety of other mitochondrial diseases not falling into the two former groups. The combination therapy resulted in lower resting plasma lactate and urinary 8-isoprostanes, as well as attenuation of the decline in peak ankle dorsiflexion strength in all patient groups, whereas higher fat-free mass was observed only in the MELAS group. Together, these results suggest that combination therapies targeting multiple final common pathways of mitochondrial dysfunction favorably influence surrogate markers of cellular energy dysfunction. Future studies with larger sample sizes in relatively homogeneous groups will be required to determine whether such combination therapies influence function and quality of life.
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