The mitochondrial metabolic reprogramming agent trimetazidine as an ‘exercise mimetic’ in cachectic C26-bearing mice
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منابع مشابه
The mitochondrial metabolic reprogramming agent trimetazidine as an ‘exercise mimetic’ in cachectic C26‐bearing mice
BACKGROUND Cancer cachexia is characterized by muscle depletion and exercise intolerance caused by an imbalance between protein synthesis and degradation and by impaired myogenesis. Myofibre metabolic efficiency is crucial so as to assure optimal muscle function. Some drugs are able to reprogram cell metabolism and, in some cases, to enhance metabolic efficiency. Based on these premises, we cho...
متن کاملModulating the metabolism by trimetazidine enhances myoblast differentiation and promotes myogenesis in cachectic tumor-bearing c26 mice
Trimetazidine (TMZ) is a metabolic reprogramming agent able to partially inhibit mitochondrial free fatty acid β-oxidation while enhancing glucose oxidation. Here we have found that the metabolic shift driven by TMZ enhances the myogenic potential of skeletal muscle progenitor cells leading to MyoD, Myogenin, Desmin and the slow isoforms of troponin C and I over-expression. Moreover, similarly ...
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Diabetes mellitus is a chronic metabolic disorder, the worldwide point prevalence of which is estimated to be 8.6% in subjects more than 20 years and 20.1% in subjects more than 65 years of age. [1, 2] The major pathophysiological feature is either reduced insulin secretion or reduced insulin sensitivity resulting in hyperglycemia. Diabetes mellitus is of two major types namely type 1 and type ...
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Protein synthesis has been measured in vivo in liver and muscle of mice bearing the XK1 tumor, an appropriate model for cancer cachexia. Two different methods were used involving measurement of tracer incorporation into tissue protein either at the end of a 4-hr constant infusion of [14C]tyrosine or 10 min after i.v. injection of a flooding dose of [3H]phenylalanine. Whole-body tyrosine flux wa...
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Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is most commonly caused by the A3243G mutation of mitochondrial DNA. The capacity to utilize fatty acid or glucose as a fuel source and how such dynamic switches of metabolic fuel preferences and transcriptional modulation of adaptive mechanism in response to energy deficiency in MELAS syndrome have not ...
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ژورنال
عنوان ژورنال: Journal of Cachexia, Sarcopenia and Muscle
سال: 2017
ISSN: 2190-5991
DOI: 10.1002/jcsm.12226