Alteration in Carnitine Metabolism in Uremic Children

2015 ◽  
pp. 86-94 ◽  
Author(s):  
M. Bulla ◽  
A. Gl�ggler ◽  
P. F�rst ◽  
M. Frosch ◽  
E. Kuwertz-Br�king
Keyword(s):  
Carnitine Metabolism

Carnitine Metabolism and Deficit - When Supplementation is Necessary?

2003 ◽  
Vol 4 (3) ◽  
pp. 211-219 ◽  
Author(s):  
A. Evangeliou ◽  
D. Vlassopoulos
Keyword(s):  
Carnitine Metabolism

scholarly journals The use of an in-vitro batch fermentation (human colon) model for investigating mechanisms of TMA production from choline, l-carnitine and related precursors by the human gut microbiota

2021 ◽  
Author(s):  
Priscilla Day-Walsh ◽  
Emad Shehata ◽  
Shikha Saha ◽  
George M. Savva ◽  
Barbora Nemeckova ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Metabolic Diseases ◽  
Human Colon ◽  
Human Studies ◽  
Bacterial Strains ◽  
Increased Risk ◽  
Carnitine Metabolism ◽  
Registration Number ◽  
Vitro Model

Abstract Purpose Plasma trimethylamine-N-oxide (TMAO) levels have been shown to correlate with increased risk of metabolic diseases including cardiovascular diseases. TMAO exposure predominantly occurs as a consequence of gut microbiota-dependent trimethylamine (TMA) production from dietary substrates including choline, carnitine and betaine, which is then converted to TMAO in the liver. Reducing microbial TMA production is likely to be the most effective and sustainable approach to overcoming TMAO burden in humans. Current models for studying microbial TMA production have numerous weaknesses including the cost and length of human studies, differences in TMA(O) metabolism in animal models and the risk of failing to replicate multi-enzyme/multi-strain pathways when using isolated bacterial strains. The purpose of this research was to investigate TMA production from dietary precursors in an in-vitro model of the human colon. Methods TMA production from choline, l-carnitine, betaine and γ-butyrobetaine was studied over 24–48 h using an in-vitro human colon model with metabolite quantification performed using LC–MS. Results Choline was metabolised via the direct choline TMA-lyase route but not the indirect choline–betaine-TMA route, conversion of l-carnitine to TMA was slower than that of choline and involves the formation of the intermediate γ-BB, whereas the Rieske-type monooxygenase/reductase pathway for l-carnitine metabolism to TMA was negligible. The rate of TMA production from precursors was choline > carnitine > betaine > γ-BB. 3,3-Dimethyl-1-butanol (DMB) had no effect on the conversion of choline to TMA. Conclusion The metabolic routes for microbial TMA production in the colon model are consistent with observations from human studies. Thus, this model is suitable for studying gut microbiota metabolism of TMA and for screening potential therapeutic targets that aim to attenuate TMA production by the gut microbiota. Trial registration number NCT02653001 (http://www.clinicaltrials.gov), registered 12 Jan 2016.

Carnitine Metabolism in Lean and Obese Zucker Rats during Starvation

1986 ◽  
Vol 116 (4) ◽  
pp. 668-674 ◽  
Author(s):  
Linda J. Brady ◽  
Paul S. Brady ◽  
Lauri Albers ◽  
Alan T. Davis ◽  
Charles L. Hoppel
Keyword(s):  
Zucker Rats ◽  
Carnitine Metabolism ◽  
Obese Zucker Rats

Neonatal Carnitine Metabolism

1998 ◽  
pp. 857-863
Author(s):  
Charles A. Stanley
Keyword(s):  
Carnitine Metabolism

Influence of carnitine supplementation on muscle substrate and carnitine metabolism during exercise

1988 ◽  
Vol 64 (6) ◽  
pp. 2394-2399 ◽  
Author(s):  
M. Soop ◽  
O. Bjorkman ◽  
G. Cederblad ◽  
L. Hagenfeldt ◽  
J. Wahren
Keyword(s):  
Prolonged Exercise ◽  
Carnitine Supplementation ◽  
Bicycle Exercise ◽  
Plasma Carnitine ◽  
Human Male ◽  
Carnitine Metabolism ◽  
Exercise Induced ◽  
Induced Changes ◽  
Male Subjects ◽  
Free Plasma

We examined 1) the effect of L-carnitine supplementation on free fatty acid (FFA) utilization during exercise and 2) exercise-induced alterations in plasma levels and skeletal muscle exchange of carnitine. Seven moderately trained human male subjects serving as their own controls participated in two bicycle exercise sessions (120 min, 50% of VO2max). The second exercise was preceded by 5 days of oral carnitine supplementation (CS; 5 g daily). Despite a doubling of plasma carnitine levels, with CS, there were no effects on exercise-induced changes in arterial levels and turnover of FFA, the relation between leg FFA inflow and FFA uptake, or the leg exchange of other substrates. Heart rate during exercise after CS decreased 7–8%, but O2 uptake was unchanged. Exercise before CS induced a fall from 33.4 +/- 1.6 to 30.8 +/- 1.0 (SE) mumol/l in free plasma carnitine despite a release (2.5 +/- 0.9 mumol/min) from the leg. Simultaneously, acylated plasma carnitine rose from 5.0 +/- 1.0 to 14.2 +/- 1.4 mumol/l, with no evidence of leg release. Consequently, total plasma carnitine increased. We concluded that in healthy subjects CS does not influence muscle substrate utilization either at rest or during prolonged exercise and that free carnitine released from muscle during exercise is presumably acylated in the liver and released to plasma.

Hypothalamic carnitine metabolism integrates nutrient and hormonal feedback to regulate energy homeostasis

2015 ◽  
Vol 418 ◽  
pp. 9-16 ◽  
Author(s):  
Romana Stark ◽  
Alex Reichenbach ◽  
Zane B. Andrews
Keyword(s):  
Energy Homeostasis ◽  
Carnitine Metabolism

Carnitine Metabolism and Urinary Organic Acid Excretion in Reye's Syndrome and Salicylate Intoxication.

1990 ◽  
Vol 32 (4) ◽  
pp. 406-409 ◽  
Author(s):  
Masaki Takayanagi ◽  
Hiroaki Kakinuma ◽  
Shigenori Yamamoto ◽  
Hironori Nakajima
Keyword(s):  
Organic Acid ◽  
Acid Excretion ◽  
Urinary Organic Acid ◽  
Reye's Syndrome ◽  
Carnitine Metabolism ◽  
Salicylate Intoxication

Carnitine metabolism in human muscle fiber types during submaximal dynamic exercise

1996 ◽  
Vol 80 (3) ◽  
pp. 1061-1064 ◽  
Author(s):  
D. Constantin-Teodosiu ◽  
S. Howell ◽  
P. L. Greenhaff
Keyword(s):  
Muscle Fiber ◽  
Fiber Type ◽  
Vastus Lateralis ◽  
Group Formation ◽  
Free Carnitine ◽  
Muscle Fiber Types ◽  
Type I ◽  
Fiber Types ◽  
Carnitine Metabolism ◽  
Type I Fibers

The effect of prolonged exhaustive exercise on free carnitine and acetylcarnitine concentrations in mixed-fiber skeletal muscle and in type I and II muscle fibers was investigated in humans. Needle biopsy samples were obtained from the vastus lateralis of six subjects immediately after exhaustive one-legged cycling at approximately 75% of maximal O2 uptake from both the exercised and nonexercised (control) legs. In the resting (control) leg, there was no difference in the free carnitine concentration between type I and II fibers (20.36 +/- 1.25 and 20.51 +/- 1.16 mmol/kg dry muscle, respectively) despite the greater potential for fat oxidation in type I fibers. However, the acetylcarnitine concentration was slightly greater in type I fibers (P < 0.01). During exercise, acetylcarnitine accumulation occurred in both muscle fiber types, but accumulation was greatest in type I fibers (P < 0.005). Correspondingly, the concentration of free carnitine was significantly lower in type I fibers at the end of exercise (P < 0.001). The sum of free carnitine and acetylcarnitine concentrations in type I and II fibers at rest was similar and was unchanged by exercise. In conclusion, the findings of the present study support the suggestion that carnitine buffers excess acetyl group formation during exercise and that this occurs in both type I and II fibers. However, the greater accumulation of acetylcarnitine in type I fibers during prolonged exercise probably reflects the greater mitochondrial content of this fiber type.

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