Liver and Muscle Contribute Differently to the Plasma Acylcarnitine Pool During Fasting and Exercise in Humans

Xu, Guowang; Hansen, Jørn Bindslev; Zhao, Xinjie; Chen, S.; Hoene, Miriam; Wang, X. L.; Clemmesen, J; Secher, Niels H.; Häring, Hans‐Ulrich; Pedersen, Bente Klarlund; Lehmann, Rainer; Weigert, Cora; Plomgaard, Peter

doi:10.1210/jc.2016-1859

Cited by 54 publications

(72 citation statements)

References 31 publications

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“…52,53 Fasting has been shown to increase the release of acetylcarnitine from the hepatosplanchnic bed, whereas the release of other acylcarnitines, except propionylcarnitine, is minor. 54 Therefore, we hypothesize that the rise in plasma acetylcarnitine levels following fenofibrate treatment reflects increased hepatic export, which, in turn, could be due to a hepatic surplus of 2-carbon molecules.…”

Section: Discussionmentioning

confidence: 99%

Effects of free omega-3 carboxylic acids and fenofibrate on liver fat content in patients with hypertriglyceridemia and non-alcoholic fatty liver disease: A double-blind, randomized, placebo-controlled study

Oscarsson

Önnerhag

Risérus

et al. 2018

Journal of Clinical Lipidology

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Section: Discussionmentioning

confidence: 99%

Effects of free omega-3 carboxylic acids and fenofibrate on liver fat content in patients with hypertriglyceridemia and non-alcoholic fatty liver disease: A double-blind, randomized, placebo-controlled study

Oscarsson

Önnerhag

Risérus

et al. 2018

Journal of Clinical Lipidology

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“…Skeletal muscle is considered the main contributor to systemic ACs concentrations. However, other organs/ tissues, such as the liver and heart, may also contribute to the circulating levels of ACs (Xu et al 2016). Although no significant correlation between plasma ACs and their tissue counterparts has been found in mice, the liver has been shown to be the major contributor to plasma longchain ACs (Schooneman et al 2015).…”

Section: Discussionmentioning

confidence: 99%

Insulin‐resistance in glycogen storage disease type Ia: linking carbohydrates and mitochondria?

Rossi

Ruoppolo

Formisano

et al. 2018

J of Inher Metab Disea

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Increased plasma ACs and abnormal UOA profile suggest mitochondrial impairment in GSDIa. Correlation data suggest a possible connection between mitochondrial impairment and IR. We hypothesized that mitochondrial overload might generate by-products potentially affecting the insulin signaling pathway, leading to IR. On the basis of the available data, the possible pathomechanism for IR in GSDIa is proposed.

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“…Serum ACC undergo time-related changes in dairy cows during the transition from late pregnancy to early lactation (Kenéz et al, 2016) and differ between cows experiencing excessive versus low lipolysis, as classified via the serum FA concentrations postpartum (Humer et al, 2016). The plasma ACC profile may reflect the intramitochondrial acyl-CoA pattern; however, it is not clear to what extent circulating levels of ACC reflect tissue ACC metabolism, as plasma ACC represent the sum from different tissues, mainly skeletal muscle and liver (Schooneman et al, 2014;Xu et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Acylcarnitine profiles in serum and muscle of dairy cows receiving conjugated linoleic acids or a control fat supplement during early lactation

Yang

Sadri

Prehn

et al. 2019

Journal of Dairy Science

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Acylcarnitines (ACC) are formed when fatty acid (FA)-coenzyme A enters the mitochondria for β-oxidation and the tricarboxylic acid cycle through the carnitine shuttle. Concentrations of ACC may vary depending on the metabolic conditions, but can accumulate when rates of β-oxidation exceed those of tricarboxylic acid. This study aimed to characterize muscle and blood serum acylcarnitine profiles, to determine the mRNA abundance of muscle carnitine acyltransferases, and to test whether dietary supplementation (from d 1 in milk) with conjugated linoleic acids (CLA; 100 g/d; each 12% of trans-10,cis-12 and cis-9,trans-11 CLA; n = 11) altered these compared with control fat-supplemented cows (CTR; n = 10). Blood samples and biopsies from the semitendinosus musclewere collected on d −21, 1, 21, and 70 relative to parturition. Serum and muscle ACC profiles were quantified using a targeted metabolomics approach. The CLA supplement did not affect the variables examined. The serum concentration of free carnitine decreased with the onset of lactation. The concentrations of acetylcarnitine, hydroxybutyrylcarnitine, and the sum of short-chain ACC in serum were greater from d −21 to 21 than thereafter. The serum concentrations of long-chain ACC tetradecenoylcarnitine (C14:1) and octadecenoylcarnitine (C18:1) concentrations were greater on d 1 and 21 compared with d −21. Muscle carnitine remained unchanged, whereas short-and medium-chain ACC, including propenoylcarnitine (C3:1), hydroxybutyrylcarnitine, hydroxyhexanoylcarnitine, hexenoylcarnitine (C6:1), and pimelylcarnitine were increased on d 21 compared with d −21 and decreased thereafter. In muscle, the concentrations of long-chain ACC (from C14 to C18) were elevated on d 1. The mRNA abundance of carnitine palmitoyltransferase 1, muscle isoform (CPT1B) increased 2.8-fold from d −21 to 1, followed by a decline to nearly prepartum values by d 70, whereas that of CPT2 did not change over time. The majority of serum and muscle short-and long-chain ACC were positively correlated with the FA concentrations in serum, whereas serum carnitine and C5 were negatively correlated with FA. Time-related changes in the serum and muscle ACC profiles were demonstrated that were not affected by the CLA supplement at the dosage used in the present study. The elevated concentrations of long-chain ACC species in muscle and of serum acetylcarnitine around parturition point to incomplete FA oxidation were likely due to insufficient metabolic adaptation in response to the load of FA around parturition.

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Liver and Muscle Contribute Differently to the Plasma Acylcarnitine Pool During Fasting and Exercise in Humans

Cited by 54 publications

References 31 publications

Effects of free omega-3 carboxylic acids and fenofibrate on liver fat content in patients with hypertriglyceridemia and non-alcoholic fatty liver disease: A double-blind, randomized, placebo-controlled study

Effects of free omega-3 carboxylic acids and fenofibrate on liver fat content in patients with hypertriglyceridemia and non-alcoholic fatty liver disease: A double-blind, randomized, placebo-controlled study

Insulin‐resistance in glycogen storage disease type Ia: linking carbohydrates and mitochondria?

Acylcarnitine profiles in serum and muscle of dairy cows receiving conjugated linoleic acids or a control fat supplement during early lactation

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