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Pivotal Role of Carnitine, Its Derivatives and Carnitine System in Human and Animal Health and Diseases

A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 4371

Special Issue Editors

Dr. Sabrina Margarucci

E-Mail Website
Guest Editor
Institute on Terrestrial Ecosystems (IRET) CNR, Via P. Castellino 111, 80131 Naples, Italy
Interests: carnitine; carnitine system; human prostate disease; canine mammary tumors; gastrointestinal disease; Rett syndrome; diabetes; metabolic plasticity
Dr. Cacciola Nunzio Antonio

E-Mail Website
Guest Editor
Institute on Terrestrial Ecosystems (IRET) CNR, Via P. Castellino 111, 80131 Naples, Italy
Interests: carnitine; carnitine system; human prostate disease; canine mammary tumors; gastrointestinal disease; lung cancer; gene expression; metabolic plasticity; pharmacology; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Carnitine is an essential metabolite widely distributed in all cells, both prokaryotic and eukaryotic. It is mainly found in food from animal sources but there is limited availability in plants. In mammals, it acts as a “shuttle” of acyl moieties, since its main function is to facilitate the transport of long-chain fatty acids from the cytosol to the mitochondria for the energy production through the β-oxidation pathway.

In recent years, scientific evidence has shown that several chronic-degenerative and neoplastic diseases can be linked to mitochondrial dysfunctions and carnitine and/or carnitine systems could play an important role as a marker of such dysfunctions.

In addition, it has been demonstrated that the carnitine system, which is composed of the carnitine palmitoyltransferase 1 (CPT1) and 2 (CPT2), the carnitine acylcarnitine translocase (CACT), and the carnitine acetyltransferase (CrAT), represents a pivotal mediator in cancer metabolic plasticity.

Finally, carnitine and its pharmacological derivatives could represent a more selective and specific remedy to conventional drugs for the treatment of several disorders, such as cancer diseases.

With this Special Issue, we aim to collect the most recent findings on carnitine and its derivatives as an alternative medicine to conventional therapies in several human and animal disorders, as well as to better comprehend how the carnitine system components act in several human and animal diseases, especially in cancer diseases.

Dr. Sabrina Margarucci
Dr. Cacciola Nunzio Antonio
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Molecules is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Carnitine
  • Carnitine system
  • Metabolism
  • Fatty acid oxidation
  • Mitochondrial dysfunctions
  • Cancer diseases
  • Human and animal pathology
  • Metabolic plasticity

Published Papers (2 papers)

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Research

17 pages, 2773 KiB  
Article
The Reversible Carnitine Palmitoyltransferase 1 Inhibitor (Teglicar) Ameliorates the Neurodegenerative Phenotype in a Drosophila Huntington’s Disease Model by Acting on the Expression of Carnitine-Related Genes
by Carla Bertapelle, Maria Rosaria Carillo, Nunzio Antonio Cacciola, Yulii V. Shidlovskii, Gianfranco Peluso and Filomena Anna Digilio
Molecules 2022, 27(10), 3125; https://doi.org/10.3390/molecules27103125 - 13 May 2022
Cited by 2 | Viewed by 2013
Abstract
Huntington’s disease (HD) is a dramatic neurodegenerative disorder caused by the abnormal expansion of a CAG triplet in the huntingtin gene, producing an abnormal protein. As it leads to the death of neurons in the cerebral cortex, the patients primarily present with neurological [...] Read more.
Huntington’s disease (HD) is a dramatic neurodegenerative disorder caused by the abnormal expansion of a CAG triplet in the huntingtin gene, producing an abnormal protein. As it leads to the death of neurons in the cerebral cortex, the patients primarily present with neurological symptoms, but recently metabolic changes resulting from mitochondrial dysfunction have been identified as novel pathological features. The carnitine shuttle is a complex consisting of three enzymes whose function is to transport the long-chain fatty acids into the mitochondria. Here, its pharmacological modification was used to test the hypothesis that shifting metabolism to lipid oxidation exacerbates the HD symptoms. Behavioural and transcriptional analyses were carried out on HD Drosophila model, to evaluate the involvement of the carnitine cycle in this pathogenesis. Pharmacological inhibition of CPT1, the rate-limiting enzyme of the carnitine cycle, ameliorates the HD symptoms in Drosophila, likely acting on the expression of carnitine-related genes. Full article
(This article belongs to the Special Issue Pivotal Role of Carnitine, Its Derivatives and Carnitine System in Human and Animal Health and Diseases)
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11 pages, 1255 KiB  
Article
The Effects of Streptozotocin-Induced Diabetes and Insulin Treatment on Carnitine Biosynthesis and Renal Excretion
by Aman Upadhyay, Kate E. Boyle and Tom L. Broderick
Molecules 2021, 26(22), 6872; https://doi.org/10.3390/molecules26226872 - 15 Nov 2021
Viewed by 1775
Abstract
Carnitine insufficiency is reported in type 1 diabetes mellitus. To determine whether this is accompanied by defects in biosynthesis and/or renal uptake, liver and kidney were obtained from male Sprague-Dawley rats with streptozotocin-induced diabetes. Diabetic rats exhibited the metabolic consequences of type 1 [...] Read more.
Carnitine insufficiency is reported in type 1 diabetes mellitus. To determine whether this is accompanied by defects in biosynthesis and/or renal uptake, liver and kidney were obtained from male Sprague-Dawley rats with streptozotocin-induced diabetes. Diabetic rats exhibited the metabolic consequences of type 1 diabetes, including hypoinsulinemia, hyperglycemia, and increased urine output. Systemic hypocarnitinemia, expressed as free carnitine levels, was evident in the plasma, liver, and kidney of diabetic rats. Compared to control rats, the low free carnitine in the plasma of diabetic rats was accompanied by decreased expression of γ-butyrobetaine hydroxylase in liver and kidney, suggesting impaired carnitine biosynthesis. Expression of organic cation transporter-2 in kidney was also reduced, indicating impaired renal reabsorption, and confirmed by the presence of elevated levels of free carnitine in the urine of diabetic rats. Insulin treatment of diabetic rats reversed the plasma hypocarnitinemia, increased the free carnitine content in both kidney and liver, and prevented urinary losses of free carnitine. This was associated with increased expression of γ-butyrobetaine hydroxylase and organic cation transporter-2. The results of our study indicate that type 1 diabetes induced with streptozotocin disrupts carnitine biosynthesis and renal uptake mechanisms, leading to carnitine insufficiency. These aberrations in carnitine homeostasis are prevented with daily insulin treatment. Full article
(This article belongs to the Special Issue Pivotal Role of Carnitine, Its Derivatives and Carnitine System in Human and Animal Health and Diseases)
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