Cited by 8Muscle Physiology and DisordersCircadian rhythm and melatoninMitochondrial Function and Pathology

Melatonin Alleviates the Impairment of Muscle Bioenergetics and Protein Quality Control Systems in Leptin-Deficiency-Induced Obesity

Open access
Potes, Yaiza, Díaz-Luis, Andrea, Bermejo-Millo, Juan C., Pérez-Martínez, Zulema, de Luxán-Delgado, Beatriz, Rubio-González, Adrian, Menéndez-Valle, Iván, Gutiérrez-Rodríguez, José +4 more·2023·Antioxidants

Abstract

Leptin is critically compromised in the major common forms of obesity. Skeletal muscle is the main effector tissue for energy modification that occurs as a result of the effect of endocrine axes, such as leptin signaling. Our study was carried out using skeletal muscle from a leptin-deficient animal model, in order to ascertain the importance of this hormone and to identify the major skeletal muscle mechanisms affected. We also examined the therapeutic role of melatonin against leptin-induced muscle wasting. Here, we report that leptin deficiency stimulates fatty acid β-oxidation, which results in mitochondrial uncoupling and the suppression of mitochondrial oxidative damage; however, it increases cytosolic oxidative damage. Thus, different nutrient-sensing pathways are disrupted, impairing proteostasis and promoting lipid anabolism, which induces myofiber degeneration and drives oxidative type I fiber conversion. Melatonin treatment plays a significant role in reducing cellular oxidative damage and regulating energy homeostasis and fuel utilization. Melatonin is able to improve both glucose and mitochondrial metabolism and partially restore proteostasis. Taken together, our study demonstrates melatonin to be a decisive mitochondrial function-fate regulator in skeletal muscle, with implications for resembling physiological energy requirements and targeting glycolytic type II fiber recovery.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/antiox12111962

Cites

91 of 91 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • In mice, leptin deficiency promotes fatty acid β-oxidation, enhancing mitochondrial protection against ROS through HK-II regulation, acting on mitochondrial function and quality control mechanisms.

    “Studies in mice show that leptin deficiency promotes fatty acid β-oxidation, enhancing mitochondrial protection against ROS through HK-II regulation, acting on mitochondrial function and quality control mechanisms [76].”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Potes, Y., Díaz-Luis, A., Bermejo-Millo, J. C., Pérez-Martínez, Z., de Luxán-Delgado, B., Rubio-González, A., Menéndez-Valle, I., Gutiérrez-Rodríguez, J., Solano, J. J., Caballero, B., Vega-Naredo, I., & Coto-Montes, A.
Affiliations
  • Universidad de Oviedo (ES)
  • Department of Morphology and Cell Biology, Faculty of Medicine, University of Oviedo, 33006 Oviedo, Spain
  • Instituto de Investigación Sanitaria del Principado de Asturias (ISPA), 33011 Oviedo, Spain
  • Hospital Monte Naranco (ES)
Corresponding author
Potes, Yaiza
Venue
Antioxidants
Publisher
MDPI AG
Published
2023-11-03
Volume
12
Issue
11
Pages
1962
ISSN
2076-3921 (ISSN-L)
OpenAlex
W4388295787
Cited by
8
References
91
Citations by year
2026: 1 · 2025: 5 · 2024: 2
FWCI
0.71
Type
journal article
Language
en
Open access
Locations
  • Antioxidants (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Instituto de Salud Carlos III (Spanish Ministry of Economy and Competitiveness) (PI21/01596, IDI/2021/000033, AP184182023)
  • Government of the Principado de Asturias (PI21/01596, IDI/2021/000033, AP184182023)
  • Fundación Mutua Madrileña (PI21/01596, IDI/2021/000033, AP184182023)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
melatonin, leptin deficiency, obesity, skeletal muscle, muscle energy metabolism, mitochondrial uncoupling, fatty acid beta-oxidation, oxidative damage, proteostasis, protein quality control, myofiber degeneration, energy homeostasis, glucose metabolism

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review