High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans

Autoři: Jonathan Alcántar-Fernández aff001;  Angélica González-Maciel aff003;  Rafael Reynoso-Robles aff003;  Martha Elva Pérez Andrade aff002;  Alain de J. Hernández-Vázquez aff002;  Antonio Velázquez-Arellano aff002;  Juan Miranda-Ríos aff002
Působiště autorů: Programa de Doctorado en Ciencias Biomédicas, Universidad Nacional Autónoma de México (UNAM), Ciudad de México, México aff001;  Unidad de Genética de la Nutrición, Depto. de Biología Molecular y Biotecnología, Instituto de Investigaciones Biomédicas, UNAM e Instituto Nacional de Pediatría, Ciudad de México, México aff002;  Laboratorio de Morfología Celular y Tisular, Instituto Nacional de Pediatría, Ciudad de México, México aff003
Vyšlo v časopise: PLoS ONE 14(12)
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pone.0226652


Glucose is an important nutrient that dictates the development, fertility and lifespan of all organisms. In humans, a deficit in its homeostatic control might lead to hyperglucemia and the development of obesity and type 2 diabetes, which show a decreased ability to respond to and metabolize glucose. Previously, we have reported that high-glucose diets (HGD) induce alterations in triglyceride content, body size, progeny, and the mRNA accumulation of key regulators of carbohydrate and lipid metabolism, and longevity in Caenorhabditis elegans (PLoS ONE 13(7): e0199888). Herein, we show that increasing amounts of glucose in the diet induce the swelling of both mitochondria in germ and muscle cells. Additionally, HGD alter the enzymatic activities of the different respiratory complexes in an intricate pattern. Finally, we observed a downregulation of ceramide synthases (hyl-1 and hyl-2) and antioxidant genes (gcs-1 and gst-4), while mitophagy genes (pink-1 and dct-1) were upregulated, probably as part of a mitohormetic mechanism in response to glucose toxicity.

Klíčová slova:

Caenorhabditis elegans – Endoplasmic reticulum – Glucose – Messenger RNA – Mitochondria – Mitochondrial DNA – Polymerase chain reaction


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