High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.

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...

Full description

Bibliographic Details
Main Authors: Jonathan Alcántar-Fernández, Angélica González-Maciel, Rafael Reynoso-Robles, Martha Elva Pérez Andrade, Alain de J Hernández-Vázquez, Antonio Velázquez-Arellano, Juan Miranda-Ríos
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0226652
id doaj-813d5d9add1d451db87a30a0447d8777
record_format Article
spelling doaj-813d5d9add1d451db87a30a0447d87772021-03-04T11:20:34ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-011412e022665210.1371/journal.pone.0226652High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.Jonathan Alcántar-FernándezAngélica González-MacielRafael Reynoso-RoblesMartha Elva Pérez AndradeAlain de J Hernández-VázquezAntonio Velázquez-ArellanoJuan Miranda-RíosGlucose 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.https://doi.org/10.1371/journal.pone.0226652
collection DOAJ
language English
format Article
sources DOAJ
author Jonathan Alcántar-Fernández
Angélica González-Maciel
Rafael Reynoso-Robles
Martha Elva Pérez Andrade
Alain de J Hernández-Vázquez
Antonio Velázquez-Arellano
Juan Miranda-Ríos
spellingShingle Jonathan Alcántar-Fernández
Angélica González-Maciel
Rafael Reynoso-Robles
Martha Elva Pérez Andrade
Alain de J Hernández-Vázquez
Antonio Velázquez-Arellano
Juan Miranda-Ríos
High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
PLoS ONE
author_facet Jonathan Alcántar-Fernández
Angélica González-Maciel
Rafael Reynoso-Robles
Martha Elva Pérez Andrade
Alain de J Hernández-Vázquez
Antonio Velázquez-Arellano
Juan Miranda-Ríos
author_sort Jonathan Alcántar-Fernández
title High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
title_short High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
title_full High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
title_fullStr High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
title_full_unstemmed High-glucose diets induce mitochondrial dysfunction in Caenorhabditis elegans.
title_sort high-glucose diets induce mitochondrial dysfunction in caenorhabditis elegans.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2019-01-01
description 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.
url https://doi.org/10.1371/journal.pone.0226652
work_keys_str_mv AT jonathanalcantarfernandez highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
AT angelicagonzalezmaciel highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
AT rafaelreynosorobles highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
AT marthaelvaperezandrade highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
AT alaindejhernandezvazquez highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
AT antoniovelazquezarellano highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
AT juanmirandarios highglucosedietsinducemitochondrialdysfunctionincaenorhabditiselegans
_version_ 1714803809579958272