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...
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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 |
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