Decrement in resting and insulin-stimulated soleus muscle mitochondrial respiration is an early event in diet-induced obesity in mice.
Animals
Blood Glucose
/ drug effects
Cell Respiration
/ drug effects
Diet, High-Fat
/ adverse effects
Dietary Fats
/ metabolism
Glucose
/ metabolism
Glycogen
/ metabolism
Insulin
/ pharmacology
Insulin Resistance
/ physiology
Male
Mice
Mitochondria
/ drug effects
Mitochondria, Muscle
/ drug effects
Muscle, Skeletal
/ drug effects
Obesity
/ physiopathology
Oxidative Phosphorylation
/ drug effects
Rest
/ physiology
diet-induced obesity
insulin resistance
mitochondrial function
Journal
Experimental physiology
ISSN: 1469-445X
Titre abrégé: Exp Physiol
Pays: England
ID NLM: 9002940
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
23
08
2018
accepted:
19
12
2018
pubmed:
24
12
2018
medline:
27
8
2019
entrez:
23
12
2018
Statut:
ppublish
Résumé
What is the central question of this study? What are the temporal responses of mitochondrial respiration and mitochondrial responsivity to insulin in soleus muscle fibres from mice during the development of obesity and insulin resistance? What is the main finding and its importance? Short- and long-term feeding with a high-fat diet markedly reduced soleus mitochondrial respiration and mitochondrial responsivity to insulin before any change in glycogen synthesis. Muscle glycogen synthesis and whole-body insulin resistance were present after 14 and 28 days, respectively. Our findings highlight the plasticity of mitochondria during the development of obesity and insulin resistance. Recently, significant attention has been given to the role of muscle mitochondrial function in the development of insulin resistance associated with obesity. Our aim was to investigate temporal alterations in mitochondrial respiration, H
Substances chimiques
Blood Glucose
0
Dietary Fats
0
Insulin
0
Glycogen
9005-79-2
Glucose
IY9XDZ35W2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Pagination
306-321Informations de copyright
© 2018 The Authors. Experimental Physiology © 2018 The Physiological Society.