Intrinsic High Aerobic Capacity in Male Rats Protects Against Diet-Induced Insulin Resistance.
Adipogenesis
/ genetics
Animals
Diet, High-Fat
Energy Metabolism
/ genetics
Gene Expression Profiling
/ methods
Insulin Resistance
/ genetics
Lipid Metabolism
/ genetics
Liver
/ metabolism
Male
Muscle, Skeletal
/ metabolism
Physical Conditioning, Animal
/ physiology
Rats
Running
/ physiology
Sequence Analysis, RNA
/ methods
Journal
Endocrinology
ISSN: 1945-7170
Titre abrégé: Endocrinology
Pays: United States
ID NLM: 0375040
Informations de publication
Date de publication:
01 05 2019
01 05 2019
Historique:
received:
14
02
2019
accepted:
02
04
2019
entrez:
31
5
2019
pubmed:
31
5
2019
medline:
18
12
2019
Statut:
ppublish
Résumé
Low aerobic capacity increases the risk for insulin resistance but the mechanisms are unknown. In this study, we tested susceptibility to acute (3-day) high-fat, high-sucrose diet (HFD)-induced insulin resistance in male rats selectively bred for divergent intrinsic aerobic capacity, that is, high-capacity running (HCR) and low-capacity running (LCR) rats. We employed hyperinsulinemic-euglycemic clamps, tracers, and transcriptome sequencing of skeletal muscle to test whether divergence in aerobic capacity impacted insulin resistance through systemic and tissue-specific metabolic adaptations. An HFD evoked decreased insulin sensitivity and insulin signaling in muscle and liver in LCR rats, whereas HCR rats were protected. An HFD led to increased glucose transport in skeletal muscle (twofold) of HCR rats while increasing glucose transport into adipose depots of the LCR rats (twofold). Skeletal muscle transcriptome revealed robust differences in the gene profile of HCR vs LCR on low-fat diet and HFD conditions, including robust differences in specific genes involved in lipid metabolism, adipogenesis, and differentiation. HCR transcriptional adaptations to an acute HFD were more robust than for LCR and included genes driving mitochondrial energy metabolism. In conclusion, intrinsic aerobic capacity robustly impacts systemic and skeletal muscle adaptations to HFD-induced alterations in insulin resistance, an effect that is likely driven by baseline differences in oxidative capacity, gene expression profile, and transcriptional adaptations to an HFD.
Identifiants
pubmed: 31144719
pii: 5434897
doi: 10.1210/en.2019-00118
pmc: PMC6482035
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1179-1192Subventions
Organisme : BLRD VA
ID : I01 BX003271
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30 DK020572
Pays : United States
Organisme : NICHD NIH HHS
ID : U54 HD090216
Pays : United States
Commentaires et corrections
Type : CommentIn
Informations de copyright
Copyright © 2019 Endocrine Society.
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