High fat diet altered cardiac metabolic gene profile in Psammomys obesus gerbils.
Animals
Carnitine O-Palmitoyltransferase
/ genetics
Diet, High-Fat
/ adverse effects
Disease Models, Animal
Energy Metabolism
/ drug effects
Fatty Acid Binding Protein 3
/ genetics
Gene Expression Regulation
/ drug effects
Gerbillinae
/ genetics
Glucose Transporter Type 1
/ genetics
Humans
Insulin
/ genetics
Metabolome
/ genetics
Myocardium
/ metabolism
Oxidation-Reduction
/ drug effects
PPAR alpha
/ genetics
Protein Kinases
/ genetics
Apoptosis
Cardiomyopathy
High fat diet
Lipotoxicity
Psammomys obesus
Journal
Lipids in health and disease
ISSN: 1476-511X
Titre abrégé: Lipids Health Dis
Pays: England
ID NLM: 101147696
Informations de publication
Date de publication:
03 Jun 2020
03 Jun 2020
Historique:
received:
01
12
2019
accepted:
22
05
2020
entrez:
5
6
2020
pubmed:
5
6
2020
medline:
17
4
2021
Statut:
epublish
Résumé
In metabolic disorders, myocardial fatty infiltration is critically associated with lipotoxic cardiomyopathy. Twenty Psammomys obesus gerbils were randomly assigned to normal plant or high fat diet. Sixteen weeks later, myocardium was sampled for pathobiological evaluation. A sixteen-week high fat diet resulted in myocardial structure disorganization, with collagen deposits, lipid accumulation, cardiomyocyte apoptosis and inflammatory cell infiltration. Myocardial expressions of glucose transporter GLUT1 and pyruvate dehydrogenase (PDH) inhibitor, PDH kinase (PDK)4 increased, while insulin-regulated GLUT4 expression remained unchanged. Myocardial expressions of molecules regulating fatty acid transport, CD36 and fatty acid binding protein (FABP)3, were increased, while expression of rate-controlling fatty acid β-oxidation, carnitine palmitoyl transferase (CPT)1B decreased. Myocardial expression of AMP-activated protein kinase (AMPK), decreased, while expression of peroxisome proliferator activated receptors (PPAR)-α and -γ did not change. In high fat diet fed Psammomys obesus, an original experimental model of nutritionally induced metabolic syndrome mixing genetic predisposition and environment interactions, a short period of high fat feeding was sufficient to induce myocardial structural alterations, associated with altered myocardial metabolic gene expression in favor of lipid accumulation.
Sections du résumé
BACKGROUND
BACKGROUND
In metabolic disorders, myocardial fatty infiltration is critically associated with lipotoxic cardiomyopathy.
METHODS
METHODS
Twenty Psammomys obesus gerbils were randomly assigned to normal plant or high fat diet. Sixteen weeks later, myocardium was sampled for pathobiological evaluation.
RESULTS
RESULTS
A sixteen-week high fat diet resulted in myocardial structure disorganization, with collagen deposits, lipid accumulation, cardiomyocyte apoptosis and inflammatory cell infiltration. Myocardial expressions of glucose transporter GLUT1 and pyruvate dehydrogenase (PDH) inhibitor, PDH kinase (PDK)4 increased, while insulin-regulated GLUT4 expression remained unchanged. Myocardial expressions of molecules regulating fatty acid transport, CD36 and fatty acid binding protein (FABP)3, were increased, while expression of rate-controlling fatty acid β-oxidation, carnitine palmitoyl transferase (CPT)1B decreased. Myocardial expression of AMP-activated protein kinase (AMPK), decreased, while expression of peroxisome proliferator activated receptors (PPAR)-α and -γ did not change.
CONCLUSION
CONCLUSIONS
In high fat diet fed Psammomys obesus, an original experimental model of nutritionally induced metabolic syndrome mixing genetic predisposition and environment interactions, a short period of high fat feeding was sufficient to induce myocardial structural alterations, associated with altered myocardial metabolic gene expression in favor of lipid accumulation.
Identifiants
pubmed: 32493392
doi: 10.1186/s12944-020-01301-y
pii: 10.1186/s12944-020-01301-y
pmc: PMC7271448
doi:
Substances chimiques
Fatty Acid Binding Protein 3
0
Glucose Transporter Type 1
0
Insulin
0
PPAR alpha
0
Carnitine O-Palmitoyltransferase
EC 2.3.1.21
Protein Kinases
EC 2.7.-
pyruvate dehydrogenase kinase 4
EC 2.7.1.-
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
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