Dietary supplementation with decaffeinated green coffee improves diet-induced insulin resistance and brain energy metabolism in mice.
Nutr Neurosci
; 15(1): 37-45, 2012 Jan.
Article
em En
| MEDLINE
| ID: mdl-22305652
OBJECTIVES: There is accumulating evidence that coffee consumption may reduce risk for type 2 diabetes, a known risk factor for Alzheimer's and other neurological diseases. Coffee consumption is also associated with reduced risk for Alzheimer's disease and non-Alzheimer's dementias. However, preventive and therapeutic development of coffee is complicated by the cardiovascular side effects of caffeine intake. As coffee is also a rich source of chlorogenic acids and many bioactive compounds other than caffeine, we hypothesized that decaffeinated coffee drinks may exert beneficial effects on the brain. METHODS: We have investigated whether dietary supplementation with a standardized decaffeinated green coffee preparation, Svetol®, might modulate diet-induced insulin resistance and brain energy metabolism dysfunction in a high-fat diet mouse model. RESULTS: As expected, dietary supplementation with Svetol® significantly attenuated the development of high-fat diet-induced deficits in glucose-tolerance response. We have also found that Svetol®) treatment improved brain mitochondrial energy metabolism as determined by oxygen consumption rate. Consistent with this evidence, follow-up gene expression profiling with Agilent whole-genome microarray revealed that the decaffeinated coffee treatment modulated a number of genes in the brain that are implicated in cellular energy metabolism. DISCUSSION: Our evidence is the first demonstration that dietary supplementation with a decaffeinated green coffee preparation may beneficially influence the brain, in particular promoting brain energy metabolic processes.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Cafeína
/
Resistência à Insulina
/
Café
/
Suplementos Nutricionais
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Metabolismo Energético
/
Dieta Hiperlipídica
Tipo de estudo:
Etiology_studies
/
Observational_studies
/
Prognostic_studies
/
Risk_factors_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2012
Tipo de documento:
Article