Dietary supplementation with decaffeinated green coffee improves diet-induced insulin resistance and brain energy metabolism in mice
Authors: Ho, Lap1; Varghese, Merina1; Wang, Jun1; Zhao, Wei1; Chen, Fei1; Knable, Lindsay Alexis1; Ferruzzi, Mario2; Pasinetti, Giulio M.1
Source: Nutritional Neuroscience, Volume 15, Number 1, January 2012 , pp. 37-45(9)
Publisher: Maney Publishing
Abstract:
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.
Keywords: Chlorogenic acid; Coffee; Dementia; Alzheimer's disease; Mitochondria; Alzheimer's disease
Document Type: Research Article
DOI: http://dx.doi.org/10.1179/1476830511Y.0000000027
Affiliations: 1: Department of Neurology, Mount Sinai School of Medicine, New York, NY, USA 2: Departments of Food Science and Foods & Nutrition, Purdue University, West Lafayette, IN, USA
Publication date: 2012-01-01
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- By this author: Ho, Lap ; Varghese, Merina ; Wang, Jun ; Zhao, Wei ; Chen, Fei ; Knable, Lindsay Alexis ; Ferruzzi, Mario ; Pasinetti, Giulio M.

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