| Literature DB >> 26797515 |
Daniela Dimer Leffa1, Gislaine Tezza Rezin2, Francine Daumann3, Luiza M Longaretti3, Ana Luiza F Dajori3, Lara Mezari Gomes4, Milena Carvalho Silva4, Emílio L Streck4, Vanessa Moraes de Andrade3.
Abstract
Obesity is a multifactorial disease that comes from an imbalance between food intake and energy expenditure. Moreover, studies have shown a relationship between mitochondrial dysfunction and obesity. In the present study, we investigated the effect of acerola juices (unripe, ripe, and industrial) and its main pharmacologically active components (vitamin C and rutin) on the activity of enzymes of energy metabolism in the brain of mice fed a palatable cafeteria diet. Two groups of male Swiss mice were fed on a standard diet (STA) or a cafeteria diet (CAF) for 13 weeks. Afterwards, the CAF-fed animals were divided into six subgroups, each of which received a different supplement for one further month (water, unripe, ripe or industrial acerola juices, vitamin C, or rutin) by gavage. Our results demonstrated that CAF diet inhibited the activity of citrate synthase in the prefrontal cortex, hippocampus, and hypothalamus. Moreover, CAF diet decreased the complex I activity in the hypothalamus, complex II in the prefrontal cortex, complex II-III in the hypothalamus, and complex IV in the posterior cortex and striatum. The activity of succinate dehydrogenase and creatine kinase was not altered by the CAF diet. However, unripe acerola juice reversed the inhibition of the citrate synthase activity in the prefrontal cortex and hypothalamus. Ripe acerola juice reversed the inhibition of citrate synthase in the hypothalamus. The industrial acerola juice reversed the inhibition of complex I activity in the hypothalamus. The other changes were not reversed by any of the tested substances. In conclusion, we suggest that alterations in energy metabolism caused by obesity can be partially reversed by ripe, unripe, and industrial acerola juice.Entities:
Keywords: Acerola; Energy metabolism; Krebs cycle; Obesity; Respiratory mitochondrial chain
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Year: 2016 PMID: 26797515 DOI: 10.1007/s12035-016-9691-y
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590