Association between Polyphenol Intake and Lipid Profile of Adults and Elders in a Northeastern Brazilian Capital.

This research was aimed at evaluating the relationship between the estimated polyphenol intake and the atherogenic lipid profile in adult and elder residents in the city of Teresina, located in the Northeastern Region of Brazil. This study was a cross-sectional population-based survey with 501 adults and elders, conducted in Teresina, Brazil. Food intake was obtained by 24-h food recall. The estimated polyphenol intake was calculated by multiplying the food consumption data from the recall by the polyphenol content in the foods described in the Phenol-Explorer database. The mean intake of total polyphenols was 1006.53 mg/day. The phenolic acids was the class with the highest intake, followed by the flavonols. Coffee, beans and apples were the main foods contributing to the total polyphenol intake. In the individuals with elevated serum concentrations of total cholesterol and triglycerides, the intake of total polyphenols was significantly higher. The intake of total polyphenols, phenolic acids and lignans was higher in the subjects with dyslipidemia. This article provides, for the first time, data on the intake of the total polyphenol classes and subclasses in the evaluated population and the relationship with the lipid profile. The individuals with a higher intake of total polyphenols had a worse lipid profile, which may be a consequence of an improved diet in those individuals who present with dyslipidemia.

Altered release and uptake of gamma-aminobutyric acid in the cerebellum of dystrophin-deficient mice.

Dystrophin deficiency caused by mutations of the related gene leads to muscle wasting in Duchenne muscular dystrophy (DMD). Some patients with DMD also present with intellectual disability and various degrees of neurological disorders, which have been related to a decreased number of postsynaptic gamma-aminobutyric acid type A receptors (GABAARs) in the hippocampus (HPC) and cerebellum (CBL). The aim of this study was to examine the relevance of dystrophin in the presynaptic GABAergic function in brain regions in which this protein is normally abundant. [3H]-GABA release, induced by nicotinic receptor (nAChR) activation or K+ depolarization, and [3H]-GABA uptake were determined using synaptosomes extracted from the cortex (CTX), HPC, and CBL of littermate control and mdx mice. Superfusion of the synaptosomes with nicotine or high K+ solutions led to a concentration-dependent and Ca2+-dependent [3H]-GABA release in control and mdx synaptosomes. [3H]-GABA release induced by 10 µM nicotine in mdx CBL synaptosomes was 47% less than that in control mice. K+-induced [3H]-GABA release did not differ between control and mdx synaptosomes. α7-containing and ß2-containing nAChRs were involved in nicotine-induced [3H]-GABA release in control and mdx synaptosomes. Kinetic analysis of [3H]-GABA uptake in mdx CBL synaptosomes showed a reduced (50%) half-maximal uptake time (t1/2) and increased (44%) rate of [3H]-GABA uptake (Vmax) compared to controls. The apparent transporter affinity (Km) for GABA was not altered. Our findings show that dystrophin deficiency in mdx mice is associated with significant changes in the release and uptake of GABA in the CBL. These presynaptic alterations may be related to the reported decrease in postsynaptic GABAAR in the same brain region. The results indicate possible dysfunction of GABAergic synapses associated with dystrophin deficiency in the CBL, which may contribute to the cognitive and neurobehavioral disorders in mdx mice and patients with DMD.