Catecholaminergic and cholinergic systems of mouse brain are modulated by LMN diet, rich in theobromine, polyphenols and polyunsaturated fatty acids

Fernández-Fernández, Laura; Esteban, Gerard; Giralt, Mercedes; Valente, Tony; Bolea, Irène; Solé, Montse; Sun, Ping; Benítez, Susana; Morelló, José Ramón; Reguant, Jordi; Ramírez, Bartolomé; Hidalgo, Juan; Unzeta, Mercedes

doi:10.1039/c5fo00052a

Cited by 21 publications

(11 citation statements)

References 29 publications

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“…For example, quercetin, a type of flavonoid, suppressed a decrease in brain serotonin concentration via inhibition of monoamine oxidase A (Maoa; an enzyme that metabolizes serotonin) 33 . In mice fed theobromine for 20 days, significant increases in DA and NE concentrations in the striatum in association with elevated Th expression in the SN have been reported 34 . The expression of Th significantly increased in the cerebral cortex when rosemary extract containing 4% RA was orally administered for one week 22 .…”

Section: Discussionmentioning

confidence: 99%

Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion

Hase

Shishido

Yamamoto

et al. 2019

Sci Rep

106

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A new mechanism is revealed by which a polyphenol, rosmarinic acid (RA), suppresses amyloid β (Aβ) accumulation in mice. Here we examined the brains of mice (Alzheimer’s disease model) using DNA microarray analysis and revealed that the dopamine (DA)-signaling pathway was enhanced in the group fed RA versus controls. In the cerebral cortex, the levels of monoamines, such as norepinephrine, 3,4-dihydroxyphenylacetic acid, DA, and levodopa, increased after RA feeding. The expression of DA-degrading enzymes, such as monoamine oxidase B (Maob), was significantly downregulated in the substantia nigra and ventral tegmental area, both DA synthesis regions. Following in vitro studies showing that monoamines inhibited Aβ aggregation, this in vivo study, in which RA intake increased concentration of monoamine by reducing Maob gene expression, builds on that knowledge by demonstrating that monoamines suppress Aβ aggregation. In conclusion, RA-initiated monoamine increase in the brain may beneficially act against AD.

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Section: Discussionmentioning

confidence: 99%

Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion

Hase

Shishido

Yamamoto

et al. 2019

Sci Rep

106

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“…the -adrenergic receptor [28][29][30] in part because they share a similar chemical structure with catecholamine [31].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Grape pomace extract induced beige cells in white adipose tissue from rats and in 3T3-L1 adipocytes

Lanzi

Perdicaro

Landa

et al. 2018

The Journal of Nutritional Biochemistry

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This study investigated the effects of a grape pomace extract (GPE) rich in phenolic compounds on brown-like adipocyte induction and adiposity in spontaneously hypertensive (SHR) and control normotensive Wistar-Kyoto (WKY) rats fed a high-fat diet (HFD). HFD consumption for 10 weeks significantly increased epididymal white adipose tissue (eWAT) in WKY but not in SHR rats. Supplementation with GPE (300 mg/kg body weight/day) reduced adipocyte diameter and increased levels of proteins that participate in adipogenesis and angiogenesis, i.e., peroxisome-proliferator activated receptor gamma (PPARγ), vascular endothelial grow factor-A (VEGF-A) and its receptor 2 (VEGF-R2), and partially increased the uncoupling protein 1 (UCP-1) in WKY. In both strains, GPE attenuated adipose inflammation. In eWAT from SHR, GPE increased the expression of proteins involved in adipose tissue "browning," i.e., PPARγ-coactivator-1α (PGC-1α), PPARγ, PR domain containing 16 (PRDM16) and UCP-1. In primary cultures of SHR adipocytes, GPE-induced UCP-1 up-regulation was dependent on p38 and ERK activation. Accordingly, in 3T3-L1 adipocytes treated with palmitate, the addition of GPE (30 μM) activated the β-adrenergic signaling cascade (PKA, AMPK, p38, ERK). This led to the associated up-regulation of proteins involved in mitochondrial biogenesis (PGC-1α, PPARγ, PRDM16 and UCP-1) and fatty acid oxidation (ATGL). These effects were similar to those exerted by (-)-epicatechin and quercetin, major phenolic compounds in GPE. Overall, in HFD-fed rats, supplementation with GPE promoted brown-like cell formation in eWAT and diminished adipose dysfunction. Thus, winemaking residues, rich in bioactive compounds, could be useful to mitigate the adverse effects of HFD-induced adipose dysfunction.

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“…(2015) showing a significant decrease of cognitive impairment when mice were fed with a diet rich in theobromine, polyphenols, and polyunsaturated acids (LMN diet). The mechanism in the mouse brain may likely involve the modulation of the catecholaminergic and cholinergic systems .…”

Section: Mtxs and Neurodegenerative Diseasesmentioning

confidence: 99%

Health benefits of methylxanthines in neurodegenerative diseases

Oñatibia-Astibia¹,

Franco

Martínez‐Pinilla

2017

Molecular Nutrition Food Res

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Methylxanthines (MTXs) are consumed by almost everybody in almost every area of the world. Caffeine, theophylline and theobromine are the most well-known members of this family of compounds; they are present, inter alia, in coffee, tea, cacao, yerba mate and cola drinks. MTXs are readily absorbed in the gastrointestinal tract and are able to penetrate into the central nervous system, where they exert significant psychostimulant actions, which are more evident in acute intake. Coffee has been paradigmatic, as its use was forbidden in many diseases, however, this negative view has radically changed; evidence shows that MTXs display health benefits in diseases involving cell death in the nervous system. This paper reviews data that appraise the preventive and even therapeutic potential of MTXs in a variety of neurodegenerative diseases. Future perspectives include the use of MTXs to advance the understanding the pathophysiology of, inter alia, Alzheimer's disease (AD) and Parkinson's disease (PD), and the use of the methylxanthine chemical moiety as a basis for the development of new and more efficacious drugs.

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Catecholaminergic and cholinergic systems of mouse brain are modulated by LMN diet, rich in theobromine, polyphenols and polyunsaturated fatty acids

Abstract: LMN diet could benefit the cognitive reserve reducing Alzheimer's disease risk.

Cited by 21 publications

References 29 publications

Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion

Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion

Grape pomace extract induced beige cells in white adipose tissue from rats and in 3T3-L1 adipocytes

Health benefits of methylxanthines in neurodegenerative diseases

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