Skip to main page content
Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
, 5, 33
eCollection

Consumption of Alcopops During Brain Maturation Period: Higher Impact of Fructose Than Ethanol on Brain Metabolism

Affiliations

Consumption of Alcopops During Brain Maturation Period: Higher Impact of Fructose Than Ethanol on Brain Metabolism

Dounia El Hamrani et al. Front Nutr.

Abstract

Alcopops are flavored alcoholic beverages sweetened by sodas, known to contain fructose. These drinks have the goal of democratizing alcohol among young consumers (12-17 years old) and in the past few years have been considered as fashionable amongst teenagers. Adolescence, however, is a key period for brain maturation, occurring in the prefrontal cortex and limbic system until 21 years old. Therefore, this drinking behavior has become a public health concern. Despite the extensive literature concerning the respective impacts of either fructose or ethanol on brain, the effects following joint consumption of these substrates remains unknown. Our objective was to study the early brain modifications induced by a combined diet of high fructose (20%) and moderate amount of alcohol in young rats by 13C Nuclear Magnetic Resonance (NMR) spectroscopy. Wistar rats had isocaloric pair-fed diets containing fructose (HF, 20%), ethanol (Et, 0.5 g/day/kg) or both substrates at the same time (HFEt). After 6 weeks of diet, the rats were infused with 13C-glucose and brain perchloric acid extracts were analyzed by NMR spectroscopy (1H and 13C). Surprisingly, the most important modifications of brain metabolism were observed under fructose diet. Alterations, observed after only 6 weeks of diet, show that the brain is vulnerable at the metabolic level to fructose consumption during late-adolescence throughout adulthood in rats. The main result was an increase in oxidative metabolism compared to glycolysis, which may impact lactate levels in the brain and may, at least partially, explain memory impairment in teenagers consuming alcopops.

Keywords: 13C NMR; alcopops; astrocytes; brain metabolism; designer drinks; high fructose; moderate ethanol; rat.

Figures

Figure 1
Figure 1
Body weight (A) and food intake (B) of rats fed with control diet (CT), high fructose diet (HF), ethanol (Et), or a mix (HFEt) during 6 weeks. Values are mean ± SEM (n = 8/diet for each time point). a: Statistical difference between CT vs. HF, Et, and HFEt from the 10th day until the end of the protocol. b: Statistical difference between HFEt vs. HF and Et from the 17th day until the end of the protocol.
Figure 2
Figure 2
Ratio glycemia/insulinemia in rats after 6-week diet with either control (CT), high fructose (HF), ethanol (Et), or a mix diet (HFEt) and prior infusion of [1-13C]D-glucose. Glucose and insulin content were measured in a blood sample collected just before [1-13C]glucose infusion and after 6 weeks of diet to detect any disturbance in insulin and therefore glucose metabolism homeostasis at this time point. Values are mean ± SEM. *Statistical difference between CT and HFEt.
Figure 3
Figure 3
Specific enrichment of glucose 13C (% 13C) obtained in the brain following 1 h of [1-13C]D-glucose infusion in rats fed with control (CT), high fructose (HF), ethanol (Et), or a mix diet (HFEt). Specific enrichments were normalized to the Glucose C1 specific enrichment in each group.
Figure 4
Figure 4
Schematic representation of metabolite labeling from [1-13C]glucose during the first tricarboxylic acid (TCA) cycle turn. In astrocytes, [1-13C]glucose follows either the pyruvate dehydrogenase (PDH; formula image) or the pyruvate carboxylase (PC; formula image), but only the PDH pathway occurs in neurons. At the end of the glycolysis, [1-13C]glucose provides [3-13C]pyruvate which can take two paths: either pyruvate dehydrogenase (PDH; formula image) or pyruvate carboxylase (PC; formula image). In the PDH pathway, [3-13C]pyruvate gives [2-13C]AcCoA which enters in the TCA cycle and leads to [4-13C]citrate, then to [4-13C] αKG. This intermediate αKG forms [4-13C]glutamate, which is metabolized in [4-13C]glutamine. Through TCA cycle, by the symmetry of some intermediates, [4-13C]αKG gives two isotopomers of OAA: [2-13C]OAA (50%) and [3-13C]OAA (50%). Then, it provides Asparate labeled in [2-13C] (50%) and [3-13C](50%). In the PC pathway (only in astrocyte compartment), [3-13C]pyruvate is converted in [3-13C]OAA which enters TCA cycle to form [2-13C]αKetoGlu which leads to [2-13C]glutamate and then to [2-13C]glutamine. α-KG, α-ketoglutarate; Ala, alanine; AcCoA, acetyl-CoA; Glu, glutamate; Gln, glutamine; GABA, γ-aminobutyric acid; Lac, lactate; OAA, oxaloacetate.
Figure 5
Figure 5
13C-specific enrichments (%) of some carbon positions of some brain metabolites after 1 h infusion of [1-13C]glucose in rats fed with control (CT), high fructose (HF), ethanol (Et) or mixed (HFEt) diet. *Statistical difference between CT and HF.

Similar articles

See all similar articles

References

    1. Metzner C, Kraus L. The impact of alcopops on adolescent drinking: a literature review. Alcohol Alcohol. (2008) 43:230–9. 10.1093/alcalc/agm148 - DOI - PubMed
    1. Federal Trade Commission (2003). Alcohol Marketing and Advertising. A Report to Congress. Available online at: https://www.ftc.gov/sites/default/files/documents/reports/alcohol-marketing-and-advertising-federal-trade-commission-report-congress-september-2003/alcohol08report.pdf (media resource library).
    1. Albers AB, Siegel M, Ramirez RL, Ross C, DeJong W, Jernigan DH. Flavored alcoholic beverage use, risky drinking behaviors, and adverse outcomes among underage drinkers: results from the ABRAND Study. Am J Public Health (2015) 105:810–5. 10.2105/AJPH.2014.302349 - DOI - PMC - PubMed
    1. Jones SC, Reis S. Not just the taste: why adolescents drink alcopops. Health Educ. (2011) 112:61–74. 10.1108/09654281211190263 - DOI
    1. Bava S, Tapert SF. Adolescent brain development and the risk for alcohol and other drug problems. Neuropsychol Rev. (2010) 20:398–413. 10.1007/s11065-010-9146-6 - DOI - PMC - PubMed
Feedback