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Introduction

Sweet taste perception is an innate capacity that depends on two G-protein-coupled subunit receptors, T1R2 and T1R3, located on the tongue [1][2]. The stimulation of these receptors by diets rich in sweet tastants, such as, for instance, sugar-sweetened beverages (soft drinks, colas, fruit beverages), generates a sensation that most humans and other mammals, including rodents, find intensely rewarding [3][6]. Once reserved to a small elite, the consumption of highly sweetened diets is now highly prevalent in developed countries and is escalating elsewhere [7][8]. Though difficult to estimate, sweet sensations evoked by sugar-sweetened foods and drinks are probably one of the most precocious, frequent and intense sensory pleasures of modern humans [7][9]. However, the current pursuit of sweet sensations far exceeds metabolic needs and is thought to contribute, together with several other factors [10][13], to drive the current obesity epidemic [7][14].

The passive overconsumption of sugar-sweetened diets has often been compared to drug addiction, though this parallel was based until very recently more on anecdotal evidence than on solid scientific grounds. More recently, mounting evidence from experimental research on animals, especially rats, have unearthed deep commonalities between overconsumption of sugars and drug addiction [15][17]. First, both sweet tastants [18][19] and drugs of abuse [20][21] stimulate dopamine signaling in the ventral striatum, a brain signaling pathway critically involved in reward processing and learning [22][23]. Second, both cross-tolerance [24][25] and cross-dependence [26][28] have been observed between sugars and drugs of abuse. For instance, animals with a long history of sucrose consumption become tolerant to the analgesic effects of morphine [25]. In addition, naloxone–an opiate antagonist–precipitates in rats with sugar overconsumption some of the behavioral and neurochemical signs of opiate withdrawal [28]. This latter observation is important because it shows that overconsumption of sugar-sweetened beverages may induce a dependence-like state. Finally, recent neuroimaging studies in humans have recently discovered neuroadaptations in the brain of obese individuals that mimic those previously observed in individuals addicted to cocaine and other drugs of abuse [29][30].

Overall, there are many behavioral and biological commonalities between sugar-sweetened beverages and drugs of abuse. However, the addictive potential of the former relative to the latter is much less clear. Previous research showed that concurrent access to highly sweetened water (saccharin plus glucose) can reduce self-administration of low doses of cocaine in non-dependent rats [31][32], suggesting that sweetened water may surpass cocaine reward–one of the most addictive and harmful substance currently known [33]. Whether this effect results from a genuine preference for intense sweetness or other factors (e.g., use of a suboptimal dose of cocaine and/or lack of cocaine dependence) has not been established yet, however. The present series of experiments was designed to directly address this question. We developed a discrete-trials choice procedure to measure the reward value of an intense sweet taste relative to intravenous cocaine. This procedure was first tested in non-restricted, naïve rats to determine how, without any prior experience with cocaine or intense sweetness, animals learn to differentially value both types of reward. Then, the same procedure was applied to rats following an extended access to cocaine self-administration. Previous research showed that with prolonged access to cocaine, most rats develop the major signs of addiction, including drug intake escalation [34], compromised brain reward processing [35]and difficulty to stop drug seeking despite negative consequences [36].

Original article in its entirety can be found here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1931610/?fbclid=IwAR3bFnXDmOP3Qgnl2vmd0zcy5ZajKOCTLizr_epH-M2D1O28hTVlzcmyggc
Original article was published from the US National Library of Medicine National Institutes of Health

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