Abstract
The modern diet has become highly sweetened, resulting in unprecedented levels of sugar consumption, particularly among adolescents. While chronic long-term sugar intake is known to contribute to the development of metabolic disorders including obesity and type II diabetes, little is known regarding the direct consequences of long-term, binge-like sugar consumption on the brain. Because sugar can cause the release of dopamine in the nucleus accumbens (NAc) similarly to drugs of abuse, we investigated changes in the morphology of neurons in this brain region following short- (4 weeks) and long-term (12 weeks) binge-like sucrose consumption using an intermittent two-bottle choice paradigm. We used Golgi-Cox staining to impregnate medium spiny neurons (MSNs) from the NAc core and shell of short- and long-term sucrose consuming rats and compared these to age-matched water controls. We show that prolonged binge-like sucrose consumption significantly decreased the total dendritic length of NAc shell MSNs compared to age-matched control rats. We also found that the restructuring of these neurons resulted primarily from reduced distal dendritic complexity. Conversely, we observed increased spine densities at the distal branch orders of NAc shell MSNs from long-term sucrose consuming rats. Combined, these results highlight the neuronal effects of prolonged binge-like intake of sucrose on NAc shell MSN morphology.
Highlights
Over the last 40 years, there has been a documented rise in the consumption of sugar-sweetened beverages and foods containing added sugars (Nielsen et al, 2002; Popkin, 2010; Ng et al, 2012), with reports estimating that up to 75% of all foods and beverages contain high amounts of added sugars (Ford and Dietz, 2013; Bray and Popkin, 2014)
Following short-term (4 weeks) sucrose consumption, there were no significant differences in nucleus accumbens (NAc) shell medium spiny neurons (MSNs) morphometric parameters (Table 1)
We used a model of binge-sucrose consumption in rats to determine the effects of short- (4 weeks) and long-term (12 weeks) sucrose consumption on neuronal morphology of MSNs in the NAc, a key component of the overlapping reward circuitry that is modulated by sugar and addictive drugs
Summary
Over the last 40 years, there has been a documented rise in the consumption of sugar-sweetened beverages and foods containing added sugars (Nielsen et al, 2002; Popkin, 2010; Ng et al, 2012), with reports estimating that up to 75% of all foods and beverages contain high amounts of added sugars (Ford and Dietz, 2013; Bray and Popkin, 2014). Because binge-eating individuals often exhibit a loss of control and an inability to self-limit their sugar intake, it is likely that these behaviors arise as a result of neurological adaptations in brain regions that evaluate the hedonic value of highly palatable food (Saper et al, 2002; Lutter and Nestler, 2009; Kenny, 2011) This rationale is supported by evidence in humans demonstrating that sugar and sweetness can cause cravings that are similar to those induced by addictive drugs such as alcohol and nicotine (Volkow et al, 2012)
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