Abstract
Sugar consumption in the United States exceeds recommendations from the American Heart Association. Overconsumption of sugar is linked to risk for obesity and metabolic disease. Animal studies suggest that high-sugar diets alter functions in brain regions associated with reward processing, including the dorsal and ventral striatum. Human neuroimaging studies have shown that these regions are responsive to food cues, and that the gut-derived satiety hormones, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), suppress striatal food-cue responsivity. We aimed to determine the associations between dietary added sugar intake, striatal responsivity to food cues, and postprandial GLP-1 and PYY levels. Twenty-two lean volunteers underwent a functional magnetic resonance imaging (fMRI) scan during which they viewed pictures of food and non-food items after a 12-h fast. Before scanning, participants consumed a glucose drink. A subset of 19 participants underwent an additional fMRI session in which they consumed water as a control condition. Blood was sampled for GLP-1, and PYY levels and hunger ratings were assessed before and ~75 min after drink consumption. In-person 24-h dietary recalls were collected from each participant on three to six separate occasions over a 2-month period. Average percent calories from added sugar were calculated using information from 24-h dietary recalls. A region-of-interest analysis was performed to compare the blood oxygen level-dependent (BOLD) response to food vs. non-food cues in the bilateral dorsal striatum (caudate/putamen) and ventral striatum (nucleus accumbens). The relationships between added sugar, striatal responses, and hormone changes after drink consumption were assessed using Spearman’s correlations. We observed a positive correlation between added sugar intake and BOLD response to food cues in the dorsal striatum and a similar trend in the nucleus accumbens after glucose, but not water, consumption. Added sugar intake was negatively associated with GLP-1 response to glucose. Post hoc analysis revealed a negative correlation between GLP-1 response to glucose and BOLD response to food cues in the dorsal striatum. Our findings suggest that habitual added sugar intake is related to increased striatal response to food cues and decreased GLP-1 release following glucose intake, which could contribute to susceptibility to overeating.
Highlights
The average intake of added sugars in the United States has increased by 19% over the last three decades
A number of studies in animal models have shown that high-sugar diets alter the striatal dopamine system [15,16,17], including a recent study that found that 7 months of high-sugar feeding increased basal glucose metabolism in mesolimbic reward regions independent of insulin sensitivity or weight gain in Yucatan mini pigs [18]
We found that increased dietary added sugar intake, independent of sex, adiposity, and physical activity, correlates with increased striatal reactivity to food cues following glucose consumption
Summary
The average intake of added sugars in the United States has increased by 19% over the last three decades. A number of studies in animal models have shown that high-sugar diets alter the striatal dopamine system [15,16,17], including a recent study that found that 7 months of high-sugar feeding increased basal glucose metabolism in mesolimbic reward regions independent of insulin sensitivity or weight gain in Yucatan mini pigs [18]. It is currently unknown whether habitual dietary added sugar consumption is related to striatal food-cue reactivity in humans
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