Abstract
It has been hypothesized that the incretin hormone, glucagon-like peptide-1 (GLP-1), decreases overeating by influencing mesolimbic brain regions that process food-cues, including the dorsal striatum. We previously showed that habitual added sugar intake was associated with lower glucose-induced circulating GLP-1 and a greater striatal response to high calorie food cues in lean individuals. Less is known about how dietary added sugar and obesity may interact to affect postprandial GLP-1 and its relationship to striatal responses to food cues and feeding behavior. The current study aimed to expand upon previous research by assessing how circulating GLP-1 and striatal food cue reactivity are affected by acute glucose consumption in participants with varied BMIs and amounts of habitual consumption of added sugar. This analysis included 72 participants from the Brain Response to Sugar Study who completed two study visits where they consumed either plain water or 75g glucose dissolved in water (order randomized; both drinks were flavored with non-caloric cherry flavoring) and underwent repeated blood sampling, a functional magnetic resonance imaging (fMRI) based food-cue task, and an ad-libitum buffet meal. Correlations between circulating GLP-1 levels, striatal food-cue reactivity, and food intake were assessed, and interactions between obesity and added sugar on GLP-1 and striatal responses were examined. An interaction between BMI and dietary added sugar was associated with reduced post-glucose GLP-1 secretion. Participants who were obese and consumed high levels of added sugar had the smallest increase in plasma GLP-1 levels. Glucose-induced GLP-1 secretion was correlated with lower dorsal striatal reactivity to high-calorie versus low-calorie food-cues, driven by an increase in reactivity to low calorie food-cues. The increase in dorsal striatal reactivity to low calorie food-cues was negatively correlated with sugar consumed at the buffet. These findings suggest that an interaction between obesity and dietary added sugar intake is associated with additive reductions in postprandial GLP-1 secretion. Additionally, the results suggest that changes to dorsal striatal food cue reactivity through a combination of dietary added sugar and obesity may affect food consumption.
Highlights
Obesity among U.S adults has reached over 40% of the total population [1]
Across all participants, paired t-tests showed that circulating glucagon-like peptide-1 (GLP-1) levels significantly increased 10 min (t(65)=6.26, 95%confidence intervals (CI) [8.01, 15.5], p
To our knowledge this is the first study to illustrate that an interaction between Body mass index (BMI) and dietary added sugar intake is associated with altered postprandial GLP-1 secretion
Summary
Obesity among U.S adults has reached over 40% of the total population [1]. In order to combat this public health crisis, recent research has been aimed at identifying interactions between neural and hormonal mechanisms that underly energy regulation and the factors that can disrupt typical functioning, inducing a cycle of overeating and excess weight gain. One hormone that has been identified as a key influence in the control of consummatory behavior is glucagon-like peptide-1 (GLP-1). Endogenous GLP-1 is elevated following glucose consumption [4] and improves glucose metabolism by augmenting glucose stimulated insulin secretion [5] and decreasing glucagon levels [4]. Along with its effects on glucose metabolism, GLP-1 has been implicated in altering the brain’s processing of both food and drug rewards [6] through its influence on the mesolimbic system [7,8,9]. A previous study from our laboratory [15] found a negative correlation between GLP-1 response to oral glucose and activation of the dorsal striatum in response to high-calorie food images, relative to nonfood images, in lean young adults
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