Abstract 19: Stimulatory Effects of Fructose vs. Glucose on Brain Reward Activation and Hunger are Heightened in Obese Young Adults

Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Kathleen Page ◽  
Shan Luo ◽  
Sandra Huang ◽  
Ana Romero ◽  
John Monterosso

Increases in consumption of sugar-sweeteners are linked to obesity, diabetes and cardiovascular disease. Studies by our group and others suggest that the fructose component of sugar-sweeteners may act centrally to promote overeating behavior. Using functional magnetic resonance imaging (fMRI), we previously demonstrated that, unlike glucose, fructose ingestion failed to reduce neuronal activity in brain appetite and reward regions and failed to increase satiety in normal-weight adults. The objective of this study was to test the hypothesis that fructose compared to glucose ingestion would cause greater food-cue reactivity in brain reward areas and greater hunger, and that these differential effects would be heightened in obese compared to lean individuals. This study is part of a larger ongoing double-blinded, random-order crossover study on brain, hormone and appetitive responses to acute consumption of drinks containing 75 grams (300kcal) fructose or an equivalent dose of glucose. fMRI scans were performed using a 3-Tesla scanner on 13 participants, 5 obese (3 female,2 male; age 22±2, BMI 37±3.8) and 8 lean (3 female,5 male; age 21±2, BMI 22.8±1.7). Scanning was performed while participants viewed images of high-calorie food pictures and non-food items using a block design. Appetite scales were obtained before and 60 min after drink ingestion. Blood-oxygen level dependent (BOLD) sequences were used to measure brain responses to food and non-food cues after drink ingestion. Paired-t tests were performed to examine drink effects on BOLD responses to high-calorie food vs. non-food cues and hunger responses. Obese vs. lean comparison of drink effects were analyzed using independent samples T-tests. In the total group, fructose vs. glucose ingestion resulted in greater activation of the amygdala (9.1±4, p=.045) and the nucleus accumbens (11.4±6, p=.07), brain regions that mediate reward and pleasure. There were no significant differences in baseline hunger ratings between sessions. However, hunger ratings were significantly greater after consumption of fructose compared to glucose (1.9±0.6, p=.011). Body mass index (BMI) group interactions were seen with drink condition. Amygdala activation was significantly greater after fructose vs. glucose ingestion in the obese group (t(1,4)=4.406, p=0.01), but not the lean group (t(1,7)=0.754, p=0.48). Ratings of hunger tended to be higher after fructose vs. glucose ingestion in the obese compared to the lean group but the differences were not statistically significant with this sample size (p=0.15). In conclusion, these results demonstrate that acute consumption of fructose compared to glucose results in greater brain reward activation to high-calorie food cues and increased hunger. These disparate responses to fructose vs. glucose ingestion were heightened in obese individuals and may play a role in promoting overeating behavior.

2015 ◽  
Vol 112 (20) ◽  
pp. 6509-6514 ◽  
Author(s):  
Shan Luo ◽  
John R. Monterosso ◽  
Kayan Sarpelleh ◽  
Kathleen A. Page

Prior studies suggest that fructose compared with glucose may be a weaker suppressor of appetite, and neuroimaging research shows that food cues trigger greater brain reward responses in a fasted relative to a fed state. We sought to determine the effects of ingesting fructose versus glucose on brain, hormone, and appetitive responses to food cues and food-approach behavior. Twenty-four healthy volunteers underwent two functional magnetic resonance imaging (fMRI) sessions with ingestion of either fructose or glucose in a double-blinded, random-order cross-over design. fMRI was performed while participants viewed images of high-calorie foods and nonfood items using a block design. After each block, participants rated hunger and desire for food. Participants also performed a decision task in which they chose between immediate food rewards and delayed monetary bonuses. Hormones were measured at baseline and 30 and 60 min after drink ingestion. Ingestion of fructose relative to glucose resulted in smaller increases in plasma insulin levels and greater brain reactivity to food cues in the visual cortex (in whole-brain analysis) and left orbital frontal cortex (in region-of-interest analysis). Parallel to the neuroimaging findings, fructose versus glucose led to greater hunger and desire for food and a greater willingness to give up long-term monetary rewards to obtain immediate high-calorie foods. These findings suggest that ingestion of fructose relative to glucose results in greater activation of brain regions involved in attention and reward processing and may promote feeding behavior.


Obesity ◽  
2013 ◽  
Vol 21 (10) ◽  
pp. 2029-2036 ◽  
Author(s):  
Shan Luo ◽  
Ana Romero ◽  
Tanja C. Adam ◽  
Houchun H. Hu ◽  
John Monterosso ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Sabrina Jones ◽  
Shan Luo ◽  
Hilary M. Dorton ◽  
Alexandra G. Yunker ◽  
Brendan Angelo ◽  
...  

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.


2017 ◽  
Vol 43 (5) ◽  
pp. 1987-2000 ◽  
Author(s):  
Qiang Li ◽  
Rongbing Jin ◽  
Hao Yu ◽  
Hongmei Lang ◽  
Yuanting Cui ◽  
...  

Background/Aims: Obesity and high salt intake are major risk factors for hypertension and cardiometabolic diseases. Obese individuals often consume more dietary salt. We aim to examine the neurophysiologic effects underlying obesity-related high salt intake. Methods: A multi-center, random-order, double-blind taste study, SATIETY-1, was conducted in the communities of four cities in China; and an interventional study was also performed in the local community of Chongqing, using brain positron emission tomography/computed tomography (PET/CT) scanning. Results: We showed that overweight/obese individuals were prone to consume a higher daily salt intake (2.0 g/day higher compared with normal weight individuals after multivariable adjustment, 95% CI, 1.2-2.8 g/day, P < 0.001), furthermore they exhibited reduced salt sensitivity and a higher salt preference. The altered salty taste and salty preference in the overweight/obese individuals was related to increased activity in brain regions that included the orbitofrontal cortex (OFC, r = 0.44, P= 0.01), insula (r = 0.38, P= 0.03), and parahippocampus (r = 0.37, P= 0.04). Conclusion: Increased salt intake among overweight/obese individuals is associated with altered salt sensitivity and preference that related to the abnormal activity of gustatory cortex. This study provides insights for reducing salt intake by modifying neural processing of salty preference in obesity.


Author(s):  
M. A. Stopyra ◽  
H.-C. Friederich ◽  
N. Lavandier ◽  
E. Mönning ◽  
M. Bendszus ◽  
...  

Abstract Objectives Food intake in obesity has been found to be reward-based and less contingent on homeostatic needs. Accordingly, previous studies investigating neural processing of food cues observed aberrant processing in reward- and control-related brain regions in obesity. To further investigate the relation between homeostasis and food intake, this study investigated the influence of glucose metabolism on the neuronal response during the regulation of food craving in participants with obesity. Methods Twenty-five normal-weight and 25 women with obesity were examined on two occasions after receiving either water or glucose directly into the stomach using a nasogastric tube. Participants were blinded to the type of infusion and were required to refrain from eating for 16 h before each visit. An event-related fMRI paradigm was used to investigate the effect of intestinal glucose load on the neuronal response during the regulation of food craving. Results A 2 × 2 mixed-model ANOVA revealed that craving regulation was associated with increased activation in fronto-parietal regions in participants with obesity when compared to healthy controls. However, this effect was observed independently from homeostatic satiety. A regression analysis revealed that the reduction of food craving was related to increased activation in the lingual gyrus in individuals with obesity following the infusion of water. Conclusions In participants with obesity, the neuronal response during the regulation of food craving is associated with increased neural cognitive top-down control and increased visual food processing. Since this observation was independent from satiety status, our results indicate a reduced influence of homeostasis on neural processing during food craving in obesity. This study was registered on clinicaltrials.org: NCT03075371.


Appetite ◽  
2012 ◽  
Vol 58 (1) ◽  
pp. 303-312 ◽  
Author(s):  
Anastasia Dimitropoulos ◽  
Jean Tkach ◽  
Alan Ho ◽  
James Kennedy
Keyword(s):  

2021 ◽  
Vol 11 (12) ◽  
pp. 1587
Author(s):  
Yingkai Yang ◽  
Qian Wu ◽  
Filip Morys

Overconsumption of high-calorie or unhealthy foods commonly leads to weight gain. Understanding people’s neural responses to high-calorie food cues might help to develop better interventions for preventing or reducing overeating and weight gain. In this review, we conducted a coordinate-based meta-analysis of functional magnetic resonance imaging studies of viewing high-calorie food cues in both normal-weight people and people with obesity. Electronic databases were searched for relevant articles, retrieving 59 eligible studies containing 2410 unique participants. The results of an activation likelihood estimation indicate large clusters in a range of structures, including the orbitofrontal cortex (OFC), amygdala, insula/frontal operculum, culmen, as well as the middle occipital gyrus, lingual gyrus, and fusiform gyrus. Conjunction analysis suggested that both normal-weight people and people with obesity activated OFC, supporting that the two groups share common neural substrates of reward processing when viewing high-calorie food cues. The contrast analyses did not show significant activations when comparing obesity with normal-weight. Together, these results provide new important evidence for the neural mechanism underlying high-calorie food cues processing, and new insights into common and distinct brain activations of viewing high-calorie food cues between people with obesity and normal-weight people.


2018 ◽  
Vol 314 (5) ◽  
pp. E522-E529 ◽  
Author(s):  
Renata Belfort-DeAguiar ◽  
Dongju Seo ◽  
Cheryl Lacadie ◽  
Sarita Naik ◽  
Christian Schmidt ◽  
...  

Blood glucose levels influence brain regulation of food intake. This study assessed the effect of mild physiological hyperglycemia on brain response to food cues in individuals with obesity (OB) versus normal weight individuals (NW). Brain responses in 10 OB and 10 NW nondiabetic healthy adults [body mass index: 34 (3) vs. 23 (2) kg/m2, means (SD), P < 0.0001] were measured with functional MRI (blood oxygen level-dependent contrast) in combination with a two-step normoglycemic-hyperglycemic clamp. Participants were shown food and nonfood images during normoglycemia (~95 mg/dl) and hyperglycemia (~130 mg/dl). Plasma glucose levels were comparable in both groups during the two-step clamp ( P = not significant). Insulin and leptin levels were higher in the OB group compared with NW, whereas ghrelin levels were lower (all P < 0.05). During hyperglycemia, insula activity showed a group-by-glucose level effect. When compared with normoglycemia, hyperglycemia resulted in decreased activity in the hypothalamus and putamen in response to food images ( P < 0.001) in the NW group, whereas the OB group exhibited increased activity in insula, putamen, and anterior and dorsolateral prefrontal cortex (aPFC/dlPFC; P < 0.001). These data suggest that OB, compared with NW, appears to have disruption of brain responses to food cues during hyperglycemia, with reduced insula response in NW but increased insula response in OB, an area involved in food perception and interoception. In a post hoc analysis, brain activity in obesity appears to be associated with dysregulated motivation (striatum) and inappropriate self-control (aPFC/dlPFC) to food cues during hyperglycemia. Hyperstimulation for food and insensitivity to internal homeostatic signals may favor food consumption to possibly play a role in the pathogenesis of obesity.


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