scholarly journals Academic stress and personality interact to increase the neural response to high-calorie food cues

Appetite ◽  
2017 ◽  
Vol 116 ◽  
pp. 306-314 ◽  
Author(s):  
Selin Neseliler ◽  
Beth Tannenbaum ◽  
Maria Zacchia ◽  
Kevin Larcher ◽  
Kirsty Coulter ◽  
...  
Trials ◽  
2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Mojca Jensterle ◽  
Simona Ferjan ◽  
Tadej Battelino ◽  
Jernej Kovač ◽  
Saba Battelino ◽  
...  

Abstract Background Preclinical studies demonstrated that glucagon-like peptide 1 (GLP-1) is locally synthesized in taste bud cells and that GLP-1 receptor exists on the gustatory nerves in close proximity to GLP-1-containing taste bud cells. This local paracrine GLP-1 signalling seems to be specifically involved in the perception of sweets. However, the role of GLP-1 in taste perception remains largely unaddressed in clinical studies. Whether any weight-reducing effects of GLP-1 receptor agonists are mediated through the modulation of taste perception is currently unknown. Methods and analysis This is an investigator-initiated, randomized single-blind, placebo-controlled clinical trial. We will enrol 30 women with obesity and polycystic ovary syndrome (PCOS). Participants will be randomized in a 1:1 ratio to either semaglutide 1.0 mg or placebo for 16 weeks. The primary endpoints are alteration of transcriptomic profile of tongue tissue as changes in expression level from baseline to follow-up after 16 weeks of treatment, measured by RNA sequencing, and change in taste sensitivity as detected by chemical gustometry. Secondary endpoints include change in neural response to visual food cues and to sweet-tasting substances as assessed by functional MRI, change in body weight, change in fat mass and change in eating behaviour and food intake. Discussion This is the first study to investigate the role of semaglutide on taste perception, along with a neural response to visual food cues in reward processing regions. The study may identify the tongue and the taste perception as a novel target for GLP-1 receptor agonists. Ethics and disseminations The study has been approved by the Slovene National Medical Ethics Committee and will be conducted in accordance with the Declaration of Helsinki and Good Clinical Practice guidelines. Results will be submitted for publication in an international peer-reviewed scientific journal. Trial registration ClinicalTrials.govNCT04263415. Retrospectively registered on 10 February 2020


2020 ◽  
Author(s):  
Yang Hu ◽  
Gang Ji ◽  
Guanya Li ◽  
Peter Manza ◽  
Wenchao Zhang ◽  
...  

Abstract The biological mediators that support cognitive-control and long-term weight-loss after laparoscopic sleeve gastrectomy (LSG) remain unclear. We measured peripheral appetitive hormones and brain functional-connectivity (FC) using magnetic-resonance-imaging with food cue-reactivity task in 25 obese participants at pre, 1 month, and 6 month after LSG, and compared with 30 normal weight controls. We also used diffusion-tensor-imaging to explore whether LSG increases brain structural-connectivity (SC) of regions involved in food cue-reactivity. LSG significantly decreased BMI, craving for high-calorie food cues, ghrelin, insulin, and leptin levels, and increased self-reported cognitive-control of eating behavior. LSG increased FC between the right dorsolateral prefrontal cortex (DLPFC) and the pregenual anterior cingulate cortex (pgACC) and increased SC between DLPFC and ACC at 1 month and 6 month after LSG. Reduction in BMI correlated negatively with increased FC of right DLPFC-pgACC at 1 month and with increased SC of DLPFC-ACC at 1 month and 6 month after LSG. Reduction in craving for high-calorie food cues correlated negatively with increased FC of DLPFC-pgACC at 6 month after LSG. Additionally, SC of DLPFC-ACC mediated the relationship between lower ghrelin levels and greater cognitive control. These findings provide evidence that LSG improved functional and structural connectivity in prefrontal regions, which contribute to enhanced cognitive-control and sustained weight-loss following surgery.


BJPsych Open ◽  
2016 ◽  
Vol 2 (4) ◽  
pp. 255-261 ◽  
Author(s):  
Stefanie Horndasch ◽  
Sophie O'Keefe ◽  
Anneka Lamond ◽  
Katie Brown ◽  
Ciara McCabe

BackgroundWe have previously shown increased anticipatory and consummatory neural responses to rewarding and aversive food stimuli in women recovered from anorexia nervosa (AN).AimsTo determine whether these differences are trait markers for AN, we examined the neural response in those with a familial history but no personal history of AN.MethodThirty-six volunteers were recruited: 15 who had a sister with anorexia nervosa (family history) and 21 control participants. Using fMRI we examined the neural response during an anticipatory phase (food cues, rewarding and aversive), an effort phase and a consummatory phase (rewarding and aversive tastes).ResultsFamily history (FH) volunteers showed increased activity in the caudate during the anticipation of both reward and aversive food and in the thalamus and amygdala during anticipation of aversive only. FH had decreased activity in the dorsal anterior cingulate cortex, the pallidum and the superior frontal gyrus during taste consumption.ConclusionsIncreased neural anticipatory but decreased consummatory responses to food might be a biomarker for AN. Interventions that could normalise these differences may help to prevent disorder onset.


2016 ◽  
Vol 108 ◽  
pp. 145
Author(s):  
Mooah Lee ◽  
Ji-Won Hur ◽  
Hyung-Jin Choi ◽  
Jang-Han Lee

2013 ◽  
Vol 120 ◽  
pp. 233-242 ◽  
Author(s):  
Matthew S. Tryon ◽  
Cameron S. Carter ◽  
Rashel DeCant ◽  
Kevin D. Laugero

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

2017 ◽  
Vol 49 (5S) ◽  
pp. 874
Author(s):  
Bruce Bailey ◽  
Jillesa Anderson ◽  
Chase Glenn ◽  
Michael Larson ◽  
James LeCheminant

2018 ◽  
Vol 115 (48) ◽  
pp. E11238-E11247 ◽  
Author(s):  
Rebecca G. Boswell ◽  
Wendy Sun ◽  
Shosuke Suzuki ◽  
Hedy Kober

Obesity rates continue to rise alarmingly, with dire health implications. One contributing factor is that individuals frequently forgo healthy foods in favor of inexpensive, high-calorie, unhealthy foods. One important mechanism underlying these choices is food craving: Craving increases with exposure to unhealthy foods (and food cues, such as advertisements) and prospectively predicts eating and weight. Prior work has shown that cognitive regulation strategies that emphasize the negative consequences of unhealthy foods reduce craving. In Studies 1 and 2, we show that cognitive strategies also increase craving for healthy foods by emphasizing their positive benefits, and change food valuation (willingness to pay) for both healthy and unhealthy foods. In Studies 3 and 4, we demonstrate that brief training in cognitive strategies (“Regulation of Craving Training”; ROC-T) increases subsequent healthy (vs. unhealthy) food choices. This was striking because this change in food choices generalized to nontrained items. Importantly, in Study 5, we show that brief training in cognitive strategies also reduces food consumption by 93–121 calories. Consumed calories correlated with changes in food choice. Finally, in Study 6, we show that the training component of ROC-T is necessary, above and beyond any effect of framing. Across all studies (NTOTAL = 1,528), we find that cognitive strategies substantially change craving and food valuation, and that training in cognitive strategies improves food choices by 5.4–11.2% and reduces unhealthy eating, including in obese individuals. Thus, these findings have important theoretical, public health, and clinical implications for obesity prevention and treatment.


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