TY - JOUR
T1 - Eating behavior modulates the sensitivity to the central effects of GLP-1 receptor agonist treatment
T2 - a secondary analysis of a randomized trial
AU - van Ruiten, Charlotte C.
AU - ten Kulve, Jennifer S.
AU - van Bloemendaal, Liselotte
AU - Nieuwdorp, Max
AU - Veltman, Dick J.
AU - IJzerman, Richard G.
N1 - Funding Information: R.G.IJ. is principal investigator of studies sponsored by research grants from AstraZeneca, Eli Lilly & Co., and Novo Nordisk. M.N. serves on the Scientific Advisory Board of Caelus Pharmaceuticals, the Netherlands, and Kaleido, USA. R.G.IJ and M.N. have reported that they received no personal payments in connection with the abovementioned activities, but all payments were directly transferred to the non-profit Amsterdam UMC. No other potential conflicts of interest relevant to this article were reported. Funding Information: This work was supported in part by a grant from Novo Nordisk. The funder had no role in the study design, data analyses or interpretation, or drafting of the manuscript, nor in the decision to submit the manuscript for publication. R.G.IJ. is financed by the Netherlands Organization for Scientific Research Innovational Research Incentives Scheme Veni (no. 91613082 ). M.N. received an unrestricted grant from AstraZeneca and is supported by a ZonMW-VIDI grant 2013 ( 016.146.327 ) and a Dutch Heart Foundation CVON IN CONTROL Young Talent Grant 2013. Publisher Copyright: © 2022 The Authors
PY - 2022/3/1
Y1 - 2022/3/1
N2 - Aims: We investigated if individuals with higher emotional eating scores are less sensitive to the effects of a GLP-1RA on central responses to food cues. Additionally, we investigated the associations of higher external and restraint eating scores with the sensitivity to the central effects of GLP-1RA. Methods: This secondary analysis of a randomized crossover study in people with obesity and type 2 diabetes, consisted of two periods of 12-week treatment with liraglutide or insulin glargine. Using functional MRI, we assessed the relation between baseline eating behavior and the effects of the GLP-1RA liraglutide compared with insulin after 10 days and 12 weeks of treatment on brain responses to food cues. Results: After 10 days, higher emotional eating scores were associated with less pronounced GLP-1RA induced reductions in brain responses to food pictures in the amygdala, insula and caudate nucleus. In addition, higher emotional eating scores tended to be associated with less pronounced GLP-1RA increases in brain responses to chocolate milk receipt in the caudate nucleus and insula. After 12 weeks, there were no significant associations between emotional eating scores and liraglutide-induced changes in brain responses to food cues. After 10 days, baseline external eating scores were associated with less pronounced GLP-1RA induced reductions in brain responses to food pictures in the insula, amygdala and orbitofrontal cortex. After 12 weeks, baseline restraint eating scores were associated with more GLP-1RA induced reductions in brain responses to food pictures in the insula and caudate nucleus, and with more GLP-1RA induced reductions in brain responses to the anticipation of chocolate milk in the caudate nucleus. Conclusions: Our findings indicate that individuals with higher baseline emotional eating scores are less sensitive to the central effect of GLP-1RA treatment. Additionally, external eating may also decrease, whereas restraint eating may increase the sensitivity to the treatment effects of GLP-1RAs. These insights may help to optimize treatment strategies for obesity and to select patient groups with better efficacy of GLP-1RA treatment.
AB - Aims: We investigated if individuals with higher emotional eating scores are less sensitive to the effects of a GLP-1RA on central responses to food cues. Additionally, we investigated the associations of higher external and restraint eating scores with the sensitivity to the central effects of GLP-1RA. Methods: This secondary analysis of a randomized crossover study in people with obesity and type 2 diabetes, consisted of two periods of 12-week treatment with liraglutide or insulin glargine. Using functional MRI, we assessed the relation between baseline eating behavior and the effects of the GLP-1RA liraglutide compared with insulin after 10 days and 12 weeks of treatment on brain responses to food cues. Results: After 10 days, higher emotional eating scores were associated with less pronounced GLP-1RA induced reductions in brain responses to food pictures in the amygdala, insula and caudate nucleus. In addition, higher emotional eating scores tended to be associated with less pronounced GLP-1RA increases in brain responses to chocolate milk receipt in the caudate nucleus and insula. After 12 weeks, there were no significant associations between emotional eating scores and liraglutide-induced changes in brain responses to food cues. After 10 days, baseline external eating scores were associated with less pronounced GLP-1RA induced reductions in brain responses to food pictures in the insula, amygdala and orbitofrontal cortex. After 12 weeks, baseline restraint eating scores were associated with more GLP-1RA induced reductions in brain responses to food pictures in the insula and caudate nucleus, and with more GLP-1RA induced reductions in brain responses to the anticipation of chocolate milk in the caudate nucleus. Conclusions: Our findings indicate that individuals with higher baseline emotional eating scores are less sensitive to the central effect of GLP-1RA treatment. Additionally, external eating may also decrease, whereas restraint eating may increase the sensitivity to the treatment effects of GLP-1RAs. These insights may help to optimize treatment strategies for obesity and to select patient groups with better efficacy of GLP-1RA treatment.
KW - Central feeding regulation
KW - Emotional eating
KW - GLP-1 receptor agonists
KW - Liraglutide
KW - Obesity
KW - Type 2 diabetes
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85122659883&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/35033928
UR - http://www.scopus.com/inward/record.url?scp=85122659883&partnerID=8YFLogxK
U2 - https://doi.org/10.1016/j.psyneuen.2022.105667
DO - https://doi.org/10.1016/j.psyneuen.2022.105667
M3 - Article
C2 - 35033928
SN - 0306-4530
VL - 137
JO - Psychoneuroendocrinology
JF - Psychoneuroendocrinology
M1 - 105667
ER -