Literature DB >> 28551112

Resting state hypothalamic response to glucose predicts glucose-induced attenuation in the ventral striatal response to food cues.

Shan Luo1, A James Melrose2, Hilary Dorton3, Jasmin Alves4, John R Monterosso5, Kathleen A Page6.   

Abstract

Feeding behavior is regulated by a complex interaction of central nervous system responses to metabolic signals that reflect nutrient availability and to food cues that trigger appetitive responses. Prior work has shown that the hypothalamus is a key brain area that senses and responds to changes in metabolic signals, and exposure to food cues induces the activation of brain areas involved in reward processing. However, it is not known how the hypothalamic responses to changes in metabolic state are related to reward responses to food cues. This study aimed to understand whether changes in hypothalamic activity in response to glucose-induced metabolic signals are linked to food-cue reactivity within brain areas involved in reward processing. We combined two neuroimaging modalities (Arterial Spin Labeling and Blood Oxygen Level Dependent) to measure glucose-induced changes in hypothalamic cerebral blood flow (CBF) and food-cue task induced changes in brain activity within reward-related regions. Twenty-five participants underwent a MRI session following glucose ingestion and a subset of twenty individuals underwent an additional water session on a separate day as a control condition (drink order randomized). Hunger was assessed before and after drink consumption. We observed that individuals who had a greater reduction in hypothalamic CBF exhibited a greater reduction in left ventral striatum food cue reactivity (Spearman's rho = 0.46, P = 0.048) following glucose vs. water ingestion. These results are the first to use multimodal imaging to demonstrate a link between hypothalamic metabolic signaling and ventral striatal food cue reactivity.
Copyright © 2017 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Appetite regulation; Brain; Eating behavior; Glucose

Mesh:

Substances:

Year:  2017        PMID: 28551112      PMCID: PMC5557629          DOI: 10.1016/j.appet.2017.05.038

Source DB:  PubMed          Journal:  Appetite        ISSN: 0195-6663            Impact factor:   3.868


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