The neuroscience of sugars in taste, gut-reward, feeding circuits, and obesity

Gutiérrez, Ranier; Fonseca, Esmeralda; Simon, Sidney A.

doi:10.1007/s00018-020-03458-2

Cited by 52 publications

(47 citation statements)

References 266 publications

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“…In this review we provide perspective on the data available to support, or contradict, the general interpretation that individuals with obesity have reduced sweet taste perception, as is frequently proposed [9]. This interpretation has typically been framed jointly with the evidence for decreased availability of striatal D 2 R in individuals with obesity, with both gustatory and dopaminergic factors proposed to contribute towards compensatory food consumption and weight gain [9].…”

Section: Discussionmentioning

confidence: 94%

Sweet taste and obesity

Ribeiro¹,

Oliveira‐Maia²

2021

European Journal of Internal Medicine

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For more than 50 years, there has been evidence for greater consumption of sweet-foods in overweight humans and animals, relative to those that have a normal weight. Furthermore, it has long been suggested that energy deficit resulting from dieting, while moving the individual from a higher weight set point, would result in heightened susceptibility to palatable tastants, namely to sweet tastants. This was the motivation behind the first studies comparing sweet taste perception between individuals with obesity and those of a normal weight. These studies, using direct measures of taste, have been characterized by significant methodological heterogeneity, contributing towards variability in results and conclusions. Nevertheless, some of these findings have been used to support the theory that patients with obesity have decreased taste perception, particularly for sweet tastants. A similar hypothesis has been proposed regarding evidence for reduced brain dopamine receptors in obesity and, in both cases, it is proposed that increased food consumption, and associated weight gain, result from the need to increase sensory and brain stimulation. However, the available literature is not conclusive on the association between obesity and reduced sweet taste perception, with both negative and contradictory findings in comparisons between individuals with obesity and normal weight control subjects, as well as within-subject comparisons before and after bariatric surgery. Nevertheless, following either Roux-en-Y gastric bypass or sleeve gastrectomy, there is evidence of changes in taste perception, particularly for reward-related measures of sweet tastants, that should be further tested and confirmed in large samples, using consensual methodology.

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Section: Discussionmentioning

confidence: 94%

Sweet taste and obesity

Ribeiro¹,

Oliveira‐Maia²

2021

European Journal of Internal Medicine

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“…The LHA is currently viewed as a hub of various cell-types (Stuber and Wise, 2016), grossly divided into two larger populations related to feeding: the glutamatergic (LHA Vglut2+ ) and GABAergic neurons (LHA Vgat+ ) (Gutierrez et al, 2020). Activation of LHA Vglut2+ neurons leads to reduced food intake and is aversive (Jennings et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Lateral Hypothalamic GABAergic neurons encode and potentiate sucrose’s palatability

Garcia

Coss

Luis-Islas

et al. 2020

Preprint

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AbstractOverconsumption of calorie-dense palatable foods, especially those with added sugars, is a contributing factor in the obesity epidemic. Although previous studies in mice have shown that GABAergic LHAVgat+ neurons evoke voracious eating, it is not known whether these neurons would be driving consumption by increasing palatability. Using optrode recordings, we measure sucrose’s palatability while VGAT-ChR2 transgenic mice performed a brief access sucrose test. We found that a subpopulation of LHAVgat+ neurons encodes palatability responses elicited by sucrose and that opto-stimulation of these neurons bias the intake towards the most palatable available tastant. In contrast, opto-self-stimulation of LHAVgat+ neurons convey a rewarding signal capable of enhancing the hedonic value of proximal stimuli. We conclude that LHAVgat+ neurons increase consumption by potentiating the palatability of the most proximal tastant available. These findings suggest that LHA GABAergic neurons could be a pharmacological target to modulate the palatability of caloric foods that produce obesity.Impact StatementSucrose is attractive due to its sweet taste and positive palatability. LHA GABAergic neurons encode sucrose’s palatability and act by increasing consumption of the most palatable and proximal tastant available.

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“…Irrespective of BMI and energy state, the prSN emerges as a key area connecting the hypothalamus with neocortical regions. The prSN processes autonomic, gut-induced rewards regulating motivational and emotional states (e.g., Gutierrez et al, 2020;Han et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

Hypothalamic effective connectivity at rest is associated with body weight and energy homeostasis

Voigt

Andrews

et al. 2021

Preprint

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Hunger and satiety states drive eating behaviours via changes in brain function. The hypothalamus is a central component of the brain networks that regulate food intake. Animal research parsed the roles of the lateral hypothalamus (LH) and the medial hypothalamus (MH) in hunger and satiety respectively. Here, we examined how hunger and satiety change information flow between human LH and MH brain networks, and how these interactions are influenced by body mass index. Forty participants (15 overweight/obese) underwent two resting-state functional MRI scans: after overnight fasting (fasted state) and following a standardised meal (sated state). The direction and valence (excitatory/inhibitory influence) of information flow between the MH and LH was modelled using spectral dynamic causal modelling. Our results revealed two core networks interacting across homeostatic state and weight status: subcortical bidirectional connections between the LH, MH and the substantia nigra pars compacta (prSN), and cortical top-down inhibition from frontoparietal and temporal areas. During fasting relative to satiety, we found higher inhibition between the LH and prSN, whereas the prSN received greater top-down inhibition from across the cortex. Individuals with higher BMI showed that these network dynamics occur irrespective of fasted or satiety states. Our findings reveal fasting affects brain dynamics over a distributed hypothalamic-midbrain-cortical network. This network is less sensitive to state-related fluctuations among people with obesity.

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The neuroscience of sugars in taste, gut-reward, feeding circuits, and obesity

Cited by 52 publications

References 266 publications

Sweet taste and obesity

Sweet taste and obesity

Lateral Hypothalamic GABAergic neurons encode and potentiate sucrose’s palatability

Hypothalamic effective connectivity at rest is associated with body weight and energy homeostasis

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