Hindbrain circuits in the control of eating behaviour and energy balance

Cheng, Wenwen; Gordian, Desiree; Ludwig, Mette Q.; Pers, Tune H.; Seeley, Randy J.; Myers, Martin G.

doi:10.1038/s42255-022-00606-9

Cited by 48 publications

(41 citation statements)

References 81 publications

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“…Although many sets of NTS neurons have been implicated in the suppression of feeding, only recently have single cell RNA sequencing methods been employed to define populations of NTS neurons in an unbiased manner (2, 5, 21, 22). Unlike Calcr, Lepr marks multiple populations of NTS neurons, including one population (GLU2) that controls respiratory function in response to leptin/energy balance (5, 22, 23).…”

Section: Discussionmentioning

confidence: 99%

“…Identifying new therapeutic targets to better combat obesity will require understanding the physiologic systems that modulate feeding and contribute to body weight maintenance. While hypothalamic circuits contribute to the control of feeding and play important roles in maintaining long-term energy balance, many hypothalamic circuits act via the brainstem to suppress food intake (2, 3). Furthermore, the brainstem receives feeding-related and other information from the gastrointestinal (GI) tract, controls the rhythmic pattern generators that mediate feeding, and can overcome hypothalamically-driven hyperphagia (2, 4).…”

Section: Introductionmentioning

confidence: 99%

“…Many of the most important food intake-controlling brainstem systems lie in the dorsal vagal complex (DVC), which includes the area postrema (AP), the nucleus tractus solitarius (NTS), and the dorsal motor nucleus of the vagus (DMV) (2, 3). The AP lies outside of the blood-brain barrier and receives circulating signals relevant to feeding, including from several anorexigenic peptides.…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Many of these brainstem circuits express receptors for peptides that suppress food intake, including the glucagon-like peptide-1 receptor (GLP1R); the calcitonin receptor (CALCR) and the related amylin receptor (AmyR-a complex of CALCR and a receptor activity modifying protein (RAMP)); and the leptin receptor (LepRb) (2, 5-7). Many of these DVC cell types may contribute to the suppression of feeding by a variety of gut peptide mimetics currently under development or in use for weight loss therapy (2). Furthermore, recent work from others and us has demonstrated that the AP and NTS neuron types that suppress food intake while mediating aversive responses associated with gut malaise are distinct from neuron types that promote non-aversive satiation (6-11).…”

Section: Introductionmentioning

confidence: 99%

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Multiple NTS Neuron Populations Synergistically Suppress Physiologic Food Intake but are Dispensable for the Response to VSG

Qui

Hutch

Wang

et al. 2022

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Several discrete groups of feeding-regulated neurons in the nucleus tractus solitarius (NTS) suppress food intake, including aversion-promoting neurons that express Cck (NTSCck cells) and distinct Lepr- and Calcr-expressing neurons (NTSLepr and NTSCalcr cells, respectively) that suppress food intake without promoting aversion. To test synergies among these cell groups we manipulated multiple NTS cell populations simultaneously. We found that activating multiple sets of NTS neurons (e.g., NTSLepr plus NTSCalcr (NTSLC), or NTSLC plus NTSCck (NTSLCK)) suppressed feeding more robustly than activating single populations. While activating groups of cells that include NTSCck neurons promoted conditioned taste avoidance (CTA), NTSLC activation produced no CTA despite abrogating feeding. Thus, the ability to promote CTA formation represents a dominant effect, but activating multiple non-aversive populations additively suppresses food intake without provoking aversion. Although silencing multiple NTS neuron groups augmented food intake and body weight more dramatically than silencing single populations, feeding activated many non-NTSLCK neurons and silencing NTSLCK neurons failed to blunt the weight loss response to vertical sleeve gastrectomy (VSG). Hence, while each of these NTS neuron populations plays crucial and additive roles in the control of energy balance, as-yet undefined cell types must make additional contributions to the control of feeding and the response to VSG.

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