Cholecystokinin and bombesin activate neuronatin neurons in the nucleus of the solitary tract

Guggenberger, Malika; Engster, Kim-Marie; Hofmann, Tobias; Rose, Matthias; Stengel, Andreas; Kobelt, Peter

doi:10.1016/j.brainres.2020.147006

Cited by 5 publications

(2 citation statements)

References 77 publications

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“…Although not addressed in our analyses, Nnat expression in other brain regions beyond the hypothalamus may also play a part in the regulation of food intake, appetitive behaviour and energy balance. For example, a recent study has implicated neuronatin neurons in the nucleus of the solitary tract as having a role in mediating the anorectic effect of the gut derived peptides cholecystokinin (CCK) and bombesin (BN) 42 . Further studies with selective perturbation of Nnat expression in different regional and neuronal population are required to build upon these observations.…”

Section: Discussionmentioning

confidence: 99%

Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

Cimino

Rimmington

Tung

et al. 2021

Sci Rep

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Neuronatin (Nnat) has previously been reported to be part of a network of imprinted genes downstream of the chromatin regulator Trim28. Disruption of Trim28 or of members of this network, including neuronatin, results in an unusual phenotype of a bimodal body weight. To better characterise this variability, we examined the key contributors to energy balance in Nnat+/−p mice that carry a paternal null allele and do not express Nnat. Consistent with our previous studies, Nnat deficient mice on chow diet displayed a bimodal body weight phenotype with more than 30% of Nnat+/−p mice developing obesity. In response to both a 45% high fat diet and exposure to thermoneutrality (30 °C) Nnat deficient mice maintained the hypervariable body weight phenotype. Within a calorimetry system, food intake in Nnat+/−p mice was hypervariable, with some mice consuming more than twice the intake seen in wild type littermates. A hyperphagic response was also seen in Nnat+/−p mice in a second, non-home cage environment. An expected correlation between body weight and energy expenditure was seen, but corrections for the effects of positive energy balance and body weight greatly diminished the effect of neuronatin deficiency on energy expenditure. Male and female Nnat+/−p mice displayed subtle distinctions in the degree of variance body weight phenotype and food intake and further sexual dimorphism was reflected in different patterns of hypothalamic gene expression in Nnat+/−p mice. Loss of the imprinted gene Nnat is associated with a highly variable food intake, with the impact of this phenotype varying between genetically identical individuals.

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Section: Discussionmentioning

confidence: 99%

Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

Cimino

Rimmington

Tung

et al. 2021

Sci Rep

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“…Studies in animals have pointed towards a role of Nnat in satiety pathways as neuronal Nnat has been shown to colocalize with various functional mediators of appetite regulation in the LHA [ 8 ], and Nnat-positive neurons in the solitary tract are activated by peripheral satiety signals such as cholecystokinin and bombesin [ 37 ]. In mice, it has been demonstrated that hypothalamic Nnat expression is downregulated during fasting and upregulated following leptin injection [ 14 ], and Nnat-deficient mice showed hyperphagia and susceptibility to obesity in old age [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

Circulating Neuronatin Levels Are Positively Associated with BMI and Body Fat Mass but Not with Psychological Parameters

Rudolph,

Stengel,

Suhs

et al. 2023

Nutrients

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Human genetic studies have associated Neuronatin gene variants with anorexia nervosa (AN) and obesity. Studies on the expression of the Neuronatin gene product, a proteolipid, are lacking. We investigated the relationship between circulating Neuronatin, body mass index (BMI), body composition (BC), physical activity (PA), and psychometric outcomes in patients with AN, normal weight, and obesity. Plasma Neuronatin was measured by ELISA in (1) 79 subjects of five BMI categories (AN/BMI < 17.5 kg/m2; normal weight/BMI 18.5–25 kg/m2; obesity/BMI 30–40 kg/m2; obesity/BMI 40–50 kg/m2; obesity/BMI > 50 kg/m2) with assessment of BC (bioimpedance analysis; BIA); (2) 49 women with AN (BMI 14.5 ± 1.8 kg/m2) with measurements of BC (BIA) and PA (accelerometry); (3) 79 women with obesity (BMI 48.8 ± 7.8 kg/m2) with measurements of anxiety (GAD-7), stress (PSQ-20), depression (PHQ-9) and eating behavior (EDI-2). Overall, a positive correlation was found between Neuronatin and BMI (p = 0.006) as well as total fat mass (FM; p = 0.036). In AN, Neuronatin did not correlate with BMI, FM, or PA (p > 0.05); no correlations were found between Neuronatin and psychometric outcomes in obesity (p > 0.05). The findings suggest an FM-dependent peripheral Neuronatin expression. The decreased Neuronatin expression in AN provides evidence that Neuronatin is implicated in the pathogenesis of eating disorders.

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Reduction of oxidative stress and inflammatory signaling in the commissural nucleus of the solitary tract (commNTS) and rostral ventrolateral medulla (RVLM) in treadmill trained rats

Farah

Nunes

et al. 2021

Brain Research

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Cholecystokinin and bombesin activate neuronatin neurons in the nucleus of the solitary tract

Cited by 5 publications

References 77 publications

Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

Murine neuronatin deficiency is associated with a hypervariable food intake and bimodal obesity

Circulating Neuronatin Levels Are Positively Associated with BMI and Body Fat Mass but Not with Psychological Parameters

Reduction of oxidative stress and inflammatory signaling in the commissural nucleus of the solitary tract (commNTS) and rostral ventrolateral medulla (RVLM) in treadmill trained rats

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