Leptin modulation of peripheral controls of meal size
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Cited by (27)
Leptin, An Adipokine With Central Importance in the Global Obesity Problem
2018, Global HeartCitation Excerpt :This is a significant finding that involves leptin and implies that afternoon appetite is unaffected by morning feeding patterns [192]. In addition, meal size is mediated by leptin by increasing inhibitory feedback of gastric load on the nucleus tractus solitarius [193]. However, the pace at which a meal is consumed does not appear to be related to leptin (though eating slowly is associated with an increased thermic effect of food, lower nonesterified fatty acids, and high adiponectin levels) [194].
Physiologic and Neural Controls of Eating
2016, Gastroenterology Clinics of North AmericaCitation Excerpt :That is, leptin enhances the dorsal hindbrain representation of ascending vagal afferent feedback signals arising from CCK or gastric preload induced gastrointestinal stimulation.165 Reducing leptin levels through food deprivation or exogenous NPY administration have the opposite result - the satiating potency of CCK is reduced166,167 and satiety related NTS activation is inhibited.165 These actions of leptin may be a downstream consequence of leptin signaling in the arcuate nucleus or directly mediated at hindbrain sites since the NTS contains receptors for both leptin and NPY.168,169
Perinatal undernutrition increases meal size and neuronal activation of the nucleus of the solitary tract in response to feeding stimulation in adult rats
2014, International Journal of Developmental NeuroscienceCitation Excerpt :Another possible way of regulation of food intake could be the modulation of NPY within NTS. Previous studies have demonstrated that injection of NPY into the NTS increases food intake (Moran et al., 2006), suggesting that the NTS exerts both negative and positive modulation on the dietary control of the meal. The present study is one of the first to demonstrate the possible changes in the activation of the NTS in response to food intake in animals submitted to perinatal undernutrition.
Circuits controlling energy balance and mood: Inherently intertwined or just complicated intersections?
2014, Cell MetabolismCitation Excerpt :Leptin, the circulating adiposity hormone, stimulates POMC neurons while reciprocally hyperpolarizing orexigenic AgRP/NPY neurons. Years of studies have also highlighted an important role for brainstem neurons in the regulation of hunger and satiety (Grill and Hayes, 2012; Moran et al., 2006). For instance, it was recently shown that neurons in the nucleus tractus solitarius (NTS) and caudal serotonergic nuclei provide excitatory inputs to the parabrachial nucleus (PBN) and inhibit food intake (Wu et al., 2012).
Integration of satiety signals by the central nervous system
2013, Current BiologyCitation Excerpt :These compensatory increases in food intake result in the restoration of weight loss and defend body energy stores. To regulate meal size, both NPY and POMC neurons send dense projections to the paraventricular nucleus [114], which in turn projects to adrenergic neurons in the nucleus of the solitary tract that regulate meal size [115–118]. By putting on weight, consequent increases in leptin increase the output from POMC neurons that ultimately render an individual more sensitive to the anorectic effect of CCK and other satiety factors [15].
Bombesin
2013, Handbook of Biologically Active Peptides