Central Ghrelin Receptors and Food Intake

Perelló, Mario; Raingo, Jesica

doi:10.1007/978-1-4939-0823-3_5

Cited by 3 publications

(2 citation statements)

References 156 publications

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“…It remains to be determined which neuronal subpopulations within the PVH translate the IL-6 effect on feeding control. A likely candidate might depict parvocellular oxytocin neurons in the PVH, which have been reported to show pSTAT3 activation upon central leptin application and to transduce the leptin-dependent effect on body weight control in rats (Perello and Raingo, 2013).…”

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confidence: 99%

IL-6 Improves Energy and Glucose Homeostasis in Obesity via Enhanced Central IL-6 trans-Signaling

et al. 2017

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Interleukin (IL)-6 engages similar signaling mechanisms to leptin. Here, we find that central application of IL-6 in mice suppresses feeding and improves glucose tolerance. In contrast to leptin, whose action is attenuated in obesity, the ability of IL-6 to suppress feeding is enhanced in obese mice. IL-6 suppresses feeding in the absence of neuronal IL-6-receptor (IL-6R) expression in hypothalamic or all forebrain neurons of mice. Conversely, obese mice exhibit increased soluble IL-6R levels in the cerebrospinal fluid. Blocking IL-6 trans-signaling in the CNS abrogates the ability of IL-6 to suppress feeding. Furthermore, gp130 expression is enhanced in the paraventricular nucleus of the hypothalamus (PVH) of obese mice, and deletion of gp130 in the PVH attenuates the beneficial central IL-6 effects on metabolism. Collectively, these experiments indicate that IL-6 trans-signaling is enhanced in the CNS of obese mice, allowing IL-6 to exert its beneficial metabolic effects even under conditions of leptin resistance.

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confidence: 99%

IL-6 Improves Energy and Glucose Homeostasis in Obesity via Enhanced Central IL-6 trans-Signaling

et al. 2017

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“…32 The distribution of specific receptors for ghrelin as well as the study of MRI images confirm the hypothesis that ghrelin not only stimulates appetite but is also involved in regulating the hedonic aspects of eating: the preference for palatable foods, the motivation to obtain one's preferred foods, the reward value/effect of one's preferred foods and the actual purchase of foods. 33,34 Recent data indicate that ghrelin also influences behaviours related to motivational aspects of eating. Thus, currently existing evidence suggests that the ghrelin/GOAT/GHSR1a system is closely linked to pathways involved in reward aspects of food intake, additionally and partially separated from those determining food intake initiation.…”

Section: Ghrelin -A Peripheral Orexigenic Peptide With Central Actionmentioning

confidence: 99%

Effects of ghrelin in energy balance and body weight homeostasis

Mihalache¹,

Gherasim²,

Niţă³

et al. 2016

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ghrelin is a gut peptide composed of 28 amino acids mostly secreted in the gastric fundus mucosa. It was isolated and described in 1999 by Kojima et al. and only three years later its specific receptor, ghsR1a, was also identified. ghrelin, the endogenous ligand for the gh secretagogue receptor, is the only peripheral orexigenic hormone that activates the receptors to be found especially in the appetite center (hypothalamus and pituitary gland). ghrelin is present in human plasma in two forms: an inactive form known as deacylated ghrelin, and an active form called acylated ghrelin synthesized under the action of ghrelin O-acyltransferase enzyme (gOAT). The literature even mentions an extremely complex ghrelin/gOAT/ghsR system involved in the regulation of human energy, metabolism and adaptation of energy homeostasis to environmental changes. In humans, there is a preprandial rise and a postprandial fall in plasma ghrelin levels, which strongly suggest that the peptide plays a physiological role in meal initiation and may be employed in determining the amount and quality of ingested food. Besides the stimulation of food intake, ghrelin determines a decrease in energy expenditure and promotes the storage of fatty acids in adipocytes. Thus, in the human body ghrelin induces a positive energy balance, an increased adiposity gain, as well as an increase in caloric storage, seen as an adaptive mechanism to caloric restriction conditions. In the current world context, when we are witnessing an increasing availability of food and a reduction of energy expenditure to a minimum level, these mechanisms have become pathogenic. As a consequence, the hypothesis that ghrelin is involved in the current obesity epidemic has been embraced by many scholars and researchers

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