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Nutrition and Appetite Regulation in Children and Adolescents with End-Stage Renal Failure
Published in Victor R. Preedy, Handbook of Nutrition and Diet in Palliative Care, 2019
Kai-Dietrich Nüsken, Jörg Dötsch
Ghrelin is a 3.24 kDa peptide hormone that is mainly secreted by the stomach (Wren et al. 2001). The orexigenic effect of ghrelin is mediated by its acetylated form (acyl-ghrelin), whereas desacyl-ghrelin and obestatin (a further product of the ghrelin gene) mediate anorexigenic effects (Naufel et al. 2010). It binds to its receptor mainly in the ARC and LHA. Acyl-ghrelin increases food intake by stimulating NPY and AGRP neurons and prevents reduction of food intake mediated by leptin (Nakazato et al. 2001). Total ghrelin, desacyl-ghrelin and obestatin concentrations are elevated in children with ESRD (Nüsken et al. 2004; Dötsch et al. 2005; Arbeiter et al. 2009; Monzani et al. 2017). As desacyl-ghrelin and obestatin inversely correlate with body mass index-standard deviation score (BMI-SDS) and/or weight SDS, they have been proposed as markers of nutritional status in children with ESRD (Monzani et al. 2017). Elevated total ghrelin concentrations are not contradictory to inappetence in ESRD, because only concentrations of desacyl-ghrelin, but not acyl-ghrelin, are increased (Büscher et al. 2010; Naufel et al. 2010).
The causes of male obesity and associated health problems
Published in Alan White, Maggie Pettifer, Hazardous Waist, 2018
In response to all these heightened sensations, we eat. The gut then contacts the brain in different ways; the nerve endings in the stomach wall transmit impulses directly via the vagal nerve to inform it that food has arrived. In addition, with increasing amounts of food entering the bowel, the cells of the gut produce a number of hormones (PYY 3-36, obestatin, cholecystokinin), which are released into the blood stream and circulate around the body. These hormones are monitored by the brain stem, and the hypothalamus, which responds by producing messenger chemicals called neuropeptides (NPY, AgRP), which give us the sensation of being satisfied, and full, so we should stop eating.
Regulation of Food Intake
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
Surya Panicker Rajeev, Ian W. Seetho, John P.H. Wilding, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
Ghrelin is the only identified orexigenic hormone. Ghrelin, originally discovered as an endogenous ligand for the growth hormone secretagogue receptor (GHS-R) [27], is a 28-amino-acid peptide hormone secreted principally by the X/A like cells in the oxyntic glands of the gastric fundus [28]. Ghrelin is cleaved from preproghrelin by prohormone convertase. Though ghrelin is synthesized in many tissues, the stomach is the largest source of circulating ghrelin. The presence of an acyl side chain attached to the serine amino acid at position three of ghrelin is necessary for its orexigenic effects [27] through binding to GHS-R as well as enhancing its ability to cross the blood–brain barrier. Ghrelin O-acyltransferase (GOAT) is the enzyme responsible for the acylation of ghrelin. Des-acylated ghrelin (which lacks the serine-3 acylation) is not orexigenic and reduces food intake in rodent models with central or peripheral administration [29]. Though des-acyl ghrelin was originally thought to be the inactive form of ghrelin, recent data has demonstrated its physiological roles in the regulation of adiposity as well as glucose homeostasis through agonistic action at the growth hormone secretagogue receptor [30]. Obestatin was identified in 2005 from the ghrelin precursor [31]. Though initially thought to have opposing effects to ghrelin, the anorexigenic effects of obestatin were subsequently not proven from clinical studies.
Blood levels of agouti-related peptide (AgRP), obestatin, corticosteroid-binding globulin (CBG), and cortisol in patients with bipolar disorder (BD): a case–control study
Published in Psychiatry and Clinical Psychopharmacology, 2019
Evrim Özkorumak Karagüzel, Birgül Vanizor Kural, Ahmet Tiryaki, İlkay Keleş Altun, Serap Yaman Özer, Filiz Civil Arslan
Agouti-related peptide (AgRP), which is synthesized in the arcuate nucleus of the hypothalamus, is a powerful orexigenic peptide that increases food intake and has been considered a gene potentially involved in human obesity [11]. The role of AgRP in schizophrenia obesity treated with antipsychotics has been investigated in a few studies [12,13]. However, its role in BD obesity has not previously been investigated but it is implicated to have a role in impaired energy homeostasis during manic episode [14]. Since during manic episode AgRP levels are reported to be higher than euthymic patients and controls, AgRP is suggested to be a state marker for manic episodes. AgRP’s orexigenic effect derives primarily from opposing the anorexigenic actions of pro-opiomelanocortin [13,15,16]. It has long-lasting orexigenic properties [17]. It increases appetite and reduces metabolism, induces obesity by antagonism of the melanocortin receptors, and stimulates adrenocorticotropic hormone and cortisol [17,18]. Glucorticoids, on the other hand, affect feeding behaviour, mainly via the modulation of orexigenic and anorexigenic neuropeptides [19]. Obestatin is a peptide derived from the ghrelin gene has still unclear metabolic actions. But it is known that obestatin levels are decreased in obesity and seem to be negatively correlated with body mass index (BMI) [20]. Obestatin levels have not been studied in BD, but recently ghrelin which is encoded from the same gene with obestatin was found higher in euthymic period of BD than the manic episode [8].
Obestatin protects and reverses nonalcoholic fatty liver disease and its associated insulin resistance in rats via inhibition of food intake, enhancing hepatic adiponectin signaling, and blocking ghrelin acylation
Published in Archives of Physiology and Biochemistry, 2019
Eman F. Khaleel, Ghada A. Abdel-Aleem
The current study aimed primarily to explore the protective and ameliorative effects of long-term obestatin administration for eight weeks on a rat’s model of HFD induced NAFLD and to investigate its possible mechanisms of protection. The main exclusive findings of the current study confirm that obestatin not only reversed weight gain, hepatic fat accumulation, and hepatomegaly but also reversed its HFD induced- hyperlipidemia and IR, an effect that is associated with inhibition of food intake. However, whether it is mediated by inhibition of food intake or by a direct effect, this study showed that obestatin acts via multiple interconnected pathways including 1) reducing IR, 2) enhancing adiponectin and possibly leptin hepatic signaling, and 3) increasing levels of total ghrelin and inhibiting its acylation.
Alteration of ghrelin/obestatin ratio in adolescence with polycystic ovarian syndrome
Published in Gynecological Endocrinology, 2018
Weiguang Wu, Xiaobin Fan, Yuecheng Yu, Zheng Wang, Yingchun Wang
Ghrelin and obestatin are two peptides isolated from the gastrointestinal tract and encoded by the same preproghrelin gene. They convey to the central nervous system information concerning the nutritional status and the energy stores. Ghrelin was initially characterized as the endogenous ligand for the growth hormone (GH) secretagogue receptor [3]. However, ghrelin has different functions such as the regulations of glucose metabolism, appetite, body weight, endocrine pancreatic and ovarian functions [4,5]. Data on ghrelin levels in women with PCOS are rather conflicting: both decreased and elevated concentrations have been reported [6–8]. Obestatin is a peptide initially described for its anorexigenic effects and its binding to G-protein-coupled receptor 39 [9]. The original study reporting the function of obestatin demonstrated that obestatin could inhibited food intake and reduced body weight [10]. Until now, all available data have suggested that obestatin is a new and relevant player in energy balance regulation. The obestatin alteration in PCOS is unclear.