Visualization of ghrelin-producing neurons in the hypothalamic arcuate nucleus using ghrelin-EGFP transgenic mice

Kageyama, Haruaki; Kitamura, Yoshitaka; Hosono, Tomohiko; Kintaka, Yuri; Seki, Mayumi; Takenoya, Fumiko; Hori, Yasunori; Nonaka, Naoko; Arata, Satoru; Shioda, Seiji

doi:10.1016/j.regpep.2007.09.026

Cited by 40 publications

(41 citation statements)

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“…Variations in published work include differences in places of localization of immunoreactivity and differences in cellular localization, for example different abilities to reveal nerve cells and nerve terminals, as we have summarized in the Introduction. At least some of the ghrelin-mimicking substance in mice is probably not a product of the ghrelin gene because, as elaborated in the Introduction, ghrelin reporter mice do not reveal expression in the CNS, whereas signal was observed in gastric endocrine cells (Wortley et al, 2004;Kageyama et al, 2008;Sakata et al, 2009). Although it might be considered that expression of transgenes is incomplete in the reporter mice, the results with the different reporter constructs all show lack of ghrelin, as do the present immunohistochemical studies.…”

Section: Discussionsupporting

confidence: 56%

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Investigation of the presence of ghrelin in the central nervous system of the rat and mouse

et al. 2011

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Section: Discussionsupporting

confidence: 56%

“…Neither antibody revealed specific immunoreactivity in the CNS, as previously reported (Wortley et al, 2004). Ghrelin reporter mice were also investigated by Kageyama et al (2008). These authors found the reporter signal, using anti-green fluorescent protein (GFP) immunofluorescence, in gastric endocrine cells that were also immunoreactive for ghrelin.…”

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confidence: 83%

Investigation of the presence of ghrelin in the central nervous system of the rat and mouse

et al. 2011

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“…Although PACAP and PAC1 expression has not yet been identified on PD/1 cells of the gastric fundus, PAC1 receptors have been characterized on ECL cells (61), which have been shown to secrete ghrelin (48). Further knowledge on ghrelin secretion processes is currently limited due to the difficulty of pure gastric mucosa cells isolation techniques (22).…”

Section: Discussionmentioning

confidence: 99%

PACAP intraperitoneal treatment suppresses appetite and food intake via PAC1 receptor in mice by inhibiting ghrelin and increasing GLP-1 and leptin

Goyal

Luong

et al. 2015

American Journal of Physiology-Gastrointestinal and Liver Physi

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PM. PACAP intraperitoneal treatment suppresses appetite and food intake via PAC1 receptor in mice by inhibiting ghrelin and increasing GLP-1 and leptin. Am J Physiol Gastrointest Liver Physiol 309: G816 -G825, 2015. First published September 3, 2015 doi:10.1152/ajpgi.00190.2015.-Pituitary adenylate cyclase-activating peptide (PACAP) is expressed within the gastroenteric system, where it has profound physiological effects. PACAP was shown to regulate food intake and thermogenesis centrally; however, PACAP peripheral regulation of appetite and feeding behavior is unknown. Therefore, we studied PACAP's effect on appetite and food intake control by analyzing feeding behavior and metabolic hormones in PAC1-deficient (PAC1Ϫ/Ϫ) and age-matched wild-type (WT) mice intraperitoneally injected with PACAP 1-38 or PACAP 1-27 before the dark phase of feeding. Food intake and feeding behavior were analyzed using the BioDAQ system. Active ghrelin, glucagon-like peptide-1 (GLP-1), leptin, peptide YY, pancreatic polypeptide, and insulin were measured following PACAP 1-38 administration in fasted WT mice. PACAP 1-38/PACAP1-27 injected into WT mice significantly decreased in a dose-dependent manner cumulative food intake and reduced bout and meal feeding parameters. Conversely, PACAP 1-38 injected into PAC1Ϫ/Ϫ mice failed to significantly change food intake. Importantly, PACAP1-38 reduced plasma levels of active ghrelin compared with vehicle in WT mice. In PAC1Ϫ/Ϫ mice, fasting levels of active ghrelin, GLP-1, insulin, and leptin and postprandial levels of active ghrelin and insulin were significantly altered compared with levels in WT mice. Therefore, PAC1 is a novel regulator of appetite/satiety. PACAP 1-38/PACAP1-27 significantly reduced appetite and food intake through PAC1. In PAC1Ϫ/Ϫ mice, the regulation of anorexigenic/orexigenic hormones was abolished, whereas active ghrelin remained elevated even postprandially. PACAP significantly reduced active ghrelin in fasting conditions. These results establish a role for PACAP via PAC1 in the peripheral regulation of appetite/satiety and suggest future studies to explore a therapeutic use of PACAP or PAC1 agonists for obesity treatment.pituitary adenylate cyclase-activating peptide; PAC1 receptor; appetite; ghrelin; GLP-1; leptin PITUITARY ADENYLATE CYCLASE-ACTIVATING POLYPEPTIDE (PACAP) was originally isolated from the ovine hypothalamus and is highly conserved among vertebrates (1). PACAP, because of its protein structure, particularly in the first 27 amino acids, belongs to the secretin-glucagon superfamily of hormones, which includes vasoactive intestinal peptide (VIP), gastric inhibitory peptide, glucagon-like peptide (GLP)-1 and GLP-2, growth hormone-releasing hormone, peptide histidine methionine, peptide histidine isoleucine, and exendins (34). PACAP exists in two variant forms: PACAP 1-27 and the COOHterminally extended form PACAP 1-38 that originates from the same precursor and stimulates adenylate cyclase activity in pituitary cells (23,35). PACAP functions through its P...

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“…Ghrelin (“hunger hormone”) was originally isolated from the stomach, but ghrelin has also been identified in other peripheral tissues, such as the pancreas, ovary and adrenal cortex14. In the brain, ghrelin-producing neurons have been identified in the pituitary and the hypothalamus glands15. In the stomach and small intestine, ghrelin is released into circulation as acyl-ghrelin16.…”

Section: Resultsmentioning

confidence: 99%

Helicobacter pylori infection can affect energy modulating hormones and body weight in germ free mice

Khosravi

Seow

Amoyo

et al. 2015

Sci Rep

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Helicobacter pylori, is an invariably commensal resident of the gut microbiome associated with gastric ulcer in adults. In addition, these patients also suffered from a low grade inflammation that activates the immune system and thus increased shunting of energy to host defense mechanisms. To assess whether a H. pylori infection could affect growth in early life, we determined the expression levels of selected metabolic gut hormones in germ free (GF) and specific pathogen-free (SPF) mice with and without the presence of H. pylori. Despite H. pylori-infected (SPFH) mice display alteration in host metabolism (elevated levels of leptin, insulin and peptide YY) compared to non-infected SPF mice, their growth curves remained the same. SPFH mice also displayed increased level of eotaxin-1. Interestingly, GF mice infected with H. pylori (GFH) also displayed increased levels of ghrelin and PYY. However, in contrast to SPFH mice, GFH showed reduced weight gain and malnutrition. These preliminary findings show that exposure to H. pylori alters host metabolism early in life; but the commensal microbiota in SPF mice can attenuate the growth retarding effect from H. pylori observed in GF mice. Further investigations of possible additional side effects of H. pylori are highly warranted.

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Visualization of ghrelin-producing neurons in the hypothalamic arcuate nucleus using ghrelin-EGFP transgenic mice

Cited by 40 publications

References 28 publications

Investigation of the presence of ghrelin in the central nervous system of the rat and mouse

Investigation of the presence of ghrelin in the central nervous system of the rat and mouse

PACAP intraperitoneal treatment suppresses appetite and food intake via PAC1 receptor in mice by inhibiting ghrelin and increasing GLP-1 and leptin

Helicobacter pylori infection can affect energy modulating hormones and body weight in germ free mice

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