Inhibitory effect of obestatin on glucose-induced insulin secretion in rats

Ren, An‐Jing; Guo, Zhian; Wang, Yang-Kai; Wang, Ligang; Wang, Weizhong; Lin, Li; Zheng, Xiaojiao; Wang, Yuan

doi:10.1016/j.bbrc.2008.02.146

Cited by 55 publications

(33 citation statements)

References 19 publications

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“…The understanding of effects of Ob on insulin secretion from pancreatic b-cell lines and pancreatic islets is still limited and controversial, as either stimulation (Granata et al 2008(Granata et al , 2010 or inhibition (Qader et al 2008, Ren et al 2008b, Unniappan et al 2008) has been reported, based also on the peptide concentrations used in the experiments. In the perfused rat pancreas, Ob potentiates glucose-induced insulin release and, when infused at a high concentration, it inhibits glucose-induced insulin release.…”

Section: Effect Of Ag Uag and Ob On Insulin Secretion In Pancreaticmentioning

confidence: 99%

Unraveling the role of the ghrelin gene peptides in the endocrine pancreas

Granata

Baragli²,

Settanni³

et al. 2010

Journal of Molecular Endocrinology

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The ghrelin gene peptides include acylated ghrelin (AG), unacylated ghrelin (UAG), and obestatin (Ob). AG, mainly produced by the stomach, exerts its central and peripheral effects through the GH secretagogue receptor type 1a (GHS-R1a). UAG, although devoid of GHS-R1a-binding affinity, is an active peptide, sharing with AG many effects through an unknown receptor. Ob was discovered as the G-protein-coupled receptor 39 (GPR39) ligand; however, its physiological actions remain unclear. The endocrine pancreas is necessary for glucose homeostasis maintenance. AG, UAG, and Ob are expressed in both human and rodent pancreatic islets from fetal to adult life, and the pancreas is the major source of ghrelin in the perinatal period. GHS-R1a and GPR39 expression has been shown in b-cells and islets, as well as specific binding sites for AG, UAG, and Ob. Ghrelin colocalizes with glucagon in a-islet cells, but is also uniquely expressed in 3-islet cells, suggesting a role in islet function and development. Indeed, AG, UAG, and Ob regulate insulin secretion in b-cells and isolated islets, promote b-cell proliferation and survival, inhibit b-cell and human islet cell apoptosis, and modulate the expression of genes that are essential in pancreatic islet cell biology. They even induce b-cell regeneration and prevent diabetes in streptozotocin-treated neonatal rats. The receptor(s) mediating their effects are not fully characterized, and a signaling crosstalk has been suggested. The present review summarizes the newest findings on AG, UAG, and Ob expression in pancreatic islets and the role of these peptides on b-cell development, survival, and function.

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Section: Effect Of Ag Uag and Ob On Insulin Secretion In Pancreaticmentioning

confidence: 99%

Unraveling the role of the ghrelin gene peptides in the endocrine pancreas

Granata

Baragli²,

Settanni³

et al. 2010

Journal of Molecular Endocrinology

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“…In contrast to ghrelin, obestatin appears to act as an anorectic hormone, decreasing food intake, slowing gastric emptying and jejunal motility, and reducing body weight gain in rodents [14]. However, additional studies have, in fact, shown that obestatin is involved in improving memory [15], regulating sleep [16], affecting cell proliferation [17,18,19], increasing the secretion of pancreatic juice enzymes [20], promoting survival of pancreatic B cells [10] and inhibiting glucose-induced insulin secretion [21]. It is also possible that circulating obestatin acts on central nervous system targets by crossing the blood-brain barrier (BBB).…”

Section: Physiological Functions Of Obestatinmentioning

confidence: 99%

Obestatin: An Interesting but Controversial Gut Hormone

Lacquaniti¹,

Donato²,

Chirico

et al. 2011

Ann Nutr Metab

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Obestatin is a 23-amino acid peptide hormone released from the stomach and is present not only in the gastrointestinal tract, but also in the spleen, mammary gland, breast milk and plasma. Obestatin appears to function as part of a complex gut-brain network whereby hormones and substances from the stomach and intestines signal the brain about satiety or hunger. In contrast to ghrelin, which causes hyperphagia and obesity, obestatin appears to act as an anorectic hormone, decreasing food intake and reducing body weight gain. Further studies have shown that obestatin is also involved in improving memory, regulating sleep, affecting cell proliferation, increasing the secretion of pancreatic juice enzymes and inhibiting glucose-induced insulin secretion. This hormone has not only been studied in the field of physiology but also in the fields of obesity and diabetes mellitus, and in patients with psychogenic eating disorders. Obestatin has a role in regulating the cell cycle by exerting proliferative effects that may be seen in cell physiology and oncology. Given the current controversy regarding the effects of obestatin and its cognate ligand, this article provides the latest review of the physiological and pathological characteristics of this hormone.

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“…Pancreas ghrelin is emerging as a key player in the regulation of insulin secretion by the ␤-cell, suggesting that it may play an important role in glucose metabolism (6,7). Recently, it was suggested that obestatin could promote pancreas ␤-cell survival (8) and, similar to the role of ghrelin in the pancreas, inhibit insulin secretion (9). However, the exact function of obestatin remains unclear (10).…”

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confidence: 99%

Ontogeny of Ghrelin, Obestatin, Preproghrelin, and Prohormone Convertases in Rat Pancreas and Stomach

et al. 2009

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ABSTRACT:The processing of preproghrelin in the stomach by prohormone convertase (PC) 1/3 produces ghrelin and possibly obestatin. In the neonate, the pancreas is also a major source of ghrelin. We compared the ontogeny of preproghrelin, ghrelin, obestatin, and PCs in the stomach and pancreas from rat embryos (day 21) and neonates (days 1, 6, 13, 21, and 28) by immunohistochemistry. In stomach, preproghrelin positive cells were present from embryonic day 21 and were in excess of ghrelin cells. The number of ghrelin positive cells progressively increased with age. When preproghrelin cells were immunoreactive for ghrelin, they were also immunoreactive for obestatin and PC1/3. In pancreas, we only found 0 to 2 preproghrelin positive cells per islet and each of these cells was also positive for ghrelin and obestatin. None of the ghrelin positive cells stained for insulin, but we observed ghrelin positive/glucagon negative and ghrelin positive/glucagon positive cells. Ghrelin positive cells contained PC1/3 or PC2. In summary, in stomach, an excess of preproghrelin positive cells compared with ghrelin/PC1/3 positive cells suggests that PC1/3 determines preproghrelin processing to ghrelin. In pancreas, the colocalization of PC1/3 or PC2 in ghrelin positive cells points to a role for both PCs in preproghrelin processing. (Pediatr Res 65: 39-44, 2009)

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Inhibitory effect of obestatin on glucose-induced insulin secretion in rats

Cited by 55 publications

References 19 publications

Unraveling the role of the ghrelin gene peptides in the endocrine pancreas

Unraveling the role of the ghrelin gene peptides in the endocrine pancreas

Obestatin: An Interesting but Controversial Gut Hormone

Ontogeny of Ghrelin, Obestatin, Preproghrelin, and Prohormone Convertases in Rat Pancreas and Stomach

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