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Obestatin (human) Sale

目录号 : GC44483

A peptide hormone

Obestatin (human) Chemical Structure

Cas No.:1081110-72-6

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500μg
¥2,209.00
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产品描述

Obestatin is a 23 amino acid peptide hormone with a conserved C-terminal glycine residue and amidation site that is formed by cleavage of the ghrelin and obestatin prepropeptide. It binds to the orphan receptor GPR39 (Kd = 1 nM) and stimulates cAMP production in CHO and HEK293 cells overexpressing human GPR39. Obestatin inhibits contraction of isolated mouse jejunum muscle strips induced by ghrelin . In vivo, obestatin (12.5-1,000 nmol/kg) suppresses food intake in a time- and dose-dependent manner and reduces body weight gain and gastric emptying in mice. Obestatin (0.22 g per animal) also reduces food intake and glucose response without affecting plasma insulin responses in fasted high-fat diet fed mice.

Chemical Properties

Cas No. 1081110-72-6 SDF
分子式 C116H176N32O33 分子量 2546.8
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mM 0.3926 mL 1.9632 mL 3.9265 mL
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Research Update

Obestatin and cardiovascular health

Peptides 2014 Feb;52:58-60.PMID:24333655DOI:10.1016/j.peptides.2013.11.023.

Obestatin, encoded by the same gene as ghrelin, was first described as a physiological opponent of ghrelin through an interaction with the orphan receptor GPR39. However, the effects of Obestatin were not totally contrary to the effects of ghrelin in cardiovascular regulations based on the recent studies. We summarize here the current evidences surrounding the cardiovascular actions of Obestatin, and the possible implications of Obestatin as a therapeutic agent in common conditions such as hypertension and heart failure.

Obestatin promotes survival of pancreatic beta-cells and human islets and induces expression of genes involved in the regulation of beta-cell mass and function

Diabetes 2008 Apr;57(4):967-79.PMID:18162507DOI:10.2337/db07-1104.

Objective: Obestatin is a newly discovered peptide encoded by the ghrelin gene whose biological functions are poorly understood. We investigated Obestatin effect on survival of beta-cells and human pancreatic islets and the underlying signaling pathways. Research design and methods: beta-Cells and human islets were used to assess Obestatin effect on cell proliferation, survival, apoptosis, intracellular signaling, and gene expression. Results: Obestatin showed specific binding on HIT-T15 and INS-1E beta-cells, bound to glucagon-like peptide-1 receptor (GLP-1R), and recognized ghrelin binding sites. Obestatin exerted proliferative, survival, and antiapoptotic effects under serum-deprived conditions and interferon-gamma/tumor necrosis factor-alpha/interleukin-1 beta treatment, particularly at pharmacological concentrations. Ghrelin receptor antagonist [D-Lys(3)]-growth hormone releasing peptide-6 and anti-ghrelin antibody prevented obestatin-induced survival in beta-cells and human islets. beta-Cells and islet cells released Obestatin, and addition of anti-obestatin antibody reduced their viability. Obestatin increased beta-cell cAMP and activated extracellular signal-related kinase 1/2 (ERK1/2) and phosphatidylinositol 3-kinase (PI 3-kinase)/Akt; its antiapoptotic effect was blocked by inhibition of adenylyl cyclase/cAMP/protein kinase A (PKA), PI 3-kinase/Akt, and ERK1/2 signaling. Moreover, Obestatin upregulated GLP-1R mRNA and insulin receptor substrate-2 (IRS-2) expression and phosphorylation. The GLP-1R antagonist exendin-(9-39) reduced Obestatin effect on beta-cell survival. In human islets, Obestatin, whose immunoreactivity colocalized with that of ghrelin, promoted cell survival and blocked cytokine-induced apoptosis through cAMP increase and involvement of adenylyl cyclase/cAMP/PKA signaling. Moreover, Obestatin 1) induced PI 3-kinase/Akt, ERK1/2, and also cAMP response element-binding protein phosphorylation; 2) stimulated insulin secretion and gene expression; and 3) upregulated GLP-1R, IRS-2, pancreatic and duodenal homeobox-1, and glucokinase mRNA. Conclusions: These results indicate that Obestatin promotes beta-cell and human islet cell survival and stimulates the expression of main regulatory beta-cell genes, identifying a new role for this peptide within the endocrine pancreas.

Ghrelin and Obestatin in human neuroendocrine tumors: expression and effect on Obestatin levels after food intake

Neuroendocrinology 2013;97(4):291-9.PMID:23147274DOI:10.1159/000345366.

Background: Ghrelin and Obestatin are derived from the same peptide hormone precursor and are mainly produced by the gastric mucosa. Ghrelin is involved in many biological processes, whereas the physiological function of Obestatin needs further investigation. The aims of the present study were to establish the incidence of ghrelin- and obestatin-immunoreactive cells in a comprehensive panel of human neuroendocrine tumors (NETs) and to investigate if blood Obestatin concentrations are influenced during a standardized meal stimulation test in healthy individuals and patients with NETs. Materials and methods: The expression of ghrelin and Obestatin was investigated in NETs (n = 149) and other endocrine-related disorders (n = 3) using immunohistochemistry with specific polyclonal antibodies. Coexpression of the peptides was evaluated by double immunofluorescence. Concentrations of Obestatin in blood were measured during a meal test in 6 healthy individuals and 5 patients with pancreatic NETs. Results: Ghrelin and Obestatin were expressed in 14/152 and 19/152 tumor tissues, respectively, mainly representing NETs of foregut origin and in pancreatic tissue from a nesidioblastosis patient. Double immunofluorescence staining showed colocalization of the peptides. During the meal test, Obestatin levels in blood were unchanged in all patients but decreased significantly in the healthy individuals. Conclusion: Only a minority of NETs express ghrelin and Obestatin. However, analysis of patients with tumors originating from tissues that express the peptides in normal conditions could be of importance. The results from the meal test indicate that the hormone levels are affected by food intake in healthy individuals, whereas Obestatin levels remained unchanged in pancreatic NET patients.

The Function and Alteration of Immunological Properties in human Milk of Obese Mothers

Nutrients 2019 Jun 6;11(6):1284.PMID:31174304DOI:10.3390/nu11061284.

Maternal obesity is associated with metabolic changes in mothers and higher risk of obesity in the offspring. Obesity in breastfeeding mothers appears to influence human milk production as well as the quality of human milk. Maternal obesity is associated with alteration of immunological factors concentrations in the human milk, such as C-reactive protein (CRP), leptin, IL-6, insulin, TNF-Alpha, ghrelin, adiponectin, and Obestatin. human milk is considered a first choice for infant nutrition due to the complete profile of macro nutrients, micro nutrients, and immunological properties. It is essential to understand how maternal obesity influences immunological properties of human milk because alterations could impact the nutrition status and health of the infant. This review summarizes the literature regarding the impact of maternal obesity on the concentration of particular immunological properties in the human milk.

Characterization of Obestatin in rat and human stomach and plasma, and its lack of acute effect on feeding behavior in rodents

J Endocrinol 2008 Aug;198(2):339-46.PMID:18480381DOI:10.1677/JOE-08-0082.

Obestatin is a 23-amino acid peptide, initially isolated from rat stomach as an endogenous ligand for the orphan G-protein-coupled receptor. Obestatin is derived from proteolytic cleavage of a 117-amino acid precursor, preproghrelin. Ghrelin increases food intake, body weight, and gastric emptying, whereas Obestatin has the opposite effects. In this study, we characterized Obestatin in both rat and human stomach, and investigated the peptide's effect on feeding behavior. Using reversed-phase high-performance liquid chromatography coupled with RIAs specific for rat and human Obestatin, we detected a very small amount of Obestatin, compared with ghrelin, in the gastric fundi. The ratios of Obestatin to ghrelin are 0.0039 and 1.94% respectively in the rat and human gastric fundi. In humans, plasma Obestatin accounted for 5.21% of the ghrelin concentration, whereas it was undetectable in rat plasma. Plasma ghrelin concentration decreased after a meal in normal subjects, whereas Obestatin concentration did not change. When administered centrally or peripherally, Obestatin did not suppress food intake in either free-feeding or fasted rodents. Administration of Obestatin did not antagonize ghrelin-induced feeding. These findings indicate that Obestatin is present at very low levels compared with ghrelin in both rat and human, and has no acute effect on feeding behavior.