Obestatin (rat)Endogenous reported anorexigenic peptide CAS# 869705-22-6 |
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Quality Control & MSDS
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| Cas No. | 869705-22-6 | SDF | Download SDF |
| PubChem ID | 71311910 | Appearance | Powder |
| Formula | C114H174N34O31 | M.Wt | 2516.84 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble to 1 mg/ml in water | ||
| Sequence | FNAPFDVGIKLSGAQYQQHGRAL (Modifications: Leu-23 = C-terminal amide) | ||
| SMILES | CCC(C)C(C(=O)NC(CCCCN)C(=O)NC(CC(C)C)C(=O)NC(CO)C(=O)NCC(=O)NC(C)C(=O)NC(CCC(=O)N)C(=O)NC(CC1=CC=C(C=C1)O)C(=O)NC(CCC(=O)N)C(=O)NC(CCC(=O)N)C(=O)NC(CC2=CNC=N2)C(=O)NCC(=O)NC(CCCNC(=N)N)C(=O)NC(C)C(=O)NC(CC(C)C)C(=O)N)NC(=O)CNC(=O)C(C(C)C)NC(=O)C(CC(=O)O)NC(=O)C(CC3=CC=CC=C3)NC(=O)C4CCCN4C(=O)C(C)NC(=O)C(CC(=O)N)NC(=O)C(CC5=CC=CC=C5)N | ||
| Standard InChIKey | OJSXICLEROKMBP-FFUDWAICSA-N | ||
| Standard InChI | InChI=1S/C114H174N34O31/c1-12-60(8)93(146-90(157)54-128-111(177)92(59(6)7)147-109(175)81(50-91(158)159)143-108(174)78(46-65-25-17-14-18-26-65)144-110(176)83-29-22-42-148(83)113(179)63(11)132-105(171)80(49-87(120)154)139-97(163)69(116)45-64-23-15-13-16-24-64)112(178)137-71(27-19-20-40-115)101(167)140-76(44-58(4)5)106(172)145-82(55-149)99(165)127-52-88(155)130-61(9)95(161)134-72(34-37-84(117)151)103(169)141-77(47-66-30-32-68(150)33-31-66)107(173)136-73(35-38-85(118)152)102(168)135-74(36-39-86(119)153)104(170)142-79(48-67-51-124-56-129-67)98(164)126-53-89(156)133-70(28-21-41-125-114(122)123)100(166)131-62(10)96(162)138-75(94(121)160)43-57(2)3/h13-18,23-26,30-33,51,56-63,69-83,92-93,149-150H,12,19-22,27-29,34-50,52-55,115-116H2,1-11H3,(H2,117,151)(H2,118,152)(H2,119,153)(H2,120,154)(H2,121,160)(H,124,129)(H,126,164)(H,127,165)(H,128,177)(H,130,155)(H,131,166)(H,132,171)(H,133,156)(H,134,161)(H,135,168)(H,136,173)(H,137,178)(H,138,162)(H,139,163)(H,140,167)(H,141,169)(H,142,170)(H,143,174)(H,144,176)(H,145,172)(H,146,157)(H,147,175)(H,158,159)(H4,122,123,125)/t60-,61-,62-,63-,69-,70-,71-,72-,73-,74-,75-,76-,77-,78-,79-,80-,81-,82-,83-,92-,93-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Endogenous peptide derived from the same prepropeptide as ghrelin. Reported to suppress food intake and reduce body weight-gain in rats. |
Obestatin (rat) Dilution Calculator
Obestatin (rat) Molarity Calculator
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Maternal High-Fat Diet during Pregnancy and Lactation Influences Obestatin and Ghrelin Concentrations in Milk and Plasma of Wistar Rat Dams and Their Offspring.[Pubmed:27127509]
Int J Endocrinol. 2016;2016:5739763.
The study aims to establish the effect of a maternal high-fat diet on obestatin concentration, total ghrelin, and ghrelin/obestatin ratio during pregnancy and lactation of Wistar rats and their offspring in the first 21 days of life. On the mating day, females were randomly allocated and fed either a high-fat diet (30% of fat; HF) or breeding diet (5% fat; BD) till the 21st day of lactation. Hormones were analyzed in the blood plasma and milk of rat dams as well as in the blood plasma of their offspring. HF resulted in a significant decrease in obestatin level on the 14th day of lactation and elevation on the 21st day. Plasma obestatin in HFD offspring was significantly higher than in BD ones. HF diet did not significantly affect dam plasma ghrelin until the 21st day of lactation. The ghrelin concentrations in milk after both diets were significantly lower than in blood plasma. Milk ghrelin in HF dams was significantly higher than in the BD ones. Plasma ghrelin from HF offspring was significantly higher than that from BD dams. Our results demonstrate that a maternal HF diet during pregnancy and lactation influences ghrelin and obestatin level in both dams and their offspring.
Changes in obestatin gene and GPR39 receptor expression in peripheral tissues of rat models of obesity, type 1 and type 2 diabetes.[Pubmed:27106635]
J Diabetes. 2017 Apr;9(4):353-361.
BACKGROUND: Obestatin has a role in regulating food intake and energy expenditure, but the roles of obestatin and the GPR39 receptor in obesity and type 1 and type 2 diabetes mellitus (T1DM and T2DM, respectively) are not well understood. The aim of the present study was to investigate changes in obestatin and GPR39 in pathophysiological conditions like obesity, T1DM, and T2DM. METHODS: Using rat models of diet-induced obesity (DIO), T1DM and T2DM (n = 14 per group), obestatin, its precursor protein preproghrelin, and GPR39 expression was investigated in tissues involved in glucose and lipid homeostasis regulation. Furthermore, serum obestatin and ghrelin concentrations were determined. RESULTS: Serum obestatin concentrations were positively correlated with glucagon (r = 0.6456; P < 0.001) and visfatin (r = 0.5560; P < 0.001), and negatively correlated with insulin (r = -0.4362; P < 0.05), adiponectin (r = -0.3998; P < 0.05), and leptin (r = -0.4180; P < 0.05). There were differences in GPR39 and preproghrelin expression in the three animal models. Hepatic GPR39 and preproghrelin mRNA expression was greater in T1DM, T2DM, and obese rats than in lean controls, whereas pancreatic GPR39 mRNA and protein and preproghrelin mRNA expression was decreased in T1DM, T2DM, and DIO rats. Higher GPR39 and preproghrelin protein and mRNA levels were found in adipose tissues of T1DM compared with control. In adipose tissues of T2DM and DIO rats, GPR39 protein levels were lower than in lean or T1DM rats. Preproghrelin mRNA was higher in adipose tissues of T1DM, T2DM, and DIO than lean rats. CONCLUSION: We hypothesize that changes in obestatin, GPR39, and ghrelin may contribute to metabolic abnormalities in T1DM, T2DM, and obesity.
The role of obestatin in Roux-en-Y gastric bypass surgery in the obese, type 2 diabetes Zucker rat.[Pubmed:27449711]
Diabetes Res Clin Pract. 2016 Sep;119:57-64.
AIMS: Roux-en-Y gastric bypass (RYGB) is a novel therapy for diabetes and the exact mechanisms of this procedure remain unclear. Obestatin is an important gut hormone. We aimed to explore the role of obestatin in the therapeutic mechanism of RYGB. METHODS: Twenty obese Zucker rats and twenty Wistar rats were randomly assigned to two groups: RYGB and sham surgery. We evaluated plasma obestatin and insulin levels pre- and post-RYGB. Additionally, obestatin expression levels in the gastrointestinal tract were assessed using immunohistochemical staining. RESULTS: In Zucker rats, plasma obestatin and insulin levels gradually increased after RYGB. At post-operation week 7, plasma levels of obestatin were higher in the RYGB group than the sham operation group, and fasting plasma insulin levels were significantly increased the in RYGB group compared with the sham operation group. Furthermore, we observed a positive relationship between obestatin and insulin plasma levels. Among 10 zucker rats, high expression of obestatin was only seen in the jejunum of 2 rats before the operation; however, high expression of obestatin was seen in the Roux limb of 8 rats and in the ileum of 7 rats after RYGB. The expression of obestatin was significantly higher in the intestine in the RYGB group than the sham operation group postoperatively. CONCLUSIONS: We propose that obestatin maybe a potential mediator to improve glucose homeostasis after RYGB. The increase of obestatin secretion may be an important mechanism through which RYGB alleviates obesity and type 2 diabetes mellitus.
Obestatin modulates ghrelin's effects on the basal and stimulated testosterone secretion by the testis of rat: an in vitro study.[Pubmed:27782745]
Physiol Res. 2017 Mar 31;66(1):93-98. Epub 2016 Oct 26.
The functional antagonism between obestatin and ghrelin in the testis is under investigation. We investigated the ability of obestatin to counteract the inhibitory effect of ghrelin on basal and stimulated testosterone (T) secretion in vitro. Testicular strips from adult rats were incubated with 10 ng/ml and 100 ng/ml of obestatin alone, ghrelin alone and obestatin + ghrelin. Obestatin modulation of stimulated T secretion was evaluated by incubation of testicular samples with 10 ng/ml and 100 ng/ml obestatin, ghrelin and obestatin + ghrelin in the absence and presence of 10 IU of human chorionic gonadotrophin (hCG). T concentrations in the hCG treated groups were significantly (P<0.0001) higher than those in the control groups. Obestatin caused a significant increase in basal T secretion in a dose-dependent manner; however, obestatin at the both 10 ng/ml and 100 ng/ml significantly (P<0.0001) increased hCG-stimulated T secretion. In contrast, ghrelin in a dose-dependent manner significantly (P<0.001) decreased both basal and hCG-induced T secretion by testicular slices. Obestatin opposed the inhibitory effect of ghrelin on T secretion under both basal and hCG-stimulated conditions at all doses tested. In conclusions, administration of obestatin was able to antagonize the inhibitory effect of ghrelin on testosterone secretion in vitro.
Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intake.[Pubmed:16284174]
Science. 2005 Nov 11;310(5750):996-9.
Ghrelin, a circulating appetite-inducing hormone, is derived from a prohormone by posttranslational processing. On the basis of the bioinformatic prediction that another peptide also derived from proghrelin exists, we isolated a hormone from rat stomach and named it obestatin-a contraction of obese, from the Latin "obedere," meaning to devour, and "statin," denoting suppression. Contrary to the appetite-stimulating effects of ghrelin, treatment of rats with obestatin suppressed food intake, inhibited jejunal contraction, and decreased body-weight gain. Obestatin bound to the orphan G protein-coupled receptor GPR39. Thus, two peptide hormones with opposing action in weight regulation are derived from the same ghrelin gene. After differential modification, these hormones activate distinct receptors.
