Oxyntomodulin RIA Kit

Catalog Number

Product Name

Quantity

$US

RKU-028-22

Oxyntomodulin (Human, Rat, Mouse) , Ultra-Sensitive RIA Kit

125 tubes

475

RK-028-22

Oxyntomodulin RIA Kit

125 tubes

475

028-27

C-terminal octapeptide [Oxyntomodulin (30-37)] (H, R, M)

200 ug

120

T-028-27

C-terminal octapeptide [Oxyntomodulin (30-37)] (H, R, M), Iodine 125 labeled tracer

10uCi

595

028-29

Oxyntomodulin (32-37) (H, R, M)

200 ug

100

028-30

Oxyntomodulin (19-37) (H, R, M)

100 ug

150

EK-028-14

Glucagon-Like Peptide-2 (GLP-2) EIA Kit

96 wells

350

H-028-22

Oxyntomodulin (Human, Mouse, Rat) Antiserum

100ul

450

G-028-22

Oxyntomodulin (Human, Mouse, Rat) Purified IgG

200ug

450

B-G-028-22

Oxyntomodulin (Human, Mouse, Rat) Purified IgG, Biotin labeled

100ul

495

FG-G-028-22-A

Oxyntomodulin (Human, Mouse, Rat) Purified IgG, FAM labeled

100ul

495

FG-G-028-22-B

Oxyntomodulin (Human, Mouse, Rat) Purified IgG, FITC labeled

100ul

495

FC3-G-028-22

Oxyntomodulin (Human, Mouse, Rat) Purified IgG, Cy3 labeled

100ul

595

T-G-028-22

Oxyntomodulin (Human, Mouse, Rat) Purified IgG, Iodine 125 labeled tracer

10uCi

650

H-028-05

Glucagon (19-29) (Human, Mouse, Rat) Antibody

100 ul

275

G-028-05

Glucagon (19-29) (Human, Mouse, Rat) Antibody, Purified IgG

200 ug

450

H-028-16

Oxyntomodulin (Porcine), Antiserum for immunohistochemistry

100ul

450

G-028-16

Oxyntomodulin (Porcine), Purified IgG

200ug

450

B-G-028-16

Oxyntomodulin (Porcine), Purified IgG, Biotin labeled

100ul

495

FG-G-028-16-A

Oxyntomodulin (Porcine), Purified IgG, FAM labeled

100ul

495

FG-G-028-16-B

Oxyntomodulin (Porcine), Purified IgG, FITC labeled

100ul

495

FC3-G-028-16

Oxyntomodulin (Porcine), Purified IgG, Cy3 labeled

100ul

595

T-G-028-16

Oxyntomodulin (Porcine) Purified IgG, Iodine 125 labeled tracer

10uCi

650

028-22

Oxyntomodulin (Human, Mouse, Rat)

100 �g

200

T-028-22

Oxyntomodulin (Human, Mouse, Rat), 125I labeled

10 �Ci

595

B-028-22

Oxyntomodulin (Human, Mouse, Rat), Biotin labeled

20 �g

350

FC3-028-22

Oxyntomodulin (Human, Mouse, Rat), Cy3 labeled

1 nmol

450

FC5-028-22

Oxyntomodulin (Human, Mouse, Rat), Cy3 labeled

1 nmol

450

FG-028-22

Oxyntomodulin (Human, Mouse, Rat), FAM labeled

1 nmol

350

FR-028-22

Oxyntomodulin (Human, Mouse, Rat), Rhodamine labeled

1 nmol

350

Central pre-proglucagon derived peptides: opportunities for treatment of obesity

Modern societies have moved from famine to feast and obesity and its co-morbidities now sweep the world as a global epidemic. Numerous scientific laboratories and pharmaceutical companies have taken the challenge and are now exploiting novel molecular targets for treatment of obesity. The pre-proglucagon system constitutes interesting candidates as potential targets for new anti-obesity drugs. In the periphery, pre-proglucagon derived peptides, Glucagon-Like Peptide-1 (GLP-1), Glucagon-Like Peptide-2 (GLP-2) and oxyntomodulin (OXM) are involved in a wide variety of physiological functions, including glucose homeostasis, gastric emptying, intestinal growth, insulin secretion as well as the regulation of food intake. Peripheral administration of GLP-1 derivatives and analogues to both rodents and man have shown promising effects on food intake and body weight suggesting that such therapies constitute potential anti-obesity treatment. In the central nervous system, pre-proglucagon and hence GLP-1, GLP-2 and OXM are exclusively found in a small population of nerve cells in the nucleus of the solitary tract. These constitute a neural pathway linking the "viscero-sensory" brainstem to hypothalamic nuclei involved in energy homeostasis. Intracerebroventricular administration of all of the three derived peptides robustly decrease food intake. It is evident that central GLP-1 agonism probably in combination with GLP-2 and/or OXM agonism constitute a potential pharmacological tool to reduce food intake and maybe also enhance energy expenditure. This and other aspects of the current state of the role of central pre-proglucagon in energy homeostasis are reviewed.

Larsen PJ, Vrang N, Tang-Christensen M. Curr Pharm Des. 2003;9(17):1373-82.

Peripheral oxyntomodulin reduces food intake and body weight gain in rats

Oxyntomodulin (OXM) is a circulating gut hormone released post-prandially from cells of the gastrointestinal mucosa. Given intracerebroventricularly to rats, it inhibits food intake and promotes weight loss. Here we report that peripheral (intraperitoneal; IP) administration of OXM dose-dependently inhibited both fast-induced and dark phase food intake without delaying gastric emptying. Peripheral OXM administration also inhibited fasting plasma ghrelin. In addition, there was a significant increase in c-fos immunoreactivity, a marker of neuronal activation, in the arcuate nucleus (ARC). OXM injected directly into the ARC caused a potent and sustained reduction in refeeding following a fast. The anorectic actions of IP OXM were blocked by prior intra-ARC administration of the GLP-1 receptor antagonist, exendin9-39, suggesting that the ARC, lacking a complete blood-brain barrier, could be a potential site of action for circulating OXM. The actions of IP GLP-1, however, were not blocked by prior intra-ARC administration of exendin9-39, indicating the potential existence of different OXM and GLP-1 pathways. Seven-day IP administration of OXM caused a reduction in the rate of body weight gain and adiposity. Circulating OXM may have a role in the regulation of food intake and body weight.

Dakin CL, Small CJ, Batterham RL, Neary NM, Cohen MA, Patterson M, Ghatei MA, Bloom SR. Endocrinology. 2004 Mar 4 [Epub ahead of print]

Oxyntomodulin inhibits food intake in the rat

Oxyntomodulin is derived from proglucagon processing in the intestine and the central nervous system. To date, no role in the central nervous system has been demonstrated. We report here that oxyntomodulin inhibits refeeding when injected intracerebroventricularly and into the hypothalamic paraventricular nucleus of 24-h fasted rats [intracerebroventricularly and into the paraventricular nucleus, 1 h, oxyntomodulin (1 nmol), 3.1 0.5 g; saline, 6.2 0.4 g; P < 0.005]. In addition, oxyntomodulin inhibits food intake in nonfasted rats injected at the onset of the dark phase (intracerebroventricularly, 1 h: oxyntomodulin, 3 nmol, 1.1 0.19 g vs. saline, 2.3 0.2 g; P < 0.05). This effect of oxyntomodulin on feeding is of a similar time course and magnitude as that of an equimolar dose of glucagon-like peptide-1. Other proglucagon-derived products investigated [glucagon, glicentin (intracerebroventricularly, 3 nmol; into the paraventricular nucleus, 1 nmol), and spacer peptide-1 (intracerebroventricularly and into the paraventricular nucleus, 3 nmol)] had no effect on feeding at any time point examined. The anorectic effect of oxyntomodulin (intracerebroventricularly, 3 nmol; into the paraventricular nucleus, 1 nmol) was blocked when it was coadministered with the glucagon-like peptide-1 receptor antagonist, exendin-(9-39) (intracerebroventricularly, 100 nmol; into the paraventricular nucleus, 10 nmol). However, oxyntomodulin has a lower affinity for the glucagon-like peptide-1 receptor compared with glucagon-like peptide-1 (IC(50): oxyntomodulin, 8.2 nM; glucagon-like peptide-1, 0.16 nM). One explanation for this is that there might be an oxyntomodulin receptor to which exendin-(9-39) can also bind and act as an antagonist.

Dakin CL, et al. Endocrinology. 2001 Oct;142(10):4244-50

Oxyntomodulin suppresses appetite and reduces food intake in humans

Oxyntomodulin (OXM) is released from the gut postprandially, in proportion to energy intake, and circulating levels of OXM are elevated in several conditions associated with anorexia. Central injection of OXM reduces food intake and weight gain in rodents, suggesting that OXM signals food ingestion to hypothalamic appetite-regulating circuits. We investigated the effect of iv OXM (3.0 pmol/kg.min) on appetite and food intake in 13 healthy subjects (body mass index, 22.5 0.9 kg/m(2)) in a randomized, double-blind, placebo-controlled, cross-over study. Infusion of OXM significantly reduced ad libitum energy intake at a buffet meal (mean decrease, 19.3 5.6%; P < 0.01) and caused a significant reduction in scores for hunger. In addition, cumulative 12-h energy intake was significantly reduced by infusion of OXM (mean decrease, 11.3 6.2%; P < 0.05). OXM did not cause nausea or affect food palatability. Preprandial levels of the appetite-stimulatory hormone, ghrelin, were significantly suppressed by OXM (mean reduction, 44 10% of postprandial decrease; P < 0.0001). Elevated levels of endogenous OXM associated with disorders of the gastrointestinal tract may contribute to anorexia.

Cohen MA, et al. J Clin Endocrinol Metab. 2003 Oct;88(10):4696-701

Data Sheet

Oxyntomodulin (Human) RIA Kit for Pharmacokinetic Study

Data Sheet

Data Sheet

Data / Protocol

Data / Protocol

Immunohistochemistry (peroxidase method with DAB colorization) for GLP-1 (1/500 dilution antiserum for human GLP-17–37 (Phoenix Pharmaceuticals, Mountain View, California, USA) in pancreata from vehicle-treated (a) or STZ-treated (c and d) rats. This antiserum recognizes GLP-17-37 and GLP-11-37) and may recognize proglucagon and MPGF, but not amidated forms of GLP-1 or glucagon. A large increase in GLP-1 immunoreactivity is seen in the STZ-treated islets corresponding to cells that stain for glucagon. Scale bar = 50 µm; 2 animals per group. Nie Y., et al. J Clin Invest, April 2000, Volume 105, Number 7, 955-965

Data Sheet / Protocol

Structure of proglucagon and biological actions of GLP-1 and GLP-2. The principal target cell types for GLP-1 (islet � cells stained with insulin antiserum) and GLP-2 (intestinal endocrine cells stained with GLP-2 receptor antiserum) are shown below the peptide sequences. The biological actions of the peptides are summarized below. GRPP, Glicentin-related pancreatic polypeptide; IP, intervening peptide; GLP-2R, glucagon-like peptide-2 receptor.

Drucker DJ. Endocrinology. 2001 Feb;142(2):521-7.







Mads Tang-Christensen et al. The proglucagon-derived peptide, glucagon-like peptide-2, is a neurotransmitter involved in the regulation of food intake. Nature Medicine 6, 802 - 807 (2000)


Comparison of the effects of ICV and iPVN proglucagonderived and related products on food intake in fasted rats. A, Cumulative food intake (grams) up to 8 h after ICV injection of GLP-1, OXM, glucagon, or glicentin (all 3 nmol) into fasted animals. , P < 0.05 vs.* saline control, B, Cumulative food intake (grams) up to 24 h after an acute iPVN injection of GLP-1, OXM (both 1 nmol), or exendin-4 (0.03 nmol) into fasted animals. , P < 0.01 vs.* saline control for all groups at 1, 2, and 4 h. , P < 0.05 vs.* saline control for exendin-4 only at 8 h. Dakin CL, et al. Endocrinology. 2001 Oct;142(10):4244-50	Effects of ICV and iPVN OXM on food intake in fasted rats. A, Cumulative food intake (grams) up to 8 h after an acute ICV injection of OXM (0.3, 1, 3, or 10 nmol). B, Cumulative food intake (grams) up to 8 h after an acute iPVN injection of OXM (0.1, 0.3, or 1.0 nmol) into fasted animals. , P < 0.05 vs.* saline control. Dakin CL, et al. Endocrinology. 2001 Oct;142(10):4244-50

Inhibition of OXM and GLP-1 effects on food intake by exendin-(9�39). A, Food intake 1 h after an acute ICV injection of GLP-1 (3 nmol), GLP-1 plus exendin-(9�39) (30 nmol), OXM (3 nmol), OXM and exendin- (9�39) (30 nmol), or exendin- (9�39) alone (30 nmol). B, Food intake after an acute iPVN injection of GLP-1 (1 nmol), GLP-1 and exendin-(9�39) (10 nmol), OXM (1 nmol), OXM and exendin-(9�39) (10 nmol), or exendin-(9�39) alone (10 nmol) into fasted animals. *, P < 0.005 vs.* saline control.	Effect of ICV OXM at the onset of the dark phase. Sated rats received an ICV injection of OXM, GLP-1 (3 nmol), or saline at the onset of the dark phase. Food intake (grams; A) and behaviors (B) at 1 h postinjection were determined. , P < 0.05 vs.* saline control.