RIA Kits

Oxyntomodulin (Human) RIA Kit (RK-028-22) specially designed for Pharmacokinetic Studies and Ultra-Sensitive Oxyntomodulin RIA Kit (RKU-028-22) for

Mapping in Human Pancreas Cancer Tissue (H-028-22)

Mapping in Rat/Mouse Intestine Tissue (H-028-22)

Protocol for antibody staining

Mapping in Human Pancreas Tissues by Glucagon (H-028-05)

Protocol for antibody staining

Related Articles

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 et al. 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 et al. Endocrinology. 2004 Jun;145(6):2687-95.

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.

                                               Plasma levels of OLI ( Oxyntomodulin-like immunoactivity)

Infusion of OXM elevated plasma OLI from 62 ± 5 pmol/liter ( 275.89 ± 22. 24 pg/ml ) to a peak of 907 ± 32 pmol/liter ( 4036.06 ± 142.39 pg/ml) at t60 . In comparison, on the saline infusion day, consumption of the buffet meal led to a peak postprandial OLI level of 151 ± 18 pmol/liter at 195 min. Gel permeation analysis of plasma samples during OXM infusion demonstrated a single immunoreactive peak eluting in the same position as synthetic OXM (Kav = 0.6). Thus, intact full-length OXM was the principle circulating form.
Cohen et al. J Clin Endocrinol Metab. 2003 Oct;88(10):4696-701.

The role of oxyntomodulin and peptide tyrosine–tyrosine (PYY) in appetite control

Oxyntomodulin and PYY(3–36) act as circulating satiety signals. In the intestinal tract, nutrient intake stimulates release of oxyntomodulin and PYY from specialized enteroendocrine L cells. The action of DPP-4 on PYY produces the biologically active truncated form PYY(3–36), which together with oxyntomodulin crosses the blood–brain barrier and binds to receptors on neurons in the ARC.

                                                Oxyntomodulin and PYY3–36 act as circulating satiety signals

In the intestinal tract, nutrient intake stimulates release of oxyntomodulin and PYY from specialized enteroendocrine L cells. The action of DPP-4 on PYY produces the biologically active truncated form PYY3–36, which together with oxyntomodulin crosses the blood–brain barrier and binds to receptors on neurons in the ARC. Abbreviations: 3V, third ventricle; ARC, arcuate nucleus; DPP-4, dipeptidyl peptidase 4; GLP-1R, glucagon-like peptide 1 receptor; PVN, paraventricular nucleus; PYY, peptide tyrosine–tyrosine; Y2R, Y2 receptor.
Wynne et al. Nat Clin Pract Endocrinol Metab. 2006 Nov;2(11):612-20.

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