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PubMed1988

Isolation of alligator gar (Lepisosteus spatula) glucagon, oxyntomodulin, and glucagon-like peptide: amino acid sequences of oxyntomodulin and glucagon-like peptide.

Oxyntomodulin, glucagon, and a glucagon-like peptide (GLP) have been isolated from the endocrine pancreas of the alligator gar (Lepisosteus spatula), a ganoid fish. The three peptides were isolated by gel filtration and HPLC and were identified by size, composition, and glucagon-like immunoreactivity. The amino acid sequences of the oxyntomodulin and GLP were determined. The oxyntomodulin contains 36 amino acid residues and its sequence is H S Q G T F T N D Y S K Y L D T R R A Q D F V Q W L M S T K R S G G I T. The composition of the glucagon is identical to the N-terminal 29 residues of the gar oxyntomodulin. The single form of GLP found contains 34 amino acid residues in the following sequence: H A D G T Y T S D V S S Y L Q D Q A A K K F V T W L K Q G Q D R R E. These findings suggest that all three peptides are derived from a common precursor.

Amino Acid Sequence↗

PubMed1991

Oxyntomodulin and its (19-37) and (30-37) fragments inhibit histamine-stimulated gastric acid secretion in the conscious rat.

Oxyntomodulin, a hormone released from jejuno-ileum and composed of the glucagon sequence extended by a C-terminal octapeptide displays original tissue specificity for the gastric mucosa. The aim of this study was to compare the effect of oxyntomodulin on histamine (0.4 mg/kg per h)-stimulated gastric acid secretion in the conscious rat to that of three of its fragments: oxyntomodulin-(19-37) produced from oxyntomodulin by enzymatic cleavage, oxyntomodulin-(30-37) corresponding to the molecular difference between oxyntomodulin and glucagon and oxyntomodulin-(32-37) produced during proglucagon processing to glucagon. The metabolic clearance rate (MCR) in the anesthetized rat was evaluated for each peptide. Oxyntomodulin, oxyntomodulin-(19-37) and oxyntomodulin-(30-37) inhibited the histamine-stimulated gastric acid secretion dose dependently. The dose-response curves for oxyntomodulin and oxyntomodulin-(19-37) were parallel. The potency of oxyntomodulin (19-37) (ED50 approximately 70 pmol/kg) was the same as that of oxyntomodulin (ED50 approximately 35 nmol/kg) after correction of the curve for the MCR (two-fold higher for the fragment). Although the dose-response curve for oxyntomodulin-(30-37) was not entirely parallel to that of the two other peptides, its maximal inhibition (at 15 nmol/kg) was the same as that of oxyntomodulin-(19-37). Thus, oxyntomodulin-(30-37) was an efficient as the longer molecules but approximately 150-fold less potent than oxyntomodulin. The MCR for oxyntomodulin-(30-37) was approximately 250 fold higher than that of oxyntomodulin, partly explaining the difference in potency. The (32-37) fragment, which is naturally released from the endocrine pancreas, was devoid of activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Oxyntomodulin: a cAMP-dependent stimulus of rat parietal cell function via the receptor for glucagon-like peptide-1 (7-36)NH2.

We have previously shown that in highly enriched rat gastric parietal cells the intestinal peptide hormones oxyntomodulin and glucagon-like peptide-2 (GLP-2) compete for receptor-binding with glucagon-like peptide-1 (GLP-1), a potent cAMP-dependent stimulus of H+ production in vitro. It is, however, unknown whether oxyntomodulin and GLP-2 elicit a biological response by interacting with the GLP-1 receptor. Therefore, we used enriched rat parietal cells to investigate the effects of both hormones on the production of cAMP and H+ ([14C]aminopyrine accumulation). Both parameters were stimulated by oxyntomodulin in a concentration-dependent manner. EC50 values were 6.2.10(-8) and 2.5.10(-7) M oxyntomodulin for stimulation of H+ and cAMP production, respectively. The maximally effective concentrations for stimulation of [14C]aminopyrine accumulation and cAMP production were 1.10(-6) and 1.10(-5) M oxyntomodulin, respectively. At these concentrations oxyntomodulin was nearly as effective as 10(-4) M histamine and equally effective as 10(-8) M GLP-1 (7-36)NH2. In the enriched parietal cell preparation there was no immunocytochemical evidence of contaminating D cells. Accordingly, the responses to oxyntomodulin and GLP-1 (7-36)NH2 were not augmented by incubating the cells in the presence of a polyclonal anti-somatostatin antibody. [14C]Aminopyrine accumulation in response to oxyntomodulin was inhibited by the GLP-1 (7-36)NH2 receptor antagonist, exendin (9-39)NH2, but not by the H2-receptor antagonist, ranitidine. Oxyntomodulin and carbachol acted additively to stimulate [14C]aminopyrine accumulation. GLP-2 (10(-7) to 10(-5)M) was without effect on basal H+ and cAMP production; however, at 10(-5) M GLP-2 markedly inhibited oxyntomodulin-stimulated [14C]aminopyrine accumulation. It is concluded that, by interacting with parietal cell receptors for GLP-1 (7-36)NH2, oxyntomodulin, but not GLP-2, directly stimulates H+ production by activating the adenylate cyclase.

Aminopyrine↗

PubMed2001

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.

Animals↗

PubMed1995

Comparative effects of GLP-1-(7-36) amide, oxyntomodulin and glucagon on rabbit gastric parietal cell function.

We have investigated in vitro, the effects of glucagon-like peptide-1-(7-36) amide (GLP-1-(7-36) amide), oxyntomodulin and glucagon on two rabbit parietal cell-enriched fractions (F3, F3n), with parietal cell contents of 60% and 88%, respectively. Histamine (10(-5) M) stimulated [14C]aminopyrine accumulation to an amount of 850% in excess of the basal level, whereas GLP-1-(7-36) amide (10(-7) M) and oxyntomodulin (10(-6) M) induced increases of 50% and 30%, respectively. With a histamine concentration of 10(-6) M, [14C]aminopyrine accumulation was stimulated to 498% in excess of the basal level; GLP-1-(7-36) amide (10(-7) M) and oxyntomodulin (10(-7) M) induced increases of 18% and 15%, respectively. With these parameters, oxyntomodulin[19-37] and glucagon were without effect. Specific binding of [125I]GLP-1-(7-36) amide to parietal cell plasma membranes was inhibited dose-dependently by GLP-1-(7-36) amide, oxyntomodulin and glucagon with inhibitory concentrations of 0.25 nM, 65 nM and 800 nM, respectively. No specific binding of [125I]oxyntomodulin or [125I]glucagon was detectable. GLP-1-(7-36) amide receptor mRNA was only detected in parietal cell-enriched fractions. GLP-1-(7-36) amide, oxyntomodulin and glucagon stimulated parietal cell cAMP production to similar maximal levels with median values close to 0.28 nM, 10.5 nM and 331.7 nM, whereas oxyntomodulin[19-37] had no effect. The maximal cAMP production induced by GLP-1-(7-36) amide, oxyntomodulin or glucagon was additive to that induced by histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyrine↗

PubMed1989

Oxyntomodulin from distal gut. Role in regulation of gastric and pancreatic functions.

We studied the effects of intravenous infusion of synthetic oxyntomodulin (proglucagon 33-69), a potential hormone from the ileal mucosa, on fasting and postprandial gastric acid secretion, gastric emptying, gastroduodenal motility, and pancreatic secretion of trypsin and lipase measured simultaneously in six normal volunteers using multilumen tubes for infusion of markers, manometry, and aspiration of gastric and duodenal contents. The infusion resulted in plasma concentrations of 203 +/- 21 pmol/liter (mean +/- SEM) of oxyntomodulin, regarded as high but not unphysiological concentrations of the peptide. Oxyntomodulin almost abolished basal acid secretion and inhibited postprandial acid secretion by 35 +/- 10%. Gastric emptying decreased significantly; the time for 50% to leave the stomach increased from 17.3 +/- 2.2 min to 34.7 +/- 8.0 min. The postprandial gastroduodenal motility was massively inhibited by oxyntomodulin. Postprandial trypsin and lipase output was significantly inhibited by 56 +/- 12% and 42 +/- 11%, respectively, during oxyntomodulin infusion. However, pancreatic enzyme output was linearly related to gastric emptying and oxyntomodulin did not influence this relationship, suggesting that oxyntomodulins effect was due to its effect on gastric emptying. Oxyntomodulin seems to play an important role in the small intestinal inhibitory control of gastropancreatic functions.

Adult↗

PubMed2006

Oxyntomodulin increases energy expenditure in addition to decreasing energy intake in overweight and obese humans: a randomised controlled trial.

BACKGROUND: Oxyntomodulin has recently been found to decrease body-weight in obese humans and may be a potential anti-obesity therapy. OBJECTIVE: To determine whether oxyntomodulin alters energy expenditure, in addition to reducing energy intake, in 'free-living' overweight and obese volunteers. DESIGN: Randomized double-blind controlled cross-over trial. SETTING: Community and hospital-based. PARTICIPANTS: Fifteen healthy overweight and obese men and women (age: 23-49 years, BMI: 25.1-39.0 kg/m(2)). All volunteers completed the study protocol. INTERVENTIONS: Four-day subcutaneous self-administration of pre-prandial oxyntomodulin, three times daily. Participants were advised to maintain their normal dietary and exercise regimen. MEASUREMENTS: (1) Energy expenditure, measured by indirect calorimetry and combined heart rate and movement monitoring; (2) energy intake, measured during a study meal. RESULTS: Oxyntomodulin administration reduced energy intake at the study meal by 128+/-29 kcal (P=0.0006) or 17.3+/-5.5% (P=0.0071), with no change in meal palatability. Oxyntomodulin did not alter resting energy expenditure; but increased activity-related energy expenditure by 143+/-109 kcal/day or 26.2+/-9.9% (P=0.0221); total energy expenditure by 9.4+/-4.8% (P=0.0454) and physical activity level by 9.5+/-4.6% (P=0.0495). A reduction in body weight of 0.5+/-0.2% was observed during the oxyntomodulin administration period (P=0.0232). CONCLUSION: Oxyntomodulin increases energy expenditure while reducing energy intake resulting in negative energy balance. This data supports the role of oxyntomodulin as a potential anti-obesity therapy.

Adult↗

PubMed2006

Oxyntomodulin : a novel potential treatment for obesity.

The prevalence of obesity is increasing rapidly and the associated morbidity and mortality has led to an urgent need for potential therapeutic targets to reduce appetite and food intake. Gut hormones released after eating that coordinate digestive activity and promote satiety are novel potential treatments for obesity. Oxyntomodulin is a gut hormone that is produced by the L cells in the small intestine and reduces food intake. It is timely to review some of the original literature on oxyntomodulin, to evaluate what is already known about the peptide, and also to set the recent findings on its effects on food intake and bodyweight into context.Recent studies have shown that long-term peripheral administration of oxyntomodulin to rats leads to reduced food intake and reduced weight gain. Studies in humans have demonstrated that acute administration reduces food intake by 19%. When given preprandially by subcutaneous injection three times daily, oxyntomodulin resulted in a reduction in food intake and mean weight loss of 2.8kg over 4 weeks. Oxyntomodulin thus represents a potential therapy for obesity.The mechanism of action of oxyntomodulin is not known. Current evidence suggests that it acts via the glucagon-like peptide 1 (GLP-1) receptor. There may be an additional receptor in the gastric mucosa mediating its effects on gastric acid secretion. Although oxyntomodulin probably acts via the GLP-1 receptor, the two peptides differentially regulate food intake and energy expenditure in the mouse.Oxyntomodulin represents a potential therapy for obesity. Further work will help to clarify its mechanisms of action.

Animals↗

PubMed1994

Stable expression of the rat GLP-I receptor in CHO cells: activation and binding characteristics utilizing GLP-I(7-36)-amide, oxyntomodulin, exendin-4, and exendin(9-39).

Glucagon-like peptide-I (GLP-I) is a potent insulinotropic peptide that mediates its actions at pancreatic B-cells via specific receptors. In the present study we stably expressed the rat B-cell GLP-I receptor in CHO cells and studied binding characteristics and receptor activation utilizing the naturally occurring receptor agonist GLP-I(7-36)-amide (GLP-I), the proglucagon-derived GLP-I-related peptide oxyntomodulin, the GLP-I receptor agonist exendin-4, and the specific antagonist exendin(9-39). The potencies to displace [125I]GLP-I from the receptor were GLP-I > exendin-4 > exendin(9-39) > oxyntomodulin, and to displace [125I]exendin-4 GLP-I = exendin-4 > exendin(9-39) > oxyntomodulin. cAMP production was stimulated equally by GLP-I and exendin-4. Oxyntomodulin was less potent to stimulate cAMP generation. Exendin(9-39) blocked the stimulatory action of GLP-I and exendin-4 on cAMP production, but not that of oxyntomodulin. This study shows that GLP-I and exendin-4 are potent agonists at the transfected rat B-cell GLP-I receptor whereas oxyntomodulin is only a weak GLP-I receptor agonist. Furthermore, exendin(9-39) is a potent GLP-I receptor antagonist. This peptide is a valuable tool to further study the physiological actions of GLP-I.

Animals↗

PubMed2026

Interlaboratory Comparison of a Glucagon and Oxyntomodulin Immuno-LC-MS/MS Assay: Implications for Diabetes Research.

BACKGROUND: The quantification of plasma glucagon and oxyntomodulin is important in the assessment of α-cell function, which is impaired in patients with diabetes. We aimed to transfer between laboratories a novel assay that uses liquid chromatography-tandem mass spectrometry (LC-MS/MS) for the sensitive and specific measurement of these highly homologous hormones. METHODS: Simultaneous measurement of glucagon and oxyntomodulin used immunoaffinity enrichment and LC-MS/MS. Immunoenrichment used monoclonal antibodies that are available at-cost to researchers (deposited at the Developmental Studies Hybridoma Bank). Pure synthetic glucagon, characterized for purity and concentration, was used as a calibrant and is available to others. A detailed standard operating procedure was shared between 3 laboratories and the performance of the method was evaluated with samples collected from patients with and without diabetes. Method comparison was made with 2 commercially available, FDA-registered glucagon immunoassays. RESULTS: The method was linear over the normal range (1-20 pM). When measured in duplicate, the median interlaboratory imprecision (%CV) of the measurement of 40 samples was 6.3% (IQR 4.5%) and 14.4% (IQR 12.4%) for glucagon and oxyntomodulin, respectively. Method comparison with commercially available immunoassays demonstrated good (Mercodia, R = 0.92) or fair (Ansh, R = 0.70) agreement. Multivariable linear regression using LC-MS/MS glucagon and oxyntomodulin concentrations to predict immunoassay results indicated significant cross-reactivity of each immunoassay with oxyntomodulin. CONCLUSION: We have validated a sensitive and specific assay for glucagon and oxyntomodulin that can be deployed in high-complexity clinical laboratories for research or the care of patients. Commercially available glucagon immunoassays have significant interference from molecules other than glucagon.

Journal Article↗

PubMed1997

Oxyntomodulin stimulates intestinal glucose uptake in rats.

BACKGROUND & AIMS: Enteroglucagon peptides have long been proposed as mediators of intestinal adaptation, including mucosal growth and nutrient absorptive capacity. The hypothesis that infusions of oxyntomodulin, a bioactive form of enteroglucagon, would stimulate glucose and amino acid uptake was tested and its effects were compared with those of glucagon. METHODS: Rats were infused intravenously via minipumps with either saline, rat oxyntomodulin (0.47 nmol x kg(-1) x h[-1]), or glucagon (0.88 nmol x kg(-1) x h[-1]) for 7 days, and plasma hormone levels were measured. At death, intestinal dimensions and brush border uptake of D-glucose and L-proline were measured using an in vitro everted sleeve technique. RESULTS: Plasma enteroglucagon and glucagon levels were increased 4- and 12-fold, respectively, but there were no effects on food intake, body weight, or intestinal dimensions. In contrast, oxyntomodulin and glucagon significantly stimulated total intestinal glucose uptake capacity by 44% and 53%, respectively, over controls. Oxyntomodulin most potently enhanced glucose uptake in the ileum (215%), whereas glucagon's greatest effect was in the jejunum (63%-85%). However, neither peptide affected proline uptake. CONCLUSIONS: These results support a new, specific action for oxyntomodulin in intestinal adaptation as a glucose uptake stimulator and confirm glucagon's role as a regulator of glucose uptake.

Animals↗

PubMed1988

Oxyntomodulin: a potential hormone from the distal gut. Pharmacokinetics and effects on gastric acid and insulin secretion in man.

Synthetic oxyntomodulin, a predicted product of the glucagon gene, which is produced in the human lower intestinal mucosa, was infused in doses of 100 and 400 ng kg-1 h-1 into six volunteers to study its pharmacokinetics and effects on pentagastrin-stimulated gastric acid secretion (100 ng kg-1 h-1). The concentration of oxyntomodulin in plasma measured with a cross-reacting glucagon assay increased from 37 +/- 5 to 106 +/- 17 and 301 +/- 40 pmol l-1, respectively. The metabolic clearance rate was 5.2 +/- 0.7 ml kg-1 min-1 and the half-life in plasma was 12 +/- 1 min. Oxyntomodulin reduced the pentagastrin-stimulated acid secretion by 20 +/- 9% during the low-rate infusion (P less than 0.05) and by 76 +/- 10% during the high-rate infusion (P less than 0.05). In accordance with the homology with glucagon, there was a small, significant rise in plasma concentrations of insulin and insulin C-peptide during oxyntomodulin infusion. Oxyntomodulin may therefore be included among the potential incretins and enterogastrones in man.

Gastric Acid↗

PubMed1993

Diurnal profile of oxyntomodulin-like immunoreactivity in duodenal ulcer patients.

Plasma concentrations of oxyntomodulin-like immunoreactivity, a group of intestinal peptides capable of mediating an enterogastrone signal, were measured during a 24-h period in 6 duodenal ulcer patients and compared with those of 16 age-matched controls. Each subject was submitted to 18 oxyntomodulin-like immunoreactivity determinations. Four standardized meals were given during the test. Furthermore, each patient was evaluated for peak acid output after pentagastrin stimulation. The values of the duodenal ulcer subjects were predominantly within normal acid secretion limits. Fasting levels, meal-induced variations, and nocturnal production of oxyntomodulin-like immunoreactivity were similar in the two groups. A negative correlation was observed between peak acid output and oxyntomodulin-like immunoreactivity evaluated either as nocturnal production or as maximum nyctohemeral concentration. We conclude that, taken as a whole, duodenal ulcer disease is not caused by a defect in oxyntomodulin-like immunoreactivity secretion. However, this study does not rule out the possibility of a selective deficiency of these peptides in some duodenal ulcer subgroups such as hypersecretory patients.

Adult↗

PubMedDate not supplied

The effect of oxyntomodulin (glucagon-37) and glucagon on exocrine pancreatic secretion in the conscious rat.

The inhibitory effect of glucagon on exocrine pancreas has been the subject of controversial reports. On the other hand, oxyntomodulin (bioactive enteroglucagon or glucagon-37), a 37 amino acid peptide isolated from porcine lower intestine, has been shown to be 10-20 times more potent than glucagon in inhibiting gastric acid secretion in the rat. In view of this, the effect of glucagon and oxyntomodulin on basal and caerulein-stimulated pancreatic secretion has been studied, during re-introduction of pancreatic juice into duodenum, in the conscious rat provided with pancreatic and duodenal fistulas. A depression of pancreatic function was observed with both peptides on the three parameters studied: (volume of juice secreted, bicarbonate and protein output), either under basal conditions or during stimulation by caerulein. In all the experimental conditions used, oxyntomodulin was ca. ten times more potent than glucagon in its inhibitory effect. The fact that oxyntomodulin, as what is observed in the stomach, is one order of magnitude more potent than glucagon in inhibiting pancreatic secretion suggests that the biological mechanisms by which the peptides of the glucagon-family act on exocrine pancreas are similar, or related to that present at the gastric level.

Animals↗

PubMed1984

A pure enteroglucagon, oxyntomodulin (glucagon 37), stimulates insulin release in perfused rat pancreas.

Oxyntomodulin, a gut peptide recently purified, has been tested in isolated perfused pancreases of normal rats. It was shown to stimulate insulin release monophasically in the presence of a low (6 mM) glucose concentration in the medium. Furthermore, oxyntomodulin potentiated glucose-induced insulin release (10 mM glucose) in a dose-dependent manner, although it was less powerful in this respect than equimolar concentrations of pancreatic glucagon. As oxyntomodulin belongs to the gut glucagon-like immunoreactants which are released during digestion, it is suggested that oxyntomodulin might be one of the factors that could functionally link the gut and the endocrine pancreas and contribute, at least in part, to the regulation of postprandial insulin release.

Animals↗

PubMed2005

Subcutaneous oxyntomodulin reduces body weight in overweight and obese subjects: a double-blind, randomized, controlled trial.

This study investigated the effect of subcutaneously administered oxyntomodulin on body weight in healthy overweight and obese volunteers. Participants self-administered saline or oxyntomodulin subcutaneously in a randomized, double-blind, parallel-group protocol. Injections were self-administered for 4 weeks, three times daily, 30 min before each meal. The volunteers were asked to maintain their regular diet and level of physical exercise during the study period. Subjects' body weight, energy intake, and levels of adipose hormones were assessed at the start and end of the study. Body weight was reduced by 2.3 +/- 0.4 kg in the treatment group over the study period compared with 0.5 +/- 0.5 kg in the control group (P = 0.0106). On average, the treatment group had an additional 0.45-kg weight loss per week. The treatment group demonstrated a reduction in leptin and an increase in adiponectin. Energy intake by the treatment group was significantly reduced by 170 +/- 37 kcal (25 +/- 5%) at the initial study meal (P = 0.0007) and by 250 +/- 63 kcal (35 +/- 9%) at the final study meal (P = 0.0023), with no change in subjective food palatability. Oxyntomodulin treatment resulted in weight loss and a change in the levels of adipose hormones consistent with a loss of adipose tissue. The anorectic effect was maintained over the 4-week period. Oxyntomodulin represents a potential therapy for obesity.

Adiponectin↗

PubMed1988

Isolation of peptide hormones from the pancreas of the bullfrog (Rana catesbeiana). Amino acid sequences of pancreatic polypeptide, oxyntomodulin, and two glucagon-like peptides.

Insulin, pancreatic polypeptide, glucagon, oxyntomodulin, and two distinct glucagon-like peptides were isolated from acidic ethanol extracts of bullfrog pancreas by gel filtration followed by high pressure liquid chromatography. The amino acid sequences of pancreatic polypeptide, oxyntomodulin, and both glucagon-like peptides were determined. Frog pancreatic polypeptide contains 36 amino acid residues and has a COOH-terminal phenylalaninamide. It is more homologous with human pancreatic polypeptide (61%) than other characterized members of this family of peptides. Frog glucagon has an amino acid composition identical to the NH2-terminal 29 residues of the larger, more abundant oxyntomodulin and was not sequenced. The finding of a single form of glucagon and oxyntomodulin, but two glucagon-like peptides in frog pancreas extract is similar to that found or deduced for mammals.

Amino Acid Sequence↗

PubMed2006

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

Oxyntomodulin and peptide tyrosine-tyrosine (PYY) are released from intestinal enteroendocrine cells in response to a meal. These circulating hormones are considered to be satiety signals, as they have been found to decrease food intake, body weight and adiposity in rodents. Their effect on energy homeostasis is mediated by the hypothalamus and brainstem, and several studies have demonstrated alterations in neuropeptide signaling within the arcuate nucleus. The weight loss that has been observed in animal models after repeated administration of oxyntomodulin and PYY has led to interest in developing these peptides as antiobesity therapies in humans. Indeed, preliminary studies have found that oxyntomodulin or PYY administration reduces food intake and body weight effectively in overweight human volunteers. This research suggests that modulation of these gut hormones could prove to be effective long-term therapies in the quest to combat the obesity epidemic.

Animals↗