Peptide YY Levels Research Articles

Effects of hemorrhage and opiate antagonists on adrenal release of neuropeptides in cats

Concurrent levels of methionine-enkephalin (ME), neuropeptide Y (NPY), peptide YY (PYY), neurotensin (NT), vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK) and bombesin (BMB) were measured in adrenal vein (AD), femoral vein (FV) and femoral artery (FA) under baseline conditions and during hypotensive hemorrhage (HTH) in halothane anesthetized cats (Group II, n=6) and compared to a non-bled control group (Group I, n=6). Five cats (Group III) received an IV bolus of naltrexone (1 mg/kg) followed by a continuous infusion prior to induction of HTH. A blood volume loss of ∼40% evoked a selective increase in AD levels of ME, NPY, PYY and NT. No differences in regard to hemodynamics and pattern of neuropeptide levels were observed between Group II and Group III. Administration of naloxone (1 mg/kg, IV) in Group I and Group II at the end of the experiment led to a significant increase in MABP in both groups but did not evoke changes in neuropeptide levels. We conclude that adrenal neuropeptide release during hypotensive hemorrhage is not modulated by actions on opiate receptors in the halothane anesthetized cat.

Increased plasma levels of peptide YY in coeliac disease.

Peptide YY (PYY) is exclusively localized in endocrine cells in the gut, and these cells are most numerous in the distal small intestine, colon, and rectum. We have earlier shown that PYY coexists with enteroglucagon in the gut endocrine cells. High basal and postprandial plasma enteroglucagon concentrations have earlier been found in patients with untreated coeliac disease. PYY circulates in human plasma and is detectable in most healthy adults. We have therefore studied the basal PYY levels in patients with coeliac disease. Marked elevated basal plasma PYY levels were found in patients with coeliac disease compared with an age- and sex-matched control group. The PYY levels were inversely correlated to the concentration of folate acid in serum. The PYY levels were studied in four patients with newly diagnosed disease and had normalized within 8 months on a gluten-free diet.

Oxygen toxicity in the infant rhesus monkey: effects on regulatory peptides in lung and blood.

A total of ten 6-month-old male rhesus monkey (Macaca mulatta) infants, born full-term, were positive-pressure ventilated with greater than 95% oxygen or room air (controls). A protocol was used which closely simulated pediatric intensive care. To test if regulatory peptides were affected by the oxygen treatment, and to search for an early marker of oxygen toxicity, lung tissue samples and systemic mixed venous blood were collected at 6, 12 and 24 hours after onset of treatment. The peptides, gastrin releasing peptide (GRP), calcitonin gene-related peptide (CGRP), peptide YY (PYY), vasoactive intestinal peptide (VIP) and somatostatin (SOM), were quantitated in lung tissue extracts and plasma using radioimmunoassay. Lung tissue GRP, CGRP, and PYY levels appeared to decrease gradually with time, perhaps as a result of the positive pressure ventilation procedure. GRP and CGRP levels decreased less among monkey infants ventilated with oxygen, thus they were significantly higher at 24 hours than in air ventilated controls. VIP levels were significantly lower among tests compared to controls at that time. Blood peptide levels did not change with oxygen treatment. These results suggest that tissue concentrations of certain pulmonary regulatory peptides can become altered by ventilation with greater than 95% oxygen. A blood borne peptide marker was not identified.

Peptide YY abnormalities in patients with ulcerative colitis.

Peptide YY concentrations in both rectal mucosa and fasting plasma, which were produced by endocrine cells in the lower gastrointestinal tract, were measured in normal subjects and patients with ulcerative colitis by specific radioimmunoassay and were examined in the relation to histopathological changes and extent of lesions of ulcerative colitis. Peptide YY levels of rectal mucosa (11.0 +/- 1.4 pmol/mg protein) and fasting plasma (53.3 +/- 7.9 fmol/ml) of patients with ulcerative colitis were significantly lower (p less than 0.001) than those of normal subjects (31.5 +/- 3.4 pmol/mg protein and 160.7 +/- 19.7 fmol/ml). It appears that the decreased PYY level in rectal mucosa and fasting plasma is related to crypt destruction and reduction of mucosal cell. These changes of PYY levels in rectal mucosa and fasting plasma suggest a presence of relationship between concentrations of peptide YY and severity of lesions in patients with ulcerative colitis.

Cerebrospinal fluid peptide YY immunoreactivity in eating disorders.

Peptide YY (PYY), a recently discovered peptide, is a potent stimulant of eating behavior in rats. We developed a radioimmunoassay for PYY and measured cerebrospinal fluid (CSF) levels in subjects with anorexia nervosa, bulimia and matched normal controls. Bulimics who had abstained from bingeing for 30 days showed a dramatic increase in CSF PYY levels compared to normal values (p less than 0.001) or their own values when actively bingeing (p less than 0.01, paired t test). No differences were seen for anorexia nervosa. These results suggest that bulimic behavior may correct a central nervous system abnormality in PYY.

Peptide YY interacts with secretin and duodenal acidification to inhibit gastric acid secretion.

Previous studies have indicated that plasma levels of peptide YY (PYY) increase significantly after a meal. The purpose of this study was to characterize the interaction of PYY and secretin in the inhibition of gastric acid secretion, and to determine whether PYY can influence acid-induced inhibition of gastric acid secretion in conscious dogs. I.v. administration of PYY at 200 pmol/kg/h inhibited pentagastrin (1 microgram/kg/h)-stimulated gastric acid output (P less than 0.05). PYY further augmented i.v. secretin-induced inhibition of pentagastrin-stimulated gastric acid output by 32 +/- 7%, and intraduodenal hydrochloric acid-induced inhibition of pentagastrin-stimulated gastric acid output by 40 +/- 12%. The mean integrated release of secretin response to duodenal acidification (3.9 +/- 1.0 ng-[0-60] min/ml) was not affected by PYY (3.3 +/- 0.9 ng-[0-60] min/ml). The present study demonstrates that PYY can interact with secretin and duodenal acidification in an additive fashion to inhibit pentagastrin-stimulated gastric acid secretion. Our results suggest that several hormones that are released postprandially can interact with each other to inhibit gastric acid secretion.

Peptide YY release by fatty acids is sufficient to inhibit gastric emptying in dogs

Peptide YY is a candidate enterogastrone localized to endocrine cells of the ileocolonic mucosa. The purpose of the present study was to determine if blood levels of peptide YY observed after perfusion of the intestine with fatty acids are capable of slowing gastric emptying. Gastric emptying of a 300-ml saline meal was monitored during intravenous infusion of normal saline or graded doses of peptide YY. Gastric emptying was significantly inhibited by infusion of peptide YY in doses of 200 and 400 pmol/kg · h. During the saline control study, 229 ± 12 ml of the 300-ml saline meal emptied by 10 min. This figure was reduced (p < 0.01) to 110 ± 28 ml by the infusion of peptide YY at a dose of 200 pmol/kg · h. This dose of peptide YY produced plasma concentrations (ΔPYY = 239 ± 50 pM) that were lower than those seen in response to intestinal perfusion of oleic acid (ΔPYY = 395 ± 55 pM) in the same animals. We conclude that perfusion of the intestine with oleic acid releases peptide YY in amounts sufficient to slow gastric emptying.

Peptide YY abnormalities in gastrointestinal diseases

Plasma concentrations of peptide YY (PYY), a newly isolated peptide produced by ileal and colonic endocrine cells, were measured in several groups of patients with digestive disorders after a standardized normal breakfast. Peptide YY levels were found to be grossly elevated in patients with steatorrhea due to small intestinal mucosal atrophy (tropical sprue). Basal levels in these patients were 79 ± 18 pM, which was nearly 10-fold higher than those seen in healthy controls (8.5 ± 0.8 pM). Patients with steatorrhea due to chronic destructive pancreatitis also had substantially increased basal PYY levels (47.5 ± 6.3 pM), and their postprandial response was also greater than that of normal subjects. Moderately elevated plasma PYY concentrations were seen in patients with inflammatory bowel disease and patients recovering from acute infective diarrhea. In contrast, patients with diverticular disease, duodenal ulcer, and functional bowel disease had normal PYY responses. These changes in the secretion of PYY, which appear to result from malabsorption, may shed light on the physiologic role of this newly discovered peptide and on intestinal adaptation to common digestive disorders.

Sensitive radioimmunoassay for measurement of circulating peptide YY

A radioimmunoassay with sufficient sensitivity to detect the recently discovered, circulating peptide YY in the majority of healthy adults has been developed. The antiserum to synthetic peptide YY raised in rabbits essentially showed no cross-reactivity with bovine or porcine synthetic pancreatic polypeptide, neurotensin, or neuropeptide Y, but cross-reacted to the extent of 0.03% with synthetic peptide HI. The minimum detectable limit of the assay for plasma peptide YY was 20 pg/ml with coefficients of variation < 16%. The immunoreactivity of peptide YY isolated from healthy adult plasma had a gel-filtration chromatographic profile similar to that of synthetic peptide YY. Fasting levels of peptide YY in plasma from 127 of 137 (92.7%) ostensibly healthy adults were measurable and showed a log-normal distribution. Using the maximum-likelihood estimation method, we calculated the normal range to be 13–178 pg/ml with a geometric mean value of 49 pg/ml. The fasting plasma peptide YY levels showed no significant age or sex dependency.