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S Cataland

Publications and source records attributed to S Cataland.

72 records · Page 4Linked to original sources
PubMed1976

Effect of chronic antacid ingestion on serum gastrin and gastric secretion.

Basal gastrin and acid secretion, and histamine- and food-stimulated acid secretion were examined before and after 6 weeks of regular antacid consumption by 20 normal volunteers, in order to test the hypothesis that regular use of antacids produces gastrin cell hyperplasia, altered gastrin inhibition by acid, and gastric hypersecretion. We found no differences in fasting serum gastrin, basal or maximal histamine-stimulated acid, or acid output in response to a protein meal after consumption of commercial antacids with or without calcium carbonate. The results suggest that normal subjects do not acquire functional hyperactivity of the gastrin mechanism after a period of regular antacid use.

Adult↗
PubMed1976

Gastric inhibitory polypeptide (GIP). Intestinal distribution and stimulation by amino acids and medium-chain triglycerides.

Radioimmunoassayable gastric inhibitory polypeptide was measured in extracts of canine antrum, duodenum, jejunum, and ileum. The highest GIP concentrations were found in the duodenum (347 +/- 53 ng/g) and jejunum (300 +/- 68 ng/g). An immunochemical similarity was demonstrable between porcine GIP and canine GIP. Dogs prepared with Mann Bollman fistulae were given an amino acid (AA) mixture or medium-chain triglycerides (MTC) by intraduodenal perfusion. With AA, a peak mean serum concentration of 672 +/- 106 pg/ml was reached 15 min after starting the perfusion. MCT resulted in a peak mean serum GIP concentration of 504 +/- 55 pg/ml 30 min after beginning the perfusion. When compared to results previously reported from this laboratory, AA and MCT are not as potent as corn oil (long-chain triglyceride) or glucose in stimulating GIP release. We conclude: (1) Immunoassayable GIP concentrations are highest in the canine proximal small intestine. (2) AA and MCT are weak stimulants of GIP release in the dog.

Amino Acids↗
PubMed1976

The insulinotropic effect of endogenous gastric inhibitory polypeptide in normal subjects.

Intravenously administered porcine GIP is insulinotropic in man. This study was designed to investigate the effects of simultaneous fat ingestion, a potent stimulus for GIP release, and intravenous glucose infusion upon endogenous serum GIP and insulin concentrations in normal subjects. Seven normal volunteers were studied on three separate occasions following: a) the ingestion of 67 grams of emulsified corn oil, b) constant intravenous infusion of glucose, and c) simultaneous administration of corn oil and glucose as in parts (a) and (b) of the study. Serum glucose, insulin (IRI), and GIP concentrations were measured at intervals between 15 and 180 minutes following each stimulus. With corn oil, mean serum GIP concentrations increased from a fasting level of 290 +/- 40 (SE) pg/ml to 1936 +/- 402 pg/ml at 60 minutes without a significant change in serum IRI or glucose concentrations. The infusion of intravenous glucose alone was associated with no rise in serum GIP levels despite a substantial increase in serum IRI and glucose concentrations. With the combined stimuli, mean serum GIP increased less (P is less than .05) between 30 and 90 minutes, and total integrated incremental GIP was significantly less (P is less than .025) than that after corn oil ingestion alone. Following the combined stimuli, incremental insulin levels were higher (P is less than .05) between 15 and 90 minutes, total integrated incremental insulin was greater (P is less than .025), and glucose homeostasis was significantly enhanced (P is less than .05) at 120 and 180 minutes compared with the effects on insulin of glucose infusion alone. We conclude that the potentiation of glucose-stimulated insulin secretion induced by the ingestion of fat is associated with serum GIP levels that are within the insulinotropic range. The augmented secretion of insulin may be mediated partially or completely by endogenous GIP. The lower serum GIP concentrations observed following the combined stimuli suggest a feedback inhibition of GIP release which is perhaps mediated by insulin.

Adult↗
PubMed1976

Gastric inhibitory polypeptide (GIP) in maturity-onset diabetes mellitus.

Serum GIP, insulin, and glucose concentrations were determined during a standard oral glucose tolerance test in 80 individuals, 45 of whom were normal and 35 of whom had adult-onset diabetes mellitus according to USPHS criteria. As a group, the diabetics had fasting hyperglycemia (219 +/- 17 mg./dl.) and, in response to glucose, displayed a peak serum glucose of 373 +/- 23 mg./dl. and sustained hyperglycemia (315 +/- 24 mg./dl.) at 180 minutes. There were no statistically significant differences in absolute serum insulin levels between the two groups. However, insulin secretion was delayed, IRI increments were smaller, and the IRI concentrations were inappropriately low for the simultaneous serum glucose concentrations in the diabetics at every time interval tested. Mean fasting serum GIP was 335 +/- 30 pg./ml. in the diabetics as against 262 +/- 15 pg./ml. in normal individuals (p less than 0.025). After the ingestion of glucose, diabetics had significantly higher (p less than 0.001) mean serum GIP levels between five and 120 minutes. By 180 minutes, serum GIP levels remained above fasting in both groups, but the diabetics had higher than normal serum concentrations (p less than 0.05). Peak serum GIP concentrations, which occurred at 30 minutes in both groups, were 1,376 +/- 106 and 806 +/- 75 pg./ml. in the diabetics and normals, respectively (p less than 0.001). Total integrated serum GIP was also greater in diabetics than normals (140,852 +/- 14,208 vs. 64,602 +/- 8,719 pg.-min./ml.-1, p less than 0.001). The higher serum GIP concentrations observed following glucose ingestion in diabetics could not be attributed to obesity or age. We conclude that both fasting and glucose-stimulated GIP concentrations are higher than normal in obese adult-onset diabetics. The significance of this observation is uncertain. However, since our current understanding suggests the GIP may be an important enteric signal for the release of insulin in man, and because GIP has been shown to stimulate the release of immunoreactive glucagon, GIP may play a role in the pathogenesis of diabetes mellitus.

Adult↗
PubMed1976

Stimulation of secretion of gastric inhibitory polypeptide and insulin by intraduodenal amino acid perfusion.

The effect of intraduodenal or intravenous administration of a 30-gm mixed amino acid solution of serum gastric inhibitory polypeptide (GIP), alpha-amino nitrogen (AAN), glucose, and insulin concentrations was studied in 10 normal subjects. Initially, an intraduodenal amino acid perfusion (15 ml per min X 60 min) was performed in each subject and was followed in 1 to 2 weeks by an intravenous infusion. Peak AAN concentrations occurred at 60 min after both routes of administration, but were greater with intravenous infusion, 145 +/- 5.7 mug per ml vs. 89 +/- 4.4 mug per ml (P less than 0.001). Although serum AAN levels were significantly lower after intraduodenal administration, incremental insulin concentrations were greater after intraduodenal perfusion, 77.3 +/- 8.8 muM per ml vs. 43.1 +/- 5.6 muU per ml (P less than 0.005). Total integrated insulin secretion was also greater after intraduodenal amino acids, 5000 vs. 2400 muU-min ml-1 (P less than 0.005). With intravenous amino acid infusion, serum GIP concentrations remained below the assay detection limit. After intraduodenal perfusion, a mean maximum GIP increment of 468 pg per ml occurred at 15 min. In all subjects peak GIP concentrations occurred at 15 min and preceded the maximum insulin rise by 15 to 30 min. Total integrated GIP secretion was significantly greater after intraduodenal amino acid perfusion, 13,000 pg-min ml-1 vs. no measurable response with intravenous infusion. In separate studies performed in 12 subjects, no significant changes in serum GIP concentrations occurred after intraduodenal perfusion of 0.45% saline, 0.9% saline, or 10% mannitol. The results of this study demonstrate that intraduodenal amino acid administration stimulates the secretion of GIP and suggest that endogenously released GIP may be important in the enteric mediated release of insulin.

Adult↗
PubMed1975

Gastric inhibitory polypeptide (GIP) stimulated by fat ingestion in man.

Ten normal volunteers ingested emulsified corn oil and the immunoreactive GIP, insulin (IRI) and nonesterified fatty acid (NEFA) responses were measured. Serum GIP levels increased after the ingestion of corn oil in all subjects, rising from a mean fasting level of 272 pg/ml to 856 +/- 272 pg/ml (P less than 0.05) by 30 minutes. The peak mean serum GIP concentration of 1,345 +/- 291 pg/ml occurred at 60 minutes; and mean serum GIP levels at 180 minutes remained significantly elevated over fasting values. Serum IRI, glucose and NEFA concentrations did not change during the 180 minutes of study. No changes in serum GIP concentrations occurred when, for control purposes, six volunteers ingested water on another day. We conclude: 1) Fat is a potent stimulus for the release of GIP in normal individuals. 2) Endogenously released GIP is not insulinotropic under the conditions of this study.

Adult↗
PubMedDate not supplied

Angiotensin II and norepinephrine antagonize the secretory effect of VIP in rat ileum and colon.

Vasoactive intestinal polypeptide (VIP) induces intestinal secretion of water and electrolytes in experimental animals and man. We assessed the ability of angiotensin II (AII) and norepinephrine (NE) to block the secretion evoked by VIP, in vivo. Ileal and colonic segments in rats were perfused in situ for two hours with a physiological buffer containing [14C]-PEG-4000 as a volume marker. Saline (0.9% NaCl) was infused intravenously during the first hour and VIP or a combination of VIP plus AII or NE was infused during the second hour. All (0.7 ng/kg/min) alone enhanced water absorption significantly (p less than 0.01) in the ileum and an appreciable, although not a statistically significant, effect was observed in the colon. AII antagonized the secretory effects of VIP in the ileum as well as in the colon. Norepinephrine (5 micrograms/kg/min) also reversed the effect of VIP on the small intestine and colon. Although the mechanism by which AII antagonizes the secretory effects of VIP has not been identified, it is probable that AII promotes absorption, at least in part secondary to release of mucosal NE.

Angiotensin II↗
PubMedDate not supplied

Limitations in usefulness of single dose intermediate acting insulin: a rapid response pattern in some type I diabetics.

Ten Type I insulin-dependent diabetics who were receiving single daily injections of intermediate acting insulin were studied to assess time-response characteristics of this therapy on 24-hour profiles of both glucose and free insulin. Nine of ten patients had undetectable postprandial levels of C-peptide. All patients had insulin antibodies typical of chronically treated Type I diabetes. Mean peak free insulin levels occurred four hours post injection with free insulin rising from 12.3 +/- 1.6 microU/ml to 26.5 +/- 1.4 microU/ml; p less than 0.01. The glucose nadir for the 24-hour profile also occurred at four hours after injection with glucose declining from 199 +/- 29 mg/dl fasting to 155 +/- 5 mg/dl; p less than 0.05. There was significant negative correlation between mean glucose and free insulin throughout the first six hours after insulin injection (r = -0.74; p less than 0.02); no correlation occurred 8 to 12 hours post injection. Two of the ten patients had hypoglycemic symptoms within four hours after their morning insulin. Although free insulin levels remained above basal for 20 hours, single dose intermediate insulin therapy never really controlled postprandial glucose levels after breakfast or lunch. These data suggest there may be limitations in managing Type I diabetics with single dose intermediate insulin. Furthermore, some patients on intermediate acting insulin may have a more rapid than anticipated maximal hypoglycemic response, often within four hours.

Adult↗
PubMedDate not supplied

The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose.

To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). Serum insulin, glucose, and GIP were measured. In each of the 3 h after sugar ingestion the integrated insulin response to (S) was greater than to (G) with the 3-h total being 104% greater. The integrated glucose response to (S) was slightly greater than to (G) in the first and second hours but the differences were not significant. Integrated GIP response to (S) was greater than to (G) in hours 2 and 3. Although significant insulin and glucose responses to (F) occurred in hour 1, G + F led to insulin and glucose responses similar to G. G + F led to greater GIP levels than G in hour 3. These studies show that GIP may play a role in the augmented insulin response to S in hours 2 and 3. This may result from delayed gastric emptying and glucose absorption. The augmentation of insulin to S in the first hour may result from fructose, extra glucose equivalent of the sucrose test solution, or from endocrine mechanisms other than those subserved by GIP.

Adult↗
PubMedDate not supplied

Significance of spontaneous ketonuria and serum C-peptide levels in obese type II diabetic patients.

Patients with type II diabetes mellitus (type II DM patients) are characteristically obese, hyperinsulinemic, and non-ketosis prone. Recently, we have encountered several obese type II DM patients with either diabetic ketoacidosis or significant ketonuria after insulin withdrawal. There was no evidence of infection, stress, or starvation to explain their ketonuria. Therefore, we assessed serum connecting peptide (C-peptide) response to oral glucose in 14 obese, insulin-treated type II DM patients: 6 with and 8 without episodes of spontaneous ketonuria. The group presenting with ketonuria had low to absent basal and stimulated serum C-peptide responses. The nonketonuric group had higher basal C-peptide (P less than 0.01) concentrations that increased significantly (P less than 0.001) after oral glucose compared with those of the ketonuric group. Clinical characteristics and biochemical control were similar in both groups. Our findings confirm that obese type II diabetes mellitus is a heterogeneous disease with variable fasting and stimulated C-peptide responses. Spontaneous ketonuria could be a feature in the clinical presentation of the patients especially in the presence of both low fasting and stimulated C-peptide levels. The significance of these findings is unclear but suggests individualization in the management of type II DM patients and cautious withdrawal of insulin therapy in such patients. Furthermore, serum C-peptide levels alone cannot be recommended to classify patients into either type I or type II diabetes mellitus.

Aged↗