Selective release of gastric inhibitory polypeptide by intraduodenal amino acid perfusion in man.

Intraduodenal amino acids are known to stimulate the release of gastric inhibitory polypeptide and cholecystokinin. In order to separate and quantitate gastric inhibitory polypeptide secretion selectively, 12 normal subjects received an intraduodenal perfusion of a mixed amino acid solution (158 mM) containing either methionine, phenylalanine, tryptophan, and valine (perfusate 1), or an amino acid solution containing arginine, histidine, isoleucine, leucine, lysine, and threonine (perfusate 2). Serum concentrations of gastric inhibitory polypeptide and insulin were significantly greater in the group receiving perfusate 2 (P less than 0.

Effect of atropine on meal-stimulated gastrin and gastric inhibitory polypeptide (GIP) release.

The effect of atropine on meal-stimulated gastric inhibitory polypeptide (GIP) and gastrin release was studied in 5 purebred foxhounds and compared with control studies done in the same animals given a meal without atropine, peak incremental serum gastrin occurred between 5 and 15 min after the meal whereas the greatest increment in serum GIP occurred 60 min postcibal. Atropine had no effect on basal concentrations of gastrin or GIP. However, when atropine was given before feeding serum gastrin concentrations from 75 to 120 min postcibal were significantly higher (P less than 0.

Insulin-induced attenuation of glucose-stimulated gastric inhibitory polypeptide secretion.

Administration of exogenous insulin before and after intraduodenal glucose results in blunting of the GIP response to glucose. Physiologic levels of serum insulin were attained. Therefore, the present study suggests the existence of negative feedback regulation of GIP release by endogenous insulin (pancreatico-GIP axis).

Renal effects on serum gastric inhibitory polypeptide (GIP).

Fasting and meal-stimulated serum immunoreactive gastric inhibitory polypeptide (GIP) concentrations were measured in normal subjects and in uremic patients undergoing chronic hemodialysis. Mean fasting GIP was higher in the uremic patients (1006 +/- 145 (SE) pg/ml) than in the normal control subjects (132 +/- 31 pg/ml, p less than 0.001).

Localization of gastric inhibitory polypeptide release by intestinal glucose perfusion in man.

To determine the site of endogenous release of gastric inhibitory polypeptide (GIP), glucose perfusions (556 mmoles per liter) of duodenum, proximal jejunum, midjejunum, and ileum were performed in human volunteers using an occluding balloon perfusion technique. Preperfusion GIP concentrations were below assay sensitivity (125 pg per ml) in all subjects. After glucose perfusion, maximal serum GIP concentrations for the four groups were: duodenum, 1383 +/- 152 pg per ml; proximal jejunum, 904 +/- 87 pg per ml; midjejunum, 545 +/- 91 pg per ml, and ileum 305 +/- 38 pg per ml.

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.

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.

Primary hyperparathyroidism and anemia.

The frequency of anemia associated with primary hyperparathyroidism is uncertain. When anemia does occur, its mechanisms are obscure. Two patients with primary hyperparathyroidism and moderate normochromic, normocytic, reticulocytopenic anemia were studied in detail.

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.

The ratio "circulating red cell volume/lean body mass" in normal and hypophysectomized rats on paired feeding.

The ratio "circulating red cell volume/lean body mass" was calculated in normal and hypophysectomized male rats put on paired feeding for 90 days after hypophysectomy, and in control rats both at the beginning and the end of this experimental period. Control rats at the onset of the experiment, hypophysectomized rats, and rats on the sub-maintenance level of food consumption did not show a significant difference in their red cell volumes/lean body mass ratios. These values were significantly lower than those of sham hypophysectomized rats allowed to eat ad libitum.

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.

Propranolol as primary therapy for thyrotoxicosis.

It has been suggested that propranolol hydrochloride alone is effective in the treatment of thyrotoxicosis. To test this hypothesis, eight mildly thyrotoxic individuals were prospectively studied for an average of eight months, during which propranolol alone was administered and thyroid function tests, cardiac systolic time intervals, and body densities were sequentially measured. Two patients became euthyroid.

Tumors of the islets of Langerhans.

The islet cell tumors of the pancreas are now known to produce a variety of polypeptides in addition to insulin. These include glucagon, serotonin, corticotropin, melanocyte-stimulating hormone, gastrin and a secretinlike hormone that may be VIP or a combination of such polypeptides. The development and wide availability of the newer immunoassays for the various recognized hormones as well as candidate hormones of the gut will simplify the diagnosis of these challenging tumors, which up until this time have produced symptoms that were bizarre and often fatal to the patient.

Primary empty sella, galactorrhea, hyperprolactinemia and renal tubular acidosis.

Discussed here is a 41 year old woman with galactorrhea associated with the empty sella syndrome and mild renal tubular acidosis. Basal serum prolactin (PRL) levels were normal, but a 24 hour serum PRL secretory profile demonstrated an increased mean PRL concentration. Serum PRL was appropriately suppressed by the administration of L-dopa; however, chlorpromazine stimulation resulted in a blunted serum PRL response.