Plasma ghrelin and pancreatic polypeptide concentrations increase with sham feeding. This suggests a vagal efferent pathway mediating ghrelin release. In contrast to pancreatic polypeptide which rises with actual meal ingestion, ghrelin levels did not change.
A high-fat solid meal significantly increased overall symptoms among individuals with gastroparesis, whereas a low-fat liquid meal had the least effect. With respect to nausea, low-fat meals were better tolerated than high-fat meals, and liquid meals were better tolerated than solid meals. These data provide support for recommendations that low-fat and increased liquid content meals are best tolerated in patients with symptomatic gastroparesis.
Serum cortisol, growth hormone (GH), and luteinizing hormone (LH) were measured in 6 controls and in 9 normal subjects following oral administration of 500 mg of Levodopa (L-Dopa). Serum cortisol levels decreased similarly in both the treated and the control group over a 3 h teste period. Serum GH levels increased dramatically, whereas LH levels showed a small but significant decrease in 7 of 9 subjects. These alterations occurred during the first 2 h following L-Dopa administration. GH and LH levels did not change significantly in the controls. These results suggest that L-Dopa exerts a selective stimulatory and inhibitory influence on the secretion of anterior pituitary hormones in man.
The effect of Na pentobarbital anesthesia on serum secretin concentration and exocrine pancreatic secretian was investigated in dogs with chronic gastric and pancreatic fistulas. Na pentobarbital anesthesia was found 1) to reduce basal pancreatic flow rate by 74%, bicarbonate by 70% and protein secretions by 81 % withou t affecting basal immunoreaclive secretin (lRS) concentration; 2) to have no effect on Hel (9.6 mEq/30 min, intraduodenally) mediated IRS release but to reduce by approximately 50% Hel mediate!! bicarbonate output; 3) to have no effect on pancreatic responsiveness to stimulation by exogenous secretin (0.5 IU/kg x 30 min); 4) not to affect serum concentrations of IRS following secretin infusion. These data suggest 1) that basal pancreatic secretory functions are under con trol of tonic neural influences; 2) that Na pentobarbital anesthesia has no effect on IRS release but inhibits stimulated pancreatic bicarbonate secretion through suppression of an as yet unidentified agent; and 3) that Na pentobarbital does not affect the metaboIism of secretin. Furthermore, it was found that intraduodenal administration of 9.6 mEq of HCl and intravenous infusion of 0.5 IU/kg of secretin for 30 min both resulted in similar IRS concentrations of approximately 600 pU/mi (equivalent to 150 pg/ml).
The effects of two antiinsulin receptor antisera (AIRA) on alpha-amino-2-[14C]isobutyric acid [( 14C]AIB) uptake by and [125I]insulin binding to cultured rat hepatocytes were examined. Diluted 1:100, both antisera inhibited insulin binding by 75-80%, mainly by decreasing available high affinity insulin-binding sites. Diluted 1:500, they decreased insulin binding and high affinity binding sites by 35-40%. Neither antiserum had an effect on basal [14C]AIB uptake, but decreased insulin-stimulated AIB uptake by 83% (dilution, 1:100; 24-h incubation) and 25% (dilution, 1:500; 24-h incubation), respectively. Insulin stimulation of AIB uptake correlated positively (r = 0.96; P less than 0.01) with insulin binding to high affinity receptors on hepatocytes incubated with normal serum or AIRA. We conclude that: 1) insulin stimulation of amino acid uptake by hepatocytes was mediated through insulin receptors, especially high affinity binding sites, and was inhibited by AIRA in parallel with receptor blockade; and 2) AIRA had no insulin-like effect on basal amino acid uptake by hepatocytes.
The fasting plasma growth hormone (GH) concentration and the plasma growth hormone response to sustained hyperglycemia was examined in 8 chronically uremic subjects before and after hemodialysis employing the hyperglycemia clamp technique. The plasma glucose concentration was acutely raised and maintained at +125 mg/100 ml above basal levels. Since the glucose concentration was held constant, the glucose infusion rate is an index of glucose metabolism (M) and M divided by the plasma insulin response (I) is a measure of tissue sensitivity to insulin. Predialysis, the fasting GH concentration, 4.0 +/- 1.0 ng/ml, was significantly greater than controls, 0.3 +/- 0.1 ng/ml (p less than 0.01), and failed to suppress normally following sustained hyperglycemia. Both M, 4.23 +/- 0.36 mg/kg x min, and M/I, 5.05 +/- 0.79 mg/kg x min per microU/ml, were significantly reduced compared to controls (p less than 0.001). There was no correlation between either the fasting GH concentration or the GH response to sustained hyperglycemia and either M or M/I. Following dialysis both M, 6.30 +/- 0.64 mg/kg x min, and M/I, 8.39 +/- 1.06 mg/kg x min per microU/ml, increased (p less than 0.01) without significant change in either the fasting GH level, 4.0 +/- 1.2 ng/ml, or the plasma GH response to hyperglycemia. It is concluded that while deranged GH physiology is a common accompaniment of the uremic state, it is not responsible for the glucose intolerance and tissue insensitivity to insulin observed in uremia.
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