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Biomedical subjects

J Palmer

Publications and source records attributed to J Palmer.

At least 271 records · Page 15Linked to original sources
PubMed1977

Insulin, glucagon, and glucose exhibit synchronous, sustained oscillations in fasting monkeys.

In overnight fasted rhesus monkeys, synchronous, regular oscillations occurred in the plasma concentrations of glucose, insulin, and glucagon. The oscillations displayed a period averaging 9 minutes. The amplitudes for insulin and glucagon were ten and five times greater than for glucose. Insulin cycled in and glucagon out of phase with glucose. In baboons, oscillations of glucose and insulin were smaller than in rhesus monkeys, while in man, regular oscillations were not observed.

Animals↗
PubMed1977

Absorption, excretion, and utilization of an intramuscular iron-poly (sorbitol-gluconic acid) complex, Ferastral.

An iron-poly (sorbitol-gluconic acid) complex (Ferastral) labelled with 59Fe was administered by intramuscular injection to clinically and haematologically normal male volunteers. Urinary excretion of radioactivity was measured for the first 48 hours following injection, and was 2%-10% of the administered dose. Disappearance of radioactivity at the site of injection and accumulation of radioactivity in the liver, spleen, and sacrum were measured by external scintillation counting. Plasma radioactivity was measured at intervals for four days and red cell incorporation of 59Fe reached levels of 29%-57.5%. An unexpected finding was that the highest levels of urinary excretion of radioactivity did not coincide with the highest levels of plasma radioactivity.

Absorption↗
PubMed1977

The effect of endotoxin on the mast cell c'AMP system.

To determine whether the endotoxin induced release of histamine is mediated via the mast cell c'AMP system, hamster mast cells were isolated and incubated (prior to endotoxin-serum stimulates (ET-S) with disodium cromoglycate, isoproterenol and aminophylline. All drugs caused significant inhibition of the ET-S histamine release. The authors conclude that ET-S utilizes the c'AMP system to release histamine.

Aminophylline↗
PubMed1975

Temperature Sensitivity of the Latent Phase in Ethylene-induced Elongation.

The temperature sensitivity is reported for the latent period preceding ethylene-induced elongation in the adaxial half of the leaf petiole of Helianthus annuus. When intact plants were exposed to 10 mul of ethylene/l of air over the temperature range 18 to 35 C, the minimum latent time was 62 minutes at 28 C and the maximum was 132 minutes at 18 C. The temperature coefficient, Q(10), changed from 2.1 below 28 C, to 0.7 above. In 100 mul of ethylene/l of air, the latent time was reduced by 14% at 18 C, but was significantly increased at 28 and 38 C. These results show that the latent period in the elongation response of the petiole to ethylene cannot be reduced below about 60 minutes by raising either the leaf temperature or the atmospheric ethylene concentration.

Journal Article↗
PubMed1975

Somatostatin blockade of acute and chronic stimuli of the endocrine pancreas and the consequences of this blockade on glucose homeostasis.

The nature and extent of somatostatin-induced inhibition of pancreatic endocrine secretion were studied by administration of a number of stimuli of either glucagon or insulin to over night fasted baboons with and without an infusion of linear somatostatin. The stimuli for acute-phase insulin release were intravenous pulses of glucose, tolbutamide, isoproterenol, and secretin. When given 15 min after the start of a somatostatin infusion, these agents were essentially unable to stimulate insulin secretion. Chronic insulin secretion was stimulated by infusions of either glucose or glucagon. Within 10 min of the start of a super-imposed infusion of somatostatin, insulin levels fell to less than 40 percent of prestimulus control and remained suppressed for the duration of the somatostatin infusion. Stimulation of glucagon secretion by insulin-induced hypoglycemia was also blocked by somatostatin. Plasma glucose decreased during somatostatin infusions except when superimposed upon an infusion of glucagon. Somatostatin had no effect on glucose production in a rat liver slice preparation. We conclude: (a) Somatostatin is a potent and so far universally effective inhibitor of both acute and chronic phases of stimulated insulin and glucagon secretion (b) The inhibitory effect is quickly reversible and the pattern of recovery of secretion is appropriate to prevailing signals; (c) Present evidence suggests that the effect of somatostatin on blood glucose is mediated through its effect on blood glucagon; (d) In the overnight-fasted baboon both in the basal state and 45 min into a 4-mg/kg-min glucose infusion, a somatostatin-induced fall in serum insulin levels appears to be unable to prevent a decrease in hepatic glucose production.

Animals↗
PubMed1975

Inhibition of glucagon and insulin secretion by somatostatin in the rat pancreas perfused in situ.

Perfusion of growth hormone inhibitory factor (somatostatin) into rat pancreas inhibited secretion of glucagon and insulin into medium containing 5.5 mM glucose. A 15-min infusion of arginine (20 mM) greatly increased glucagon and insulin secretion. When perfused simultaneously with arginine, somatostatin (55 nM) abolished the increase in glucagon secretion. The acute phase of insulin secretion in response to arginine was attenuated by somatostatin, and subsequent secretion was decreased to control levels. Pretreatment for 5 min with somatostatin blocked even acute-phase insulin secretion in response to arginine. Somatostatin did not affect basal or glucose-stimulated secretion of insulin from rat pancreatic islets isolated by the collagenase technique. Arginine-stimulated secretion of insulin was enhanced by somatostatin in isolated islets. These results demonstrate a direct effect of somatostatin on the pancreas to inhibit secretion of glucagon and insulin. The failure of somatostatin to inhibit insulin secretion in pancreatic islets may be due to alterations in the beta cells produced by the isolation procedure. It is also possible that the effect of somatostatin on insulin secretion may be mediated indirectly.

Animals↗