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Biomedical subjects

T Wasada

Publications and source records attributed to T Wasada.

67 records · Page 4Linked to original sources
PubMed1981

Effect of gastric inhibitory polypeptide on plasma levels of chylomicron triglycerides in dogs.

To determine whether gastric inhibitory polypeptide (GIP) promotes the clearance of chylomicron triglycerides (TG) from the circulation in dogs, chyle collected from donor dogs via a thoracic duct fistula was infused at a rate of 2 ml/min i.v. into normal recipient dogs during an infusion of either porcine GIP (1 microgram/kg per h) or saline as a control. In the GIP-infused dogs the rise in plasma TG was significantly below that of the control animals [mean peak of 36 +/- 4 mg/dl vs. 82 +/- 18 mg/dl (P less than 0.05)]. It is concluded that GIP exerts an effect upon the removal of chylomicron TG from the blood. The results suggest that GIP may play a physiologic role in the disposition of ingested fat.

Animals↗
PubMed1981

Effect of 2-deoxy-D-glucose on plasma somatostatin levels in conscious dogs.

The effects of 2-deoxy-D-glucose (2-DG) on plasma levels of somatostatin-like immunoreactivity (SLI) were examined in conscious normal dogs. After an iv infusion of 2-DG (400 mg/kg . h for 15 min), plasma SLI rose significantly from a mean baseline of 130 +/- 5 pg/ml (mean +/- SEM) to a mean peak of 204 +/- 25 pg/ml (P less than 0.005) at 25 min. Plasma insulin and glucagon also increased significantly. Atropine (200 microgram/kg . h for 35 min, iv) and hexamethonium (5 mg/kg, iv) markedly suppressed the SLI response to 2-DG, suggesting that it might be mediated, at least in part, by the autonomic nervous system. In contrast, the plasma insulin and plasma glucagon responses to this glucose analog were only slightly affected by atropine or hexamethonium pretreatment. Carbachol (0.2 mg, sc) caused a mean maximal increase in SLI of 43 +/- 14% (P less than 0.005) and atropine (200 micrograms/kg . h, iv) caused a mean maximal decrease of 25 +/- 2% (P less than 0.001) from the respective baseline levels. Plasma insulin and glucagon rose promptly after carbachol and were unchanged by atropine. To assess th contribution of 2-DG-stimulated gastric acid secretion in the 2-DG-induced SLI rise 2-DG was infused during the infusion of the H2-receptor antagonist cimetidine (3.0 mg/kg . h). Plasma SLI, nevertheless, increased significantly from a mean baseline of 112 +/- 6 pg/ml to a mean peak of 158 +/- 19 pg/ml (P less than 0.005) at 20 min, although the magnitude of the response was substantially reduced (P = NS). These observations suggest that in the conscious dog, 2-DG stimulates SLI secretion in part via cholinergic mechanism.

Animals↗
PubMed1981

High plasma free fatty acid levels contribute to the hypersomatostatinemia of insulin deficiency.

High plasma levels of free fatty acids (FFA) stimulate the secretion of splanchnic somatostatin, and both are elevated in insulin deficiency. To determine if the hypersomatostatinemia of insulin deficiency is secondary to high FFA levels, plasma somatostatin-like immunoreactivity (SLI) was measured in a group of insulin-deprived alloxan-diabetic dogs during nicotinic acid-induced lowering of their elevated plasma FFA to normal, and in a group of nondiabetic dogs during nicotinic acid-induced lowering of their FFA to subnormal values. In insulin-deprived diabetic dogs, nicotinic acid reduced plasma FFA from 1.07 +/- 0.2 (M +/- SE) mmol/L to 0.6 +/- 0.1 mmol/L (P less than 0.02), approximately the basal FFA level in normal dogs. This was accompanied by a significant decline in plasma SLI levels from a mean baseline of 247 +/- 15 pg/ml to a mean nadir of 199 +/- 10 pg/ml (P less than 0.005). The latter was, nevertheless, significantly above the basal SLI level of the nondiabetic dogs. In contrast, in normal dogs, nicotinic acid-induced reduction in FFA from 0.54 +/- 0.02 mmol/L to 0.24 +/- 0.03 mmol/L (P less than 0.001) was associated with only a small and inconsistent decrease in SLI. These findings suggest that the hypersomatostatinemia of insulin-deficient alloxan-diabetic dogs is, in part, secondary to high plasma FFA levels.

Animals↗
PubMed1980

Evidence for a role of free fatty acids in the regulation of somatostatin secretion in normal and alloxan diabetic dogs.

To investigate the effect of acute elevation of plasma free fatty acids (FFA) on the secretion of splanchnic somatostatin-like immunoreactivity (SLI), the peripheral venous, pancreatic, and gastric venous effluent levels of SLI were measured in normal and chronic alloxan diabetic dogs before and after the infusion of a fat emulsion supplemented with heparin. In normal conscious dogs heparin injected during the infusion of a fat emulsion elevated FFA levels from a mean (+/-SE) base-line level of 0.7+/-0.1 meq/liter to a peak value of 1.5+/-0.1 meq/liter (P < 0.001) and plasma SLI rose from a mean (+/-SE) base-line value of 145+/-7 pg/ml to a peak of 253+/-44 pg/ml (P < 0.05). Neither the infusion of glycerol, of fat emulsion without heparin, of heparin alone nor of saline itself had an effect on either the plasma level of FFA or SLI. In another group of anesthetized dogs with surgically implanted catheters the administration of fat emulsion plus heparin was accompanied by more than a two-fold rise in the concentration of SLI in the venous effluent of the pancreas and of the gastric fundus and antrum in association with an elevation of FFA levels. In a group of conscious diabetic dogs fat emulsion plus heparin raised FFA from a mean base-line level of 1.2+/-0.2 to 1.6+/-0.3 meq/liter (P < 0.05) and SLI rose from a mean base-line level of 185+/-9 pg/ml to a peak value of 310+/-44 pg/ml (P < 0.01). Although SLI levels were significantly greater than in normal dogs at several time points after the rise in FFA, the magnitude of the increment in diabetic dogs did not differ from normal. These results demonstrate that a rise in FFA levels is a potent stimulus for SLI secretion from the pancreas and stomach and raise the possibility that FFA is an important physiological regulator of SLI secretion.

Animals↗
PubMed1979

A case of insulin resistant diabetes with possible antibodies to insulin receptors.

A case of a 19-year-old, non-obese female with insulin resistant diabetes mellitus and polycystic ovary syndrome was reported. The maximal insulin requirement attained 360 units per day, but a satisfactory control of diabetes did not follow. The patient's serum contained not only anti-insulin antibodies, but also possible anti-insulin receptor antibodies which were demonstrated by the 125I-insulin binding test using insulin receptors derived from human placental plasma membrane. The insulin resistance in this case was assumed to be caused primarily by possible blocking antibodies to insulin receptors and partly by anti-insulin antibodies because of the following observations. First, high serum free insulin (165 microunits/ml) without hypoglycemia indicates the presence of insulin resistance due to other factors than antiinsulin antibodies. Second, the titer of 125I-insulin binding capacity of serum was not unusually higher than those seen in chronically insulin-treated diabetics. Third, immunologically heterospecies insulin (fish insulin) was also ineffective. The clinical features such as absence of ketoacidosis and association with polycystic ovary syndrome resemble those of an unique diabetic syndrome reported previously though acanthosis nigricans and endogenous hyperinsulinemia were not found in this case. Her insulin resistance remitted spontaneously and over the next 18 months' observation, her diabetes remained regulated without insulin therapy.

Adult↗
PubMed1978

Adrenal contribution to circulating estrogens in woman.

To study the contribution of adrenal glands to circulating estrogens in woman, the concentrations of estrone (E1), estradiol-17 beta (E2), and estriol (E3) in adrenal and peripheral venous blood were measured by radioimmunoassay and the grandular secretion of estrogens after ACTH stimulation was investigated by analyzing the adrenal vein levels of these steroids in patients with breast cancer who were undergoing a therapeutic adrenal operation. Furthermore, adrenal secretion rates of estrogens and cortisol were estimated. It was shown that there existed greater concentrations of estrogens in adrenal vein than in peripheral blood; about 3 times higher for E1 (p less than 0.001), and 2 times higher for E2 and E3 (p less than 0.05). Administration of ACTH caused a significant increase of E1 and E2 concentrations in adrenal venous blood to mean 150% of the basal levels that was comparable to the increase of cortisol. Apparent adrenal secretion rates of estrogens estimated under surgical situation were calculated to be 7.7 +/- 1.7 (M +/- SE) microgram/day for E1, 1.9 +/- 0.3 microgram/day for E2, and 0.3 +/- 0.2 microgram/day for E3, while the secretion rate of cortisol was 52.7 +/- 8.2 microgram/min. The present study demonstrates that the direct adrenal secretion of not only E1, but E2 and E3 contributes to the circulating estrogen levels, and it is suggested that the adrenal glands might be responsible for the relatively important source of estrogen production in the aged woman.

Adrenal Glands↗