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Biomedical subjects

T Y Tai

Publications and source records attributed to T Y Tai.

119 records · Page 7Linked to original sources
PubMed1976

Direct stimulation by growth hormone of glucagon and insulin release from isolated rat pancreas.

The acute effects of bovine growth hormone (bGH) upon the release of glucagon and insulin from the isolated perfused rat pancreas were investigated in the presence of 5.6 mM glucose. Glucagon and insulin release occurred in response to 10(-9), 10(-8) and 10(-7)M bGH within 1-2 min and dissipated within 4 min; a significant increase was seen at 24 sec for glucagon and at 48 sec for insulin. In this concentration range, a dose-response relationship was established for both islet hormones. Upon the addition of 5 mM fumarate, glutamate, and pyruvate, glucagon and insulin release occurred also in response to 10(-11) and 10(-10)M bGH. In the absence of glucose, in response to 10(-7)M bGH, the magnitude of glucagon release was similar to that seen with 5.6 mM glucose; but the release of insulin failed to occur. In the presence of 16.7 mM glucose, the release of glucagon was blunted and that of insulin augmented. The data indicate that growth hormone can stimulate acutely the release of glucagon and insulin at physiological as well as pharmacological concentrations. These rapid and short-lived effects are likely to be direct and not mediated through the generation of somatomedin. The stimulatory effect of growth hormone appears to favor the release of glucagon under conditions of glucose lack, and of insulin under conditions of glucose abundance. These results indicate that growth hormone may have a tonic effect on islet hormone release.

Animals↗
PubMed1976

Glucagon release precedes insulin release in response to common secretagogues.

UNLABELLED: The dynamics and interrelationships of glucagon and insulin secretion were studied in the isolated perfused rat pancreas by utilizing a series of compounds that stimulate the release of both hormone. Leucine, arginine, prostaglandins F2alpha and E2, bovine growth hormone, and isoproterenol were administered individually over 60-second intervals. The release of glucagon preceded that of insulin in response to all compounds tested. The rapidity of glucagon release varied in response to different secretagogues; the time course of insulin release was fairly constant. The timing and the magnitude of glucagon and insulin release did not correlate statistically. CONCLUSIONS: (1) pancreatic alpha cells respond more rapidly than beta cells to the same stimulus; (2) antecedent release of glucagon is not the principal mediator of insulin release in response to stimuli common to both hormones; and (3) endogenous glucagon may at best modify the release of insulin evoked by certain secretagogues.

Amino Acids↗
PubMed1975

Stimulation by prostaglandin E2 of glucagon and insulin release from isolated rat pancreas.

To ascertain whether prostaglandins (PG) may play a role in the secretion of glucagon and in an attempt to elucidate the conflicting observations on the effects of PG on insulin release, the isolated intact rat pancreas was perfused with solutions containing 1.1 x 10(-9) to 1.8 x 10(-5)m PGE2. In the presence of 5.6 mM glucose significant increments in portal venous effluent levels of glucagon and insulin were observed in response to minimal concentrations of 2.8 X 10(-8) and 1.4 X 10(-7) PGE2, respectively; a dose-response relationship was evident for both hormones at higher concentrations of PGE2. When administered over 60 seconds, 1.4 X 10(-6)M PGE2 resulted in a significant increase in glucagon levels within 24 seconds and in insulin within 48 seconds. Ten-minute perfusions of 1.4 X 10(-6)M PGE2 elicited biphasic release of both islet hormones; Phase I glucagon release preceded that of insulin. Both phases of the biphasic glucagon and insulin release which occurred in response to 15-minute perfusions of 10 mM arginine were augmented by PGE2. These observations indicate that PGE2 can evoke glucagon and insulin release at concentrations close to those observed by others in the extracts of rat pancreas. We conclude that PG may be involved in the regulation of secretion of glucagon and insulin and may mediate and/or modify the pancreatic islet hormone response to other secretagogues.

Animals↗
PubMedDate not supplied

Abnormal peripheral microcirculation in seemingly normal subjects living in blackfoot-disease-hyperendemic villages in Taiwan.

Blackfoot disease (BFD) is an endemic peripheral arterial disease confined to the southwestern coast of Taiwan. The cause of the disease has been ascribed to the high-arsenic artesian well water. The purpose of this study was to examine the possible association between the long-term exposure to artesian well water and the change in microvascular circulation in the absence of peripheral arterial insufficiency. A total of 45 men living in the BFD-hyperendemic villages and another 51 age- sex- body-mass index-matched men who lived in nonendemic villages nearby were recruited into this study. All subjects were free from peripheral vascular disease (resting ankle-brachial index > 1.00), clinical claudication, cigarette smoking, diabetes mellitus, hypertension, ischemic heart disease, cerebral infarction and obesity. Laser Doppler flowmetry was used to measure the peripheral microcirculation on the big toes both at 36 degrees C (basal perfusion, Pb) and after a hyperthermic test at 42 degrees C (Ph). The time required to reach Ph (T), and the average rate (R) of increase from Pb to Ph measured by (Ph-Pb)/T were also calculated. Results showed that those living in the BFD-hyperendemic area had a lower Pb [32.8 +/- 6.0 perfusion units (PU) vs. 67.0 +/- 4.3 PU, p < 0.001], a lower Ph (193.2 +/- 13.6 vs. 231.1 +/- 6.3 PU, p < 0.005), a longer T (3.04 +/- 0.19 vs. 1.31 +/- 0.08 min, p < 0.001) and a slower rate of increase from Pb to Ph (48.0 +/- 4.8 vs. 76.2 +/- 5.4 PU/min, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

The effect of health education for diabetics in the community.

Diabetic care in the community has become a public health issue. To assess the effect of a community diabetes care program (CDCP) on knowledge acquisition and its impact on metabolic control, a 2-year study including 260 non-insulin-dependent diabetics from two different districts in Taipei city was conducted. The experimental group consisted of 140 cases. The remaining 120 cases served as controls. Preintervention knowledge scores were significantly correlated with the formal education level and the duration of diabetes [Diabetic knowledge score = 50.06 + 0.82 (duration of education in years) + 0.23 (duration of diabetes in years), p less than 0.001]. A large increase in the knowledge scores for experimental patients was noted 1 year after intervention. A significant difference in diabetic knowledge still existed between the control and experimental groups 2 years after intervention. HbAlc levels (mean +/- SD) for the experimental patients decreased from a baseline of 7.47 +/- 1.87% to 7.23 +/- 1.68% and 6.88 +/- 1.30% 1 year and 2 years after intervention, respectively. However, no significant decrease was found in the control group (7.20 +/- 2.00% at baseline and 6.98 +/- 1.96%, and 7.14 +/- 2.25% at 1 year and 2 years after intervention, respectively). Reduction in body weight was found in the experimental group. In order of baseline, 1 year and 2 years after intervention, the results were 63.6 +/- 9.6, 62.6 +/- 9.3 and 62.5 +/- 9.2 kg, respectively. There was no remarkable change in body weight in the control group during the 2-year observation period. In conclusion, an integrated approach to CDCP provides a cost-effective method for management of diabetes in the community.

Aged↗