The Pancreatic Alpha and Beta Cells Responses to 1-Arginine and Insulin-Induced Hypoglycaemia in Hyperthyroidism

Shima, Kenji; Sawazaki, N; Tanaka, Ryoichi; Morishila, S.; Tarui, Seiichiro; Nishikawa, Mitsuo

doi:10.1530/acta.0.0830114

Cited by 10 publications

(5 citation statements)

References 10 publications

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“…In the present report it has been shown that an elevation of the circulating insulin concentration to levels comparable to those (Shima et al 1976) attained ten minutes after the rapid injection of insulin. 0.1 U per kg body weight.…”

Section: Discussionsupporting

confidence: 61%

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Failure of Exogenous Insulin to Inhibit Insulin Secretion in Man

Shima¹,

Morishta²,

Sawazaki³

et al. 1977

Horm Metab Res

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In order to explore whether or not the negative feedback mechanism of insulin per se on insulin secretion exists in man, changes in plasma C-peptide immunoreactivity (CPR), as an index of pancreatic B cells secretory function, were studied in 6 nonobese healthy volunteers in the presence of high circulating levels of exogenous insulin. 10% glucose was infused concurrently so as to maintain blood sugar at the basal level. The insulin-glucose infusion was maintained for 120 minutes, achieving mean plasma levels of 140-180 mu1/ml. After this period, the insulin infusion was continued at the same rate for an additional 10 minutes while the glucose was omitted. Despite the elevated level of circulating insulin, no significant change in plasma CPR concentration was observed so long as the blood sugar was maintained at the basal levels. Following cessation of the glucose infusion, the plasma CPR levels declined with a decrease in blood sugar level. Under the conditions of the present study, no inhibitory effect of exogenous insulin on the secretory function of the B cells was noticed.

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Section: Discussionsupporting

confidence: 61%

“…have shown suppression of a secretory function of B cells in healthy subjects and patients with hyperthyroidism during insulin-induced hypoglycemia (Shima, Sawazaki, Morishita, Tanaka, Tarui and Nishikawa 1976). Similar findings were obtained in normal subjects by Horowitz, Rubenstein, Reynolds, Molnar and Yanaihara (1975).…”

Section: Introductionsupporting

confidence: 69%

Failure of Exogenous Insulin to Inhibit Insulin Secretion in Man

Shima¹,

Morishta²,

Sawazaki³

et al. 1977

Horm Metab Res

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“…However, this alteration was mainly due to a marked elevation in three of nine patients; the remaining six patients showed normal values ( Table 2). In two previous studies (10,11), basal plasma glucagon levels were reported to be normal, although no detailed data regarding individual patients were made available. Recently, it has been demonstrated that in rats rendered hyperthyroid by ip administration of T 4 (500-1500 jug/kg BW) for 9 days, portal venous plasma glucagon was markedly elevated (12).…”

Section: Discussionmentioning

confidence: 99%

Impaired Pancreatic α-Cell Response in Hyperthyroidism

Kabadi

Eisenstein

1980

The Journal of Clinical Endocrinology & Metabolism

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Recently, we observed that in hyperthyroid patients, plasma glucagon was not adequately suppressed by an oral glucose load, suggesting altered pancreatic alpha-cell sensitivity. To further assess pancreatic alpha-cell function in hyperthyroidism, plasma glucose, glucagon, and insulin resonses to a protein meal were determined in normal subjects and hyperthyroid patients. Fasting plasma glucose was normal in hyperthyroid patients. A protein meal produced an increase in plasma glucose levels in hyperthyroid patients, whereas in normal subjects protein feeding was followed by a decline in blood glucose levels. Basal glucagon was markedly elevated in three of nine hyperthyroid patients, whereas in the remaining six, fasting plasma glucagon was unaltered. In both groups, protein feeding induced a glucagon rise; however, the increment was significantly smaller in hyperthyroid patients. In hyperthyroidism, fasting plasma insulin was raised and the insulin response to a protein meal was exaggerated. Furthermore, the insulin elevations were sustained and did not return to the basal level by 180 min as observed in normal subjects. We conclude that 1) the plasma glucagon response to a protein meal is blunted in hyperthyroidism, a finding which confirms our recent observation of decreased sensitivity of the pancreatic alpha-cell in hyperthyroidism; 2) fasting hyperinsulinemia with simultaneous euglycemia is consistent with the presence of insulin resistance in hyperthyroidism; and 3) the sustained and exaggerated plasma insulin rise after ingestion of a protein meal suggests hypersensitivity of the pancreatic beta-cell in hyperthyroidism.

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“…Insulin sensitivity would have reflected the concentration of insulin receptors on target cells, which is known to be inversely related to the concentration of circulating insulin (Soll et al, 1975a,b). The secretion of insulin in response to nutrients such as glucose (Renauld et al, 1971;Cavagnini et al, 1974;Lenzen et al, 1976;Okajima & Ui, 1978) and arginine (Imura et al, 1976;Shima et al, 1976) was reported to be severely impaired in hyperthyroidism. Though the insulinaemic action of fl-adrenergic agents was conversely enhanced by hyperthyroidism (Okajima & Ui, 1978), nutritional stimuli might be more intense and more frequent than sympathetic stimuli to cause a normal daily rhythm of insulin secretion.…”

Section: Sensitivity Of Hyperthyroid Rats To Glycaemic Action Of Insulinmentioning

confidence: 99%

Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Minor role of endogenous insulin in thyroid-dependent changes in glucose turnover

Okajima¹,

Ui²

1979

Biochemical Journal

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1. Rates and rate coefficients of glucose utilization and replacement (glucose turnover) as well as its recycling were determined in rats by using [U-14C]- and [2-3H]-, [3-3H]- or [6-3H]-glucose. 2. In euthyroid rats, the blood concentration of glucose was 1.5 times and its turnover rate was 2 times as high in the fed state as in the starved state; consequently the rate coefficient, a measure of the capacity of rats to utilize blood glucose, was also higher in the former than in the latter. 3. Induction of mild diabetes by streptozotocin exerted little influence on the content and turnover of blood glucose in the starved state, whereas it caused hyperglycaemia and a decrease in the rate coefficient after feeding. 4. Induction of hyperthyroidism caused increases in rates and rate coefficients of glucose turnover to substantially the same extent whether or not the plasma concentration of insulin was lowered by treatment with streptozotocin or injection with anti-insulin serum. 5. It is concluded that thyroid hormones are capable of enhancing glucose turnover in the starved state independently of endogenous insulin, which plays a significant role in increasing glucose utilization in the fed state.

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The Pancreatic Alpha and Beta Cells Responses to 1-Arginine and Insulin-Induced Hypoglycaemia in Hyperthyroidism

Cited by 10 publications

References 10 publications

Failure of Exogenous Insulin to Inhibit Insulin Secretion in Man

Failure of Exogenous Insulin to Inhibit Insulin Secretion in Man

Impaired Pancreatic α-Cell Response in Hyperthyroidism

Metabolism of glucose in hyper- and hypo-thyroid rats in vivo. Minor role of endogenous insulin in thyroid-dependent changes in glucose turnover

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