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D C Shen

Publications and source records attributed to D C Shen.

24 records · Page 2Linked to original sources
PubMed1985

Hyperthyroid Graves' disease causes insulin antagonism.

Oral glucose tolerance and pancreatic suppression tests were carried out in six young hyperthyroid men before treatment and 2-4 weeks after thyroid function tests returned to normal and in six normal men matched for age and weight. Glucose intolerance was present in the hyperthyroid individuals. It improved, but did not return to normal, after treatment. Insulin secretion was increased, and the peak values were delayed in the patients. Treatment did not influence the amount or pattern of the insulin response. Steady state plasma glucose levels (milligrams per dl +/- SEM) were significantly (P less than 0.001) higher in the hyperthyroid patients before treatment (128.6 +/- 2.4) than in the normal subjects (86.1 +/- 3.1). Although after treatment, steady state plasma glucose levels (116.1 +/- 2.7) decreased significantly (P less than 0.001), they remained higher than those in normal subjects (P less than 0.01). Therefore, insulin action was impaired in hyperthyroidism and had not returned to normal by 2-4 weeks after thyroid function tests were in the normal range.

Adult↗
PubMed1985

Long term treatment of Graves' hyperthyroidism with sodium ipodate.

To investigate the long term usefulness of sodium ipodate (Oragrafin) in the management of Graves' hyperthyroidism, we studied the effects of ipodate (500 mg, orally, daily for 23-31 weeks) on serum T3, T4, rT3, and some clinical parameters in five newly diagnosed Graves' hyperthyroid patients. Mean pretreatment serum T3, T4, and rT3 concentrations were 780 ng/dl, 25.4 micrograms/dl, and 118 ng/dl, respectively. One day after the first dose of ipodate, serum T3 decreased by 62% (P less than 0.01), and it was within the normal range thereafter throughout treatment. The serum T4 concentration decreased by 20% (P = 0.09) at 24 h and by 43% (P less than 0.05) at 14 days. Subsequently, serum T4 was 41-65% lower than before treatment throughout the study; rT3 increased 24 h after the first dose of ipodate (118% above baseline; P = 0.1), remained elevated (97-109%) for 10 weeks, and then gradually decreased to the pretreatment level. A marked gain in body weight [5.1 +/- 1.1 (+/- SEM) kg] occurred in all patients. After discontinuation of ipodate, mean thyroid radioiodine (RAI) uptake values increased serially in four patients and were similar to pretreatment values: pretreatment, 74 +/- 6% (+/- SEM); after 7 days, 66 +/- 8%; after 14 days, 71 +/- 7%; after 28 days, 69 +/- 7%. The fifth patients's RAI uptake was 12-16% (vs. a pretreatment value of 48%) from 7-28 days after the end of a 31-week course of ipodate. He remained euthyroid without further treatment for the subsequent 4 months. We conclude that 1) ipodate (500 mg daily) reduces serum T4 and T3 levels as fast and as much as does the 1-g daily dose studied previously; 2) long term use (for 23-31 weeks) of ipodate for the treatment of Graves' hyperthyroidism is clinically feasible; no adverse effects occurred during or after ipodate treatment; and 3) RAI uptake returns to pretreatment levels as early as 7 days after the discontinuation of ipodate. Hence, use of ipodate does not prevent use of 131I therapy for those patients for whom it is otherwise desirable.

Adult↗
PubMedDate not supplied

Moderate insulinopenia can cause insulin antagonism.

Profound insulin deficiency can cause insulin antagonism. To assess whether more modest insulinopenia can also cause insulin antagonism, male Sprague-Dawley and female obese (fa/fa) Zucker rats received streptozotocin injections (20, 30 or 40 mg/kg) or citrate buffer alone. After 1 and 2 weeks, the animals underwent glucose (0.5 g/kg) and insulin (0.2 U/kg)-glucose (0.7 mg/kg) tolerance tests, respectively, after an overnight fast. In the Sprague-Dawley rats: (a) basal glucose concentrations were significantly increased in the 40 mg/kg group; (b) glucose-induced insulin responses were significantly decreased in the 30 and 40 mg/kg groups; (c) glucose disappearance rates after glucose alone were significantly decreased in the 40 mg/kg group; and (d) glucose disappearance rates after insulin and glucose were significantly decreased in both the 30 and 40 mg/kg group. All obese Zucker rats injected with 30 and 40 mg/kg died within the first week with marked hyperglycemia. In the 20 mg/kg groups: (a) basal glucose levels were significantly elevated; (b) glucose disappearance rates and insulin responses were significantly decreased; (c) glucose disappearance rates after insulin and glucose were 20% lower than in the control rats but the difference did not reach statistical significance. In conclusion, Zucker rats are much more sensitive to streptozotocin than Sprague-Dawley rats. In the Sprague-Dawley strain, a modest insulin deficiency is associated with insulin antagonism. Since these rats treated with low doses of streptozotocin are characterized by decreased glucose-induced insulin secretion and insulin antagonism, they may serve as an appropriate model for type 2 diabetes mellitus.

Animals↗