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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the relationship between the concentrations of serum T3 and hepatic nuclear T3 receptor in a reversible nonthyroidal disease, we studied these parameters in rats with streptozotocin-induced diabetes mellitus, control rats, and rats that were weight-matched to the diabetic rats by food restriction. Results were similar either 1 or 9 weeks after the induction of diabetes. A significant decrease from control in mean serum T4, T3 and free T3 index was noted in the diabetic rats. However, mean serum TSH was not altered significantly. The hepatic nuclear T3-binding capacity in the diabetic rats was similar to that in the control at both time intervals, whereas the nuclear T3-binding capacity of fasted rats was decreased. The dissociation of serum T3 and hepatic nuclear receptor concentrations in diabetic rats suggests that receptor concentration is not modified by thyroid hormones in this nonthyroidal disease.
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PMID:Dissociation of serum triiodothyronine concentration and hepatic nuclear triiodothyronine-binding capacity in streptozotocin-induced diabetic rats. 626 40

The effect of diabetes mellitus on the synthesis and secretion of thyroid hormone ws investigated in mice with streptozotocin-induced diabetes. Thyroid glands were labeled in vivo with 131I for 2 h. In control animals, TSH stimulated the synthesis of PB127I and 131I-labeled iodothyronines and simultaneously decreased the proportion of 131I-. These effects of TSH were not observed in diabetic animals but were demonstrable in diabetic animals treated with insulin. For studies of hormone secretion, labeled thyroid glands were cultured in vitro in medium containing 1 mM mononitrotyrosine. The rate of the hydrolysis of labeled thyroglobulin was measured as the proportion of 131I-labeled iodotyrosines and 131I-labeled iodothyronines recovered at the end of culture and was used as an index of thyroid secretion. TSH in vivo stimulated the rate of thyroglobulin hydrolysis for 6 h, with a peak occurring after 2 h. The diabetic mice had a diminished response to TSH, which improved on treatment with insulin. The addition of TSH and insulin to the culture medium significantly increased the rate of thyroglobulin hydrolysis in glands of diabetic mice over that resulting from the addition of dibutyryl cAMP alone. The generation of thyroidal cAMP in response to TSH was higher in diabetic mice than in controls. The rise in plasma T4 and T3 2 h after the administration of TSH was less in diabetic mice than in control mice or diabetic mice treated with insulin. Our studies, therefore, indicate that the thyroidal response to TSH is decreased in diabetes mellitus. The defect appears to be at a step beyond the generation of cAMP.
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PMID:Decreased thyroidal response to thyrotropin in diabetic mice. 627 30

Several alterations in thyroid function are found in diabetes mellitus (see Table I). The most profound changes occur in patients with insulin-dependent diabetes. Plasma T4 is normal whereas plasma T3 is diminished, and the plasma level of rT3 is elevated in diabetic ketoacidosis or in patients with severely uncontrolled diabetes. These changes arise from alterations in the monodeiodination pathways of T4. Both hypo- and hyperthyroidism occur with increased frequency in diabetes. There is an increased prevalence of thyroid autoantibodies in insulin-dependent diabetics. Animals studies suggest a defect in the hypothalamic regulation of the thyroid-pituitary feedback system and an impaired response of the thyroid gland to TSH. Clinical studies are not yet available to confirm the occurrence of these regulatory disturbances in human diabetic patients. It is not clear whether the deiodination and regulatory changes in thyroid hormone economy that are associated with diabetes result in hypothyroidism at the cellular level.
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PMID:Thyroid function in a diabetic population. 630 31

The number of nuclear thyroxine (T4) or triiodothyronine (T3) receptors and the serum values of thyroxine, triiodothyronine, reverse triiodothyronine and TSH were investigated in 13 patients with Type 1 (insulin-dependent) diabetes (group 1), in 10 patients with Type 2 (non-insulin-dependent) diabetes (group 2) and in age and weight matched non-diabetic subjects. All patients were clinically euthyroid, although serum T3 was low and reverse T3 high in group 1 compared with the non-diabetic subjects. The Type 1 diabetic patients had evidence of poor metabolic control because of weight loss and high glycosylated haemoglobin levels. The maximal specific nuclear binding capacities for T4 (1.8 X 10(-16) mol T4/10 micrograms DNA) and T3 (1.4 X 10(-16) mol T3/10 micrograms DNA) were increased in group 1 compared with the normal subjects (T4: 1.1 X 10(-16) mol T4/10 micrograms DNA, p less than 0.010, T3: 0.9 X 10(-16) mol T3/10 micrograms DNA, p less than 0.05), whereas the nuclear binding affinity for T4 (Ka = 1.5 X 10(9) l/mol) and T3 (5.1 X 10(9) l/mol) was similar to that of the normal subjects (T4, Ka = 2.0 X 10(9) l/mol; T3, Ka = 5.6 X 10(9) l/mol). In contrast, neither the nuclear binding of T4 (1.0 X 10(-16) mol T4/10 micrograms DNA) and T3 (1.1 X 10(-16) mol T3/10 micrograms DNA) nor the binding affinity for T4 (Ka = 3.3 X 10(9) l/mol) and T3 (Ka = 3.9 X 10(9) l/mol) in group 2 differed from those of the non-diabetic subjects. In conclusion, nuclear T4 and T3 receptor number in cells from patients with poorly controlled Type 1 diabetes was raised compared with normal subjects. This increase may have been responsible for the euthyroidism in these patients in whom the serum T3 was low. In contrast, cellular binding of T4 and T3 appeared normal in the Type 2 diabetic subjects.
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PMID:Nuclear thyroxine and triiodothyronine receptors in human mononuclear cells in diabetes mellitus. 630 86

The effect of experimental diabetes on T4 to T3 conversion, T3-deiodination, and the pituitary response to a dose of T4 and T3 was studied. Pituitary GH and plasma TSH were determined as a measure of the biological response to thyroid hormones. Thyroidectomized rats, 5 days after injection with saline or streptozotocin (thyroidectomized-control (Th.C) and thyroidectomized-diabetic (Th.D) rats, respectively) received an ip dose of T4 + [125I]T4 or T3 + [125I]T3. Rats from each group were sacrificed at varying intervals after thyroid hormone injection. Th.D rats had hyperglycaemia, glycosuria, and a body weight of about 80% of that of Th.C rats. The concentrations of [125I]T4 and [125I]T3 were measured in several tissues after ethanol extraction, separation by thin-layer chromatography, and identification with markers. Plasma TSH and pituitary GH were measured by specific RIAs. Diabetes decreased the conversion of T4 to T3 in several tissues, including the pituitary, but did not affect the deiodination of T3. The decrease in pituitary T3 content after a dose of T4 was accompanied by a diminution of the biological effect of the T4 dose on pituitary GH. Since diabetes also interferes with this biological response to a T3 dose, it seems likely that the reduced biological effect of thyroid hormones on pituitary GH may be related to an alteration in the somatotrophin T3 receptors, or in post-receptor events. Moreover, the data indicate that although T3 generation in the pituitary was reduced, the same dose of T4 had a greater inhibitory effect on TSH secretion in Th.D rats than in Th.C rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased T4 to T3 conversion in tissues of streptozotocin-diabetic rats. 632 20

In two girls (14 and 16 years) and one boy (19 years) with PLW-syndrome and pronounced obesity (240, 210 and 77% overweight) endocrine function tests were carried out. Growth hormone secretion was decreased but normalized after reduction of weight. Thyroxin levels as well as basal and TRH stimulated TSH concentrations were normal. HCG application in the boy induced no rise of the normal basal testosterone levels. Oral glucose tolerance test demonstrated an increased stimulation of insulin in two cases, no other symptoms of diabetes mellitus were found. In the LHRH test an insufficient rise of gonadotropins was found. However, after two weeks of pernasal application of an LHRH analogue (D-Leu6-des-Gly10-EA) the gonadotropin stimulation was distinctly improved and onset of puberty was induced in the male patient. These results are indicative of a hypothalamic disturbance in patients with PLW-syndrome.
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PMID:[Endocrine studies on the Prader-Labhart-Willi syndrome: puberty induction in a 19-year-old boy after long-term treatment with an LHRH analog]. 641 33

Altered thyroid hormone metabolism with decreased serum T3 and increased rT3 concentrations in patients with uncontrolled diabetes mellitus has been well documented. However, data regarding TSH secretion are sparse, especially the influence of glycemic control. Therefore, we examined serum T4, free T4, T3, rT3, T3 resin uptake, and TSH as well as the TSH response to TRH administration [expressed as TSH increment (delta TSH) and area under the curve (theta TSH)] in 29 newly discovered type II diabetic patients (DM) before treatment and in 12 normal subjects. The study was repeated in the DM patients after attainment of euglycemia and normalization of glycosylated hemoglobin (HbA1C) following therapy with diet and tolazamide for 8-12 weeks. Serum T4, free T4, and T3 resin uptake were not significantly different in DM compared to those in normal subjects. Serum T3 was low and rT3 was high in DM before treatment, and both normalized on achieving the euglycemic state. Basal TSH in uncontrolled DM was not significantly different from that in normal subjects and remained unchanged during treatment. However, delta TSH and theta TSH were significantly reduced (P less than 0.01) in uncontrolled DM. Both fasting plasma glucose (FBS) and HbA1C levels correlated inversely with delta TSH as well as theta TSH (FBS vs. delta TSH, r = -0.42; FBS vs. theta TSH, r = -0.38; HbA1C vs. delta TSH, r = -0.40; HbA1C vs. theta TSH, r = -0.42; P less than 0.05 for all correlations). Finally, TSH responses returned to normal on attainment of euglycemia and normal HbA1C concentrations. These studies indicate that regulation of TSH secretion is altered in DM during the decompensated state and normalizes when euglycemia is achieved.
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PMID:Impaired pituitary thyrotroph function in uncontrolled type II diabetes mellitus: normalization on recovery. 643 Sep 48

Comprehensive evaluation of thyroid hormone indices was performed in 58 children with insulin-dependent diabetes mellitus (IDDM) at the time of diagnosis and prior to insulin therapy. Two patients were found to have primary hypothyroidism, with markedly elevated TSH and very low T4, free T4, T3, and reverse T3 concentrations. The remaining 56 patients had the transient alterations in thyroid hormone indices that are characteristic of "euthyroid sick" or "low T3" syndrome. Mean TSH and reverse T3 values were significantly higher and the mean T3, T4, and free T4 levels were significantly lower than those observed in the control population. Ten of the diabetic patients had elevated TSH concentrations and normal or low free T4 values; eight had normal TSH levels and low T4 and free T4 values. The remainder of the group had thyroid indices compatible with abnormal peripheral metabolism of thyroid hormones. Elevated titers of antimicrosomal antibodies were found in 16% of the children with IDDM. We conclude that abnormal peripheral metabolism and altered hypothalamic-pituitary function are responsible for the transient changes in thyroid hormone indices in patients with untreated IDDM. The most reliable indicators of concomitant primary hypothyroidism in untreated IDDM are markedly elevated TSH and low reverse T3 values.
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PMID:Thyroid hormone abnormalities at diagnosis of insulin-dependent diabetes mellitus in children. 643 Oct 66

In order to establish whether cholinergic receptors mediate GH secretion induced by TRH in insulin-dependent diabetes, 10 patients were treated with pirenzepine, an anticholinergic agent, and tested with TRH. Basal concentrations of GH were elevated in these patients and 8 of 10 patients responded to TRH with a significant rise in GH levels. Pretreatment with pirenzepine (40 mg given iv 10 min before TRH) suppressed the TRH-induced GH rise. Pirenzepine had no effect on TRH-induced TSH release. This finding suggests that a cholinergic mechanism is involved in the paradoxical response of GH to TRH in diabetic patients.
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PMID:The growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics involves a cholinergic mechanism. 643 81

A solid-phase immunosorbent radioassay for the detection of circulating antibodies to protein hormones is described. The assay is based on the binding of the homologous 125I-labelled antigen to the antibodies which are then bound to anti-IgG antibodies covalently coupled to Sepharose. It can easily be applied as a complement to any radioimmunoassay for the detection of circulating antibodies to the ligand measured. The assay system avoids falsely elevated values due to interference of high serum concentrations of the antigen. The assay was applied to measure antibodies to FSH, LH, TSH, GH, prolactin, insulin and thyroglobulin (Tg). Among patients with chronic thyroiditis Tg antibodies were found in 100% of the sera. In diffuse toxic goitre 73% of the patients had detectable Tg antibodies. Insulin antibodies were present in 82% of the sera from patients with insulin treated diabetes. No antibodies were found against the other protein hormones tested.
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PMID:A new sensitive immunosorbent radioassay for the detection of circulating antibodies to polypeptide hormones and proteins. 643 35


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