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Nuclear thyroxine and triiodothyronine receptors in human mononuclear cells in diabetes mellitus

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) diabet...

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Published in:Diabetologia 1983-06, Vol.24 (6), p.428-432
Main Author: Kvetny, J
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Language:English
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description 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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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. 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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. 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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.</abstract><cop>Germany</cop><pmid>6309586</pmid><doi>10.1007/BF00257341</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record>
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subjects Adolescent
Adult
Aged
Cell Fractionation
Cell Nucleus - metabolism
Cell Separation
Diabetes Mellitus - blood
Humans
Middle Aged
Monocytes - metabolism
Receptors, Cell Surface - analysis
Thyroid Hormones - blood
Thyroid Hormones - metabolism
title Nuclear thyroxine and triiodothyronine receptors in human mononuclear cells in diabetes mellitus
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