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

It has been suggested that the incidence of Hashimoto's thyroiditis is increased in the presence of high iodide intake. The diabetes-prone BB/W rat develops spontaneous histological autoimmune lymphocytic thyroiditis (LT) without functional hypothyroidism between 60 and 120 days of age. Studies were carried out to determine whether iodine administration to BB/W rats would affect the incidence and severity of LT and induce hypothyroidism. Iodide (0.05% in water) or tap water (C) was administered ad libitum to 42 10-month-old BB/W rats and 71 30-day-old BB/W rats for 8 weeks. For control purposes, 0.05% iodide or tap water (C) was also administered ad libitum to 42 30-day-old nondiabetic and non-LT-prone BB/W genetically equivalent rats (W-line) for 12 weeks and 41 21-day-old Wistar rats for 7 weeks. In a separate experiment, weanling BB/W rats were fed a low iodine diet, a control iodine-sufficient (C) diet, or Purina chow (P) and tap water ad libitum for 8 weeks. In each experiment, blood was obtained at the time of death for the measurement of serum T4, T3, TSH, and antithyroglobulin antibody (anti-Tg Ab), and the thyroids were removed for histological evaluation (0 = no LT; 1-4 = LT). Iodide administration (0.05%) induced a significant increase in the incidence of LT in 30-day-old BB/W rats (I, 77%; C, 30%, P less than .001). Thyroid weight and serum T4, T3, and anti-Tg Ab concentrations were not affected by iodide administration. However, the presence of LT was associated with a significant increase in thyroid weight and anti-Tg Ab concentrations. BB/W rats subjected to a low iodine diet exhibited a significantly decreased incidence of LT (low I, 8.6%; C, 47.3%; P less than 0.01), but no statistically significant difference in anti-Tg Ab levels. Increased iodide intake did not significantly affect the incidence of LT in adult BB/W rats and did not induce LT or affect thyroid function in W-line or Wistar rats. These data show that iodine intake significantly affects the incidence of spontaneous LT in young, genetically predisposed rats.
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PMID:The effect of iodide ingestion on the development of spontaneous lymphocytic thyroiditis in the diabetes-prone BB/W rat. 375 9

Serum concentrations of thyroxine (T4),3,5,3'-triiodothyronine (T3),3,3',5'-reverse triiodothyronine (rT3),T3-binding capacity (TBC) and TSH were measured in 10 children with diabetes mellitus (mean age: 12.8 +/- 2 yr). The children were without ketoacidosis and serum glucose concentrations were 10.64 +/- 1.68 mmol/l (SD). The mean concentrations of serum T4, T3, rT3, TBC and TSH were 116.35 +/- 10.68 nmol/l (SD), 2.81 +/- 0.33 nmol/l, 0.27 +/- 0.04 nmol/l, 1.087 +/- 0.031 and 3.16 +/- 0.9 mu IU/ml, respectively, which were not significantly different from values of 10 normal control subjects (mean age: 11.6 +/- 2 yr). It seems therefore that the thyroid hormones and TSH levels between well controlled diabetic and healthy subjects of pediatric age do not differ significantly.
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PMID:Thyroid function in insulin-dependent diabetic children. 378 Aug 68

Several previous studies have reported that serum T3 and reverse T3 (rT3) concentrations are altered in uncontrolled diabetes mellitus and their normalization occurs when euglycemia is achieved. Therefore, this study was undertaken to examine the usefulness of serum T3 and rT3 levels as indices of metabolic control in diabetes mellitus. Serum T3, rT3, T4, Free T4, TSH and T3 resin uptake were determined in 18 normal subjects and 35 patients with newly discovered diabetes mellitus before initiation of therapy and reassessed after normalization of glycosylated hemoglobin (HbA1) concentration. These thyroid hormone concentrations were compared to the well established parameters of metabolic control such as fasting plasma glucose (FPG), peak plasma glucose (PPG), area under the curve of the oral glucose tolerance test (sigma G), 24 hr urinary glucose level (UG), HbA1 as well as glycosylated protein (GlyPr) and glycosylated albumin (GlyAlb) concentrations. Serum T4, T3RU, Free T4 and TSH concentrations in patients with diabetes mellitus prior to treatment were not significantly different from normal subjects and were not significantly correlated with any of the parameters of diabetic control. Serum T3 was significantly lower and serum rT3, significantly higher in diabetic patients prior to treatment as compared to normal subjects and both T3 and rT3 normalized in 20 patients studied when adequate metabolic control was achieved as reflected by normalization of HbA1 (less than 8.2%). Furthermore, significant negative and positive correlations were noted between parameters of metabolic control and serum T3 and rT3 levels respectively. Therefore, this study demonstrates that serum T3 and rT3 may be reliable indices of metabolic control in diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1986 Oct
PMID:Serum T3 and reverse T3 concentrations: indices of metabolic control in diabetes mellitus. 381 44

A 37 year old male with a strong family history of autoimmune disease presented with typical symptoms of hyperthyroidism. He had exophthalmos but no goitre. Hyperthyroidism was confirmed by failure of 131I neck uptake to suppress after 7 days treatment with triiodothyronine. Six years previously a diagnosis of primary hypothyroidism has been made. At diagnosis of hyperthyroidism, thyroglobulin antibodies, thyroidal microsomal antibodies and thyroid stimulating immunoglobulins were detected. The absence of thyroid growth stimulating immunoglobulins and presence of immunoglobulins blocking TSH-induced growth may account for the absence of goitre throughout. HLA -B8, -B, -DR3 and -DR4 genotypes, low C4 complement concentrations and islet cell autoantibodies were detected at the time of diagnosis and 1 year later diabetes mellitus developed.
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PMID:Hyperthyroidism following primary hypothyroidism in association with polyendocrine autoimmunity. 388 26

Euthyroid sick syndrome is characterized by low serum T3 and raised reverse T3 (rT3). Most of the states with this syndrome are also documented to manifest hyperglucagonemia. Furthermore, several recent studies have suggested that glucagon may play a role in T4 monodeiodination in some of these states such as starvation and uncontrolled diabetes mellitus. Therefore, hyperglucagonemia was induced by intravenous glucagon administration in euthyroid healthy volunteers and thyroid hormone levels were determined at frequent intervals up to six hours. Plasma glucose and insulin rose promptly on glucagon administration, thus establishing the physiologic effect of glucagon. Serum T4, free T4, T3 resin uptake, and TSH concentrations remained unaltered throughout the study period. Serum T3 declined to a significantly low level (P less than 0.05) between 60-90 minutes. Serum rT3 rose significantly (P less than 0.05) by four hours and the rise was progressive till the end of the study period. Therefore, these results suggest that hyperglucagonemia may be one of the factors responsible for lowering of T3 and a rise in rT3 in euthyroid sick syndrome.
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PMID:Glucagon administration induces lowering of serum T3 and rise in reverse T3 in euthyroid healthy subjects. 391 May 31

A 68-year-old male patient without any previous thyroidal disease developed three times of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Because of his diabetes mellitus, alcoholic hepatitis, chronic pancreatitis and blind loop syndrome, his nutritional balance was easily disturbed leading to PCM. Although he recurrently developed primary hypothyroidism associated with PCM, this condition was completely restored by protein-calorie repletion. The possibility of dietary iodine deficiency was negated by the observation that his daily urinary iodine secretion was more than 4 mg/day. Plasma amino acid analysis revealed severe depletion of phenylalanine, tyrosine and other essential amino acids and raised the possibility that this hypothyroidism was caused by amino acid deficiency. In order to clarify the mechanisms of this primary hypothyroidism, we have investigated the change of thyroid functions during protein-calorie repletion by total parenteral nutrition (TPN). We then removed iodine from the nutrients for TPN to ascertain that iodine deficiency was not the cause of the primary hypothyroidism in the present case. In spite of the removal of iodine, serum T4 and T3 suddenly increased from 1.1 micrograms/dl and less than 25 ng/dl to 3.5 micrograms/dl and 59 ng/dl, respectively, in a few days after the beginning of TPN. They continued to increase thereafter and reached 6.3 micrograms/dl and 115 ng/dl in 6 weeks. Serum free T4 also showed a sudden increase from 0.56 ng/dl to 1.7 ng/dl after TPN and remained above 1.3 ng/dl thereafter. Serum reverse T3 showed a rapid increase after TPN, but, 4 weeks later, returned to the previous level before TPN. Serum TSH decreased from 120 microU/ml to 17 microU/ml in a few days after TPN and reached a level within normal range in 4 weeks. Serum TBG gradually increased from 10.7 micrograms/ml to 29.2 micrograms/ml in 6 weeks. These results show that the T4 synthesis was extremely impaired by PCM in spite of the strong stimulation by TSH and that this suppression of T4 synthesis by PCM led the patient recurrently to the primary hypothyroidism. We have next investigated the possibility whether the deficiency of phenylalanine and tyrosine could cause a suppression of T4 synthesis because tyrosine is an important substrate of T4. For this purpose we removed phenylalanine and tyrosine from TPN and added iodine to prevent iodine deficiency due to prolonged iodine-depleted nutrition. Reduction of phenylalanine and tyrosine resulted in a marked decrease in serum T4, T3 and TBG in 7 weeks, but gave no change to free T4. Serum TSH remained within normal range.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Contribution of amino acid deficiency to primary hypothyroidism associated with protein-calorie malnutrition]. 393 44

Overt insulin-dependent diabetes mellitus in the rat is associated with the u haplotype of the rat major histocompatibility complex (MHC), RT1. Thyroiditis of sufficient severity to result in elevation of TSH levels is seen in Buffalo rats (RT1b). In order to examine the association of autoimmune thyroid disease with MHC gene products, we have crossed inbred Buffalo rats with diabetic BB rats and examined the RT1 genotype, the histology of thyroid and pancreatic tissue, and two indices of thyroid function. The data indicate that animals having pancreatic lymphocytic infiltration and insulinopenic overt diabetes mellitus had at least one RT1u haplotype. All but one animal having severe histological thyroid lymphocytic infiltration had at least one RT1b haplotype. Rats with severe thyroiditis had higher mean TSH levels than rats with normal histology or rats with mild thyroiditis. We conclude that gene products of the rat MHC affect the severity of spontaneous organ-specific autoimmune disease in terms of clinically apparent as well as tissue inflammatory disease.
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PMID:Association of spontaneous thyroiditis with the major histocompatibility complex of the rat. 397 12

Studies of the hypothalamic-pituitary-thyroid axis have been performed in streptozotocin (STZ)-diabetic Wistar rats and their controls. Plasma PBI concentration, plasma and pituitary TSH, contents, and hypothalamic TRH content were measured by RIA in basal and stimulated conditions. Compared to controls, rats made diabetic by 6.0 or 7.5 mg STZ/100 g BW showed decreased plasma PBI and TSH and diminished pituitary TSH content, with greater alterations in rats receiving the highest STZ dose. Both diabetic groups showed an almost 50% reduction of hypothalamic TRH content in comparison with the mean control value. After thyroidectomy, pituitary TSH secretion increased in diabetic, ad libitum fed, and semistarved animals, but it was lower in the diabetic group in which the reduction in plasma PBI was similar or greater. To evaluate pituitary sensitivity to the inhibitory action of L-T4 on TSH secretion in diabetes, thyroidectomized control (Thx-C), thyroidectomized diabetic (Thx-D), and thyroidectomized semistarved (Thx-S) rats were injected twice daily for 7 days with either saline or a fractional L-T4 dose of 0.25, 0.50, or 1.00 microgram/100 microgram/100 g BW. In Thx-D rats, a daily dose of 1.00 microgram L-T4 was sufficient to normalize pituitary TSH secretion, while a dose of 2.00 microgram was required to induce a similar effect in the Thx-C and Thx-S animals. Pituitary TSH content was increased in the Thx-C group with increasing T4 doses. No modification in this parameter was seen in the Thx-D and Thx-S animals. The fact that diabetes caused a reduction in the hypothalamic TRH content indicates that the primary cause of pituitary-thyroid alterations in STZ-diabetic rats lies in the hypothalamus, although the metabolic imbalance induced by diabetes and, in less degree, by undernutrition could also be partly responsible for some of the described modifications.
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PMID:Effect of streptozotocin diabetes on the hypothalamic-pituitary-thyroid axis in the rat. 615 7

The effects of streptozotocin-induced diabetes mellitus on the hypothalamic-pituitary-thyroid axis in rats were studied. Streptozotocin (60 mg/kg) was injected ip. Rats were decapitated at two and four weeks after the streptozotocin treatment. Thyrotropin releasing hormone (TRH), thyrotropin (TSH), thyroxine (T4), 3,3',5-triiodothyronine (T3), 3,3',5'-triiodothyronine (rT3), 3,3'-diiodothyronine (3,3'-T2) and 3',5'-diiodothyronine (3',5'-T2) were measured by means of the specific radioimmunoassay for each. Immunoreactive TRH (ir-TRH) contents in the hypothalamus significantly decreased at four weeks (p less than 0.02). Basal TSH levels in plasma significantly decreased (p less than 0.005, p less than 0.001), and plasma ir-TRH and TSH responses to cold were significantly inhibited after the streptozotocin treatment (p less than 0.001). The plasma TSH response to TRH was decreased, but not significantly. The plasma T4 and T3 levels fell significantly. RT3 did not change throughout the experiment. 3,3'-T2 levels in plasma fell significantly, whereas 3',5'-T2 increased. Blood glucose levels rose significantly after streptozotocin treatment, but insulin treatment led to partial restoration. The findings suggest that streptozotocin-induced diabetes mellitus affects various sites of the hypothalamic-pituitary-thyroid axis in rats.
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PMID:Effects of streptozotocin-induced diabetes mellitus on hypothalamic-pituitary-thyroid axis in rats. 622 95

The pattern of spontaneous GH, TSH, T4, and T3 secretion has been studied in male rats in response to a 15-day period of streptozotocin diabetes or food restriction. Beginning at 0900 h, groups of control (C), food-restricted (FR), diabetic (D), and insulin-treated D rats were killed every 60-90 min for a 8-h period. Food restriction resulted in a significant depression of the GH, TSH, T4, and T3 peaks, whereas diabetes caused complete suppression of episodic secretion of each hormone. Insulin (6 U/100 g BW X day for 12 days) administration to D rats restored the normal pattern of secretion. In D and FR rats, pituitary GH concentrations were lower than in C rats, whereas pituitary TSH concentrations were similar to those in controls. Thus, as compared to C rats, FR and D rats showed an inhibition in GH, TSH, T4, and T3 secretion, most marked in D animals. Since diabetes is associated with a deficiency of circulating thyroid hormones, the potential roles of T4 and T3 on pituitary GH concentration and secretion in D rats were evaluated. Treatment of D rats with insulin (3 U/100 g BW X day), T4 (1.8 micrograms/100 g BW X day), or T3 (0.30 microgram/100 g BW X day) for 12 days resulted in a significant but limited increase in pituitary GH content. When administered together with insulin, the net effects of T4 or T3 with insulin appeared additive. T4 administration to D rats produced a significant though limited increase in plasma GH concentrations and weight gain, whereas both values were unaffected by T3. Simultaneous administration of T4 and insulin resulted in significant increased plasma GH concentration to levels greater than those in C rats. However, plasma GH levels in rats treated with T3 plus insulin were greater than those in D rats, but lower than in C animals. The results indicate that the decreased pituitary GH content of D rats can be corrected, at least in part, by T4 and T3.
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PMID:Diurnal variations of plasma growth hormone, thyrotropin, thyroxine, and triiodothyronine in streptozotocin-diabetic and food-restricted rats. 623 18


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