Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to elucidate whether or not the 'coupling defect' observed in thyroids from diabetic rats is due to a structural defect of intrathyroidal thyroglobulin (Tg), the sedimentation pattern and the stability of the thyroidal soluble iodoproteins were studied in control (C), food restricted (FR), diabetic (D) and insulin-treated diabetic (D+I) rats fed a low iodine diet either with (NID) or without (LID) iodide supplementation and labelled with 125I: acutely, 24 h prior to sacrifice and chronically, by feeding the corresponding diet labelled for 60 days. Diabetes resulted in a decrease of thyroidal weight, an increase of both thyroidal 127I content and concentration and decreased plasma TSH, irrespective of the diet. Insulin treatment reversed these alterations. Food restriction led to an intermediate situation between C and D. The iodoamino acid distribution in the acutely labelled thyroidal soluble iodoproteins showed a significant increase in the percent of organified 125I found as iodotyrosines (MIT and DIT) and a decrease of that found as iodothyronines (T3 and T4) both in D and FR. However, in the isotopically equilibrated groups, no differences were found except in LID-D where a slight increase in DIT and a decrease in T3 was found as compared to the corresponding control. The sedimentation patterns of both acutely and chronically labelled thyroidal soluble iodoproteins from all experimental groups displayed two peaks. The main one, corresponding to Tg, had a slightly lower sedimentation coefficient than the 19 S internal marker run in parallel, while the second one, relatively small, formed probably by dissociation of the main Tg peak, sedimented more slowly (12- 14 S).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intrathyroidal thyroglobulin in streptozotocin-diabetic rats. 352 86

We have recently reported that iodine administration (0.05% iodine in drinking water) to weanling, diabetes mellitus- and lymphocytic thyroiditis (LT)-prone Biobreeding Worcester (BB/W) rats strikingly increases the incidence of LT without occurrence of iodine-induced hypothyroidism, which frequently results when excess iodine is administered to euthyroid patients with Hashimoto's thyroiditis. Since hypothyroidism did not occur in the iodine-treated BB/W rats, hemithyroidectomy was carried out in 30-day-old BB/W rats to increase thyroid mass and functional reserve. Iodine administration for 60 days markedly increased antithyroglobulin antibodies (0.40 +/- 0.08 vs. 0.15 +/- 0.06 OD; P less than 0.02), the incidence of LT (68% vs. 13%; P less than 0.001), and thyroid weight of the residual lobe (10.5 +/- 0.7 vs. 6.3 +/- 0.3 mg/100 g BW; P less than 0.001) and induced hypothyroidism (T4, 2.5 +/- 0.2 vs. 3.0 micrograms/dL; P less than 0.05; T3, 25.1 +/- 1.9 vs. 37.5 ng/dL; P less than 0.001; TSH, 252 +/- 49 vs. 61 +/- 14 microU/mL; P less than 0.02). Hypothyroidism in the iodine-treated rats occurred primarily in those with LT. Similar studies were carried out in the non-diabetes mellitus-, non-LT-prone, genetically equivalent BB/W rats (W-line), the parent strain Wistar-Furth rats, and Sprague-Dawley rats. Iodine administration did not induce LT or antithyroglobulin antibodies in these three strains and did not affect thyroid function in Wistar-Furth and Sprague-Dawley rats. However, in the W-line rats, iodine excess did induce thyroid enlargement in the residual lobe (8.4 +/- 0.2 vs. 6.4 +/- 0.2 mg/100 g BW; P less than 0.001), a decrease in serum T3 (71.5 +/- 2.9 vs. 86.0 +/- 2.5 ng/dL; P less than 0.001), and an increase in serum TSH (344 +/- 65 vs. 69 +/- 6.0 microU/mL; P less than 0.001). It is evident, therefore, that hemithyroidectomy in BB/W rats sufficiently reduces functioning thyroid tissue, resulting in iodine-induced LT and hypothyroidism, similar to iodine-induced hypothyroidism in euthyroid patients with Hashimoto's thyroiditis. It is unclear, however, why iodine administration also induced hypothyroidism in hemithyroidectomized, genetically similar, W-line rats in the absence of LT. This observation suggests that iodine-induced hypothyroidism in rats may be genetically determined.
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PMID:Iodine-induced thyroiditis and hypothyroidism in the hemithyroidectomized BB/W rat. 359 27

We report a patient with pulmonary and bony metastases due to follicular carcinoma of the thyroid, occurring 12 years after the initial diagnosis. This was brought to light by worsening diabetic control due to thyrotoxicosis from functioning malignant thyroid tissue. Following radio-active iodine therapy, she remains well with good control of her diabetes.
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PMID:Metastatic follicular carcinoma of the thyroid presenting with thyrotoxic induced impaired control of diabetes mellitus. 371 6

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

Pancreatic islets contain large-quantities of thyrotropin-releasing hormone (TRH) and of its metabolite Histidyl-Proline diketopiperazine (Cyclo His-Pro). The effects of these two putative neurotransmitters on the pancreatic B-cell function have been evaluated in vitro, with islets of normal or dysthyroid mice. TRH and Cyclo His-Pro (10(-11)-10(-6) M) were without effect on insulin release induced by 10-20 mM glucose in islets of normal mice. They transiently accelerated the slow waves of membrane potential triggered in B cells by 10 mM glucose, but did not cause any sustained change in overall electrical activity, and did not affect the rate of 86Rb+ efflux from islet cells. They were also ineffective when insulin release was stimulated by leucine or arginine, or was potentiated by forskolin, an activator of the adenylate cyclase. Hyperthyroidism (induced by injections of thyroxine) caused a fall in islet insulin content, but augmented the 2 phases of glucose-induced release. On the other hand, hypothyroidism (induced by a low iodine diet and propylthiouracil) caused an increase in islet insulin content, but depressed the second phase of release. TRH did not affect either phase of insulin release by islets of hyperthyroid or hypothyroid mice. These results show that pancreatic B cells are not a target for TRH and Cyclo His-Pro.
Diabetes Res 1985 Mar
PMID:Thyrotropin-releasing hormone and insulin release: in vitro studies with islets of normal and dysthyroid mice. 393 Jan 25

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

A total of 123 spa patients with inadequately controlled diabetes mellitus was divided into the following 3 therapeutic groups: 1. therapeutic exercise alone, 2. iodine therapy with iodine brine (including drinking cure with "iodine-brine concentrate"), 3. remedial exercise plus iodine brine therapy. All patients received a rigidly controlled diabetic diet. The following parameters were determined at the beginning and at the end of the cure: whole blood and plasma viscosity, fibrinogen, blood glucose, total and HDL-cholesterol, triglycerides, HbA1c, alpha 2-macroglobulin, total protein, microhaematocrit. A significant improvement was found in the values of whole blood viscosity, cholesterol, triglycerides and blood glucose, indicative of a beneficial effect on metabolism, primarily due to the administered diet. The largest decreases were shown by blood viscosity, relative viscosity, triglycerides, cholesterol and HbA1c in group III, and by plasma viscosity in group II. alpha 2-Macroglobulins did not change. Fibrinogen was raised in groups I and III. The importance of the improved blood rheological properties is discussed, particularly with respect to reduced erythrocyte flexibility in diabetics.
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PMID:[Comparative study on the effect of diet, exercise and iodine balneotherapy on blood rheologic parameters in diabetics within the scope of a 4 week health resort stay in Bad Hall]. 399 41

Eight women with uncomplicated progressive partial lipodystrophy and two with progressive lipodystrophy and diabetes mellitus were studied. Plasma triglyceride levels were significantly elevated in the subjects with uncomplicated lipodystrophy; serum cholesterol, phospholipid, and plasma free fatty acid levels were normal. Paper electrophoresis showed increases in serum pre-beta lipoprotein and chylomicra. Thyroid function, as measured by radioiodine and stable iodine studies, was normal. Some subjects had a raised basal metabolic rate. Intravenous glucose tolerance was normal in patients with the uncomplicated disease.
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PMID:Blood lipid levels, thyroid status, and glucose tolerance in progressive partial lipodystrophy. 601 88

In order to determine the effect of diabetes mellitus on bone mineral content, measurements with the iodine 125 isotope method of Cameron were carried out in the distal ulna and calcaneus of 40 patients. 38% of female and 20% of male diabetic patients showed abnormally low values. The most severe changes were found in patients with complications of diabetes. There was a correlation between the duration of the diabetes and the severity of the mineral loss.
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PMID:[Mineral content of the peripheral skeleton in patients with diabetes mellitus ]. 621 76

A sensitive assay was used to measure the binding of iodine-125-labeled insulin in serum obtained from 112 newly diagnosed insulin-dependent diabetics before insulin treatment was initiated. Two groups of nondiabetics served as controls: children with a variety of diseases other than diabetes and nondiabetic siblings of insulin-dependent diabetics. Eighteen of the diabetics were found to have elevated binding and 36 were above the 95th percentile of control values. The insulin-binding protein is precipitated by antibody to human immunoglobulin G, has a displacement curve that is parallel and over the same concentration range as serum from long-standing insulin-dependent diabetics, and elutes from a Sephacryl S-300 column at the position of gamma globulin. These insulin antibodies are present in a large percentage of newly diagnosed, untreated diabetics and may be an immune marker of B-cell damage.
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PMID:Insulin antibodies in insulin-dependent diabetics before insulin treatment. 636 5


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