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)

The 24-h hormonal and metabolic profiles obtained in five non-insulin-dependent diabetics receiving twice daily s.c. injections of the long-acting somatostatin analogue SMS 201-995 (50 micrograms) have been compared with those obtained following placebo injection. Injections were given 30 min before breakfast and the evening meal. GH secretion was not suppressed by the analogue administered in this manner. Despite suppression of serum insulin levels following breakfast and the evening meal, blood glucose levels were similar during the two study periods with no evidence of worsening in diabetic control. Prolonged suppression of plasma glucagon levels was observed and the nocturnal elevation in serum TSH levels was abolished. Free T4 levels fell significantly following the analogue but total T3 levels were unaffected. Blood alanine levels were elevated throughout the study period following SMS 201-995 but changes in lactate, pyruvate, glycerol and 3-hydroxybutyrate were minor. All five subjects suffered gastrointestinal side-effects. SMS 201-995 (50 micrograms) given twice daily before meals does not cause a deterioration in metabolic control, does not suppress 24-h GH secretion and causes significant side-effects in patients with non-insulin-dependent diabetes mellitus.
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PMID:Effects of somatostatin analogue SMS 201-995 in non-insulin-dependent diabetes. 288 47

Because of its wide distribution in the organism, natural somatostatin (SRIF) demonstrates an ample spectrum of actions, involving mainly the central neuroendocrine system and the enteropancreatic area. In the former, this peptide may find its field of application in conditions characterized by excessive GH, TSH or ACTH secretion, depending on the central or peripheral cause of the inappropriate hormone control. The inhibitory effect of SRIF on gastrointestinal and pancreatic hormones may be useful in the management of tumors originating in this system and also in the treatment of inflammatory processes such as pancreatitis, in malignant diarrhea, and in gastrointestinal bleeding. A complex action of SRIF and its derivative on insulin release and glucose homeostasis may offer some advantages in the control of unstable diabetes. Dampening of organic functions in the upper digestive tract may also render SRIF and its analogues useful in the exploration of the gallbladder, gastric and pancreatic functions. The effect of such peptides on tissue growth and on the regulation of blood pressure are the subject of present investigations. Cytoprotection, an interesting aspect of SRIF application, is discussed elsewhere in this compendium. Finally, some comments on the possible use of SRIF as an additive to the conventional treatment of burns and sepsis close this review.
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PMID:Clinical applications of somatostatin. 290 Feb 4

Both clinical diabetes and chemically-induced diabetes have been reported to alter control processes of the hypothalamic-pituitary-thyroid axis. One of the sites of alteration appears to be depression of thyrotrophin releasing hormone (TRH) stimulated thyrotrophin (TSH) release. The present study examined the influence of sequential administration of streptozotocin and the goitrogen thiouracil to male mice for 4 weeks in view of their possibly opposing effects on TSH release. The drugs produced the expected results when administered singly, with streptozotocin producing hyperglycemia and thiouracil causing hypothyroxinemia and goitrogenesis. Additionally, thiouracil administration produced hyperinsulinemia. Sequential administration of the drugs appeared to ameliorate the thyroid status and glycemic condition caused by individual exposure. Streptozotocin reduced the goitrogenic influence of thiouracil and thiouracil reduced the hyperglycemia of streptozotocin, but not to control levels. Thus, sequential administration resulted in mice with simultaneously elevated circulating glucose and insulin levels, and depressed thyroxine levels. Similar effects on glucose, insulin, and the thyroxine levels have been reported clinically in patients with non-insulin-dependent diabetes mellitus.
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PMID:Consequences of sequential induction of diabetes mellitus by streptozotocin and hypothyroidism by thiouracil in mice. 294 14

In an accompanying report, we describe a new test for detecting and quantitating those immunoglobulins G (IgG) related to the presence of hyperthyroidism in Graves' disease. In this procedure, an immunoprecipitate formed between the test IgG and antiserum against the Fc portion of the human IgG is incubated with 125I-labeled solubilized guinea pig fat cell membranes (SFCM). The proportion of added 125I bound to the immunoprecipitate is a measure of fat cell-binding IgG (FBI) in the test preparation. In this report we describe an improvement of the basic technique that permitted its use with serum. Here, the test specimen of serum was allowed to interact with anti-Fc IgG coupled to beads of Sepharose-4B. SFCM were then added, and the test proceeded as in the IgG-based procedure. Serum FBI values were decreased in a dose-dependent manner by bovine (b) TSH and, with lesser potency, by other glycoprotein hormones (bLH, bFSH, and hCG). Further, in experiments with sera and their corresponding IgG fractions from patients in the various groups studied, both individual serum FBI values and the extent to which they were decreased by the addition of bTSH were closely correlated with the TSH-binding inhibitory (TBI) activity of the corresponding IgG fractions. These findings indicate that FBI values in the serum-based test, as in the IgG-based test, reflect mainly the concentration of IgG that bind to the TSH receptor in SFCM. Two entirely separate evaluations of the serum-based FBI test were carried out. In the first, in sera from 21 patients with Graves' hyperthyroidism, FBI values (mean +/- SD, 1.6 +/- 0.6%) were completely separated from those in normal sera (-0.6 +/- 0.3%; n = 20), TBI-negative sera from patients with Hashimoto's disease (-0.3 +/- 0.3%; n = 21), and sera from patients with collagen-vascular disease (0 +/- 0.3%; n = 16). Positive results were also obtained in sera from 2 patients with TBI-positive Hashimoto's disease and 2 with diabetes mellitus associated with anti-insulin receptor antibodies (type B diabetes mellitus). In the latter, however, abnormal FBI values were not decreased by bTSH, but were decreased by insulin, which, conversely, had no effect on the elevated FBI values found in Graves' hyperthyroidism. In the second evaluation, FBI values were measured in 34 sera from normal subjects and 38 sera from patients with hyperthyroidism due to Graves' disease; 14 samples in the former group and 16 in the latter group were studied without knowledge of the diagnosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A new serum-based assay for fat cell-binding immunoglobulins: application to the detection of the thyrotropin receptor antibodies of Graves' disease. 299 74

We compared the circadian rhythms of anterior pituitary hormones in 15 patients with noncompensated insulin-dependent diabetes on first and second day treatment with Biostator. The rhythm was evaluated by means of a least squares analysis and presented as the circle of cosinors. In noncompensated diabetes the TSH and prolactin rhythm was maintained, whereas other hormones of the anterior pituitary showed no significant rhythm. In the course of one-day normalization of glycemia by means of Biostator the TSH and prolactin rhythm was maintained, whereas the circadian rhythm of growth hormone and ACTH levels appeared with acrophase at 18.47 and 19.59 hour, respectively. The LH rhythm did not exist, whereas the FSH rhythm was dubious. One may assume that noncompensated diabetes results in the impairment of certain pituitary hormonal rhythms and these disturbances are reversible after restoring of normoglycemia.
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PMID:Chronobiological analysis of changes in circadian rhythm of anterior pituitary hormones level during glycemia normalization by means of biostator. 303 56

The change in the levels of free thyroid hormones and the pathophysiology of the hypothalamo-pituitary-thyroid axis of patients with nonthyroidal illness (NTI) have not been clearly elucidated so far. Therefore, it was thought of interest to investigate this problem by determining free thyroid hormones and TSH in serum and the response of TSH to TRH in these patients. The subjects employed in this study were 71 cases with hemodialysis, 40 cases with diabetes mellitus, 24 cases with liver cirrhosis, 12 cases with various cancers, 10 cases with anorexia nervosa and 110 normal subjects as controls. The serum total protein, albumin, free T4, free T3, TSH and other parameters of thyroid function were determined, and the TRH test was performed on about 10 patients of each group. Serum TSH was not only determined by a conventional assay system, but with a highly sensitive method, and the data were compared with one another. It was found that the serum free T3 levels were significantly low in all the groups investigated, but the serum free T4 levels were significantly low only in the groups with hemodialysis, decompensated liver cirrhosis, cancers and anorexia nervosa. No significant lowering of serum free T4 was observed in the patients with diabetes mellitus, acute hepatitis and compensated liver cirrhosis. However, serum TSH levels tended to be higher in all the groups studied, though they were not significant. The response of TSH to TRH was low or delayed in about 20-50% of patients with hemodialysis, diabetes mellitus, liver cirrhosis, cancers and anorexia nervosa. It was observed that the serum rT3 concentration was significantly high in the patients with diabetes mellitus and anorexia nervosa but significantly low in the patients on hemodialysis. In the rest of the groups, there were found many cases who showed high levels of serum rT3 although they were not statistically significant. These results indicate that low concentrations of serum free T3 observed in the majority of the patients with severe NTI were, at least in part, due to the decrease in the peripheral conversion of T4 to T3 and the lowered sensitivity of the anterior pituitary to thyroid hormones and TRH.
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PMID:[Serum free thyroid hormones and response of TSH to TRH in nonthyroidal illnesses]. 310 Mar 46

Goiter and hypothyroidism have been reported as side effects of sulfonylurea therapy. To test the effects of glyburide, a new generation sulfonylurea drug, on thyroid function, we studied 15 male Type 2 diabetic patients before and after 6 weeks of treatment with this drug, and we repeated the studies on 9 of these patients who remained on the drug for at least 24 weeks. All hypoglycemic agents were discontinued for 1 week before the study. Patients had a baseline thyroid examination, serum T4, free T4 index (FT4I), T3, and free T3 index (FT3I), fasting serum glucose (FSG), HbA1c and a TRH test of TSH reserve. The dose of glyburide was adjusted at 2 weeks, and the tests were repeated after 6 weeks and after at least 24 (24-32) weeks of glyburide therapy. Compared to baseline, there was a significant decrease in FSG at 6 weeks and again at 24-32 weeks. Body weight, thyroid size, serum FT4I, FT3I, and TSH did not change significantly. After 6 weeks of therapy, there was no significant correlation of FSG or HbA1c with FT4I, FT3I, basal or peak TSH or TSH response area. The integrated area under the TSH response curve decreased significantly in 8 patients at 24 weeks (p less than 0.05). There was a positive correlation between FSG and the area under the TSH response curve using the combined baseline and 24 week data in these patients (r = 0.73, p less than 0.01). In this study with patients acting as their own controls, there was no effect of glyburide on thyroid function or size.
Diabetes Res 1986 Nov
PMID:Glyburide does not alter thyroid function. 310 70

The effect of domperidone, a specific blocker of dopamine receptors, on serum TSH and PRL levels was evaluated in 16 euthyroid men affected by insulin-dependent diabetes mellitus (IDDM) of different duration and in 7 age-matched normal controls. Diabetics were divided into 2 groups of 8 men according to the duration of their disease (group I: 1-9 years; group II: 11-18 years). Both groups had normal basal levels of TSH and PRL. Responses of these hormones to domperidone were similar in normal controls and in group I diabetics, whereas they were significantly reduced in patients of group II. When all 16 diabetics were studied together, a significant negative correlation was found between mean maximal peaks of TSH and PRL responses to domperidone and duration of diabetes. In order to evaluate whether the reduced effect of domperidone in diabetics was due to alterations of the dopaminergic control of TSH and PRL secretion, the domperidone test was repeated in 6 normal controls and in 6 diabetics of group II after infusion of dopamine (4 micrograms/kg/min for 2 h). Dopamine infusion induced parallel decreases in TSH and PRL concentrations, without modifying hormonal secretory patterns in response to domperidone. These data suggested that the reduced TSH and PRL responses to domperidone in diabetics were not due to alterations of the dopaminergic control of pituitary function but to a defect at the pituitary level. To test this hypothesis, TSH and PRL responses to TRH were evaluated in group I and group II diabetics and in normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:TSH and PRL responses to domperidone and TRH in men with insulin-dependent diabetes mellitus of different duration. 310 34

A man with diabetes mellitus, chronic hepatitis, chronic pancreatitis, and blind loop syndrome but without any previous thyroid disease developed three episodes of transient primary hypothyroidism associated with protein-calorie malnutrition (PCM). Clinical examinations suggested that this primary hypothyroidism was not caused by chronic thyroiditis, iodine deficiency, or iodine excess. Since the three times association of primary hypothyroidism with PCM suggested the possibility that the primary hypothyroidism was caused by PCM, we have tried to clarify its mechanism. For this purpose we have investigated the change of thyroid functions during protein-calorie repletion and the effect of amino acid deficiency. Total parenteral nutrition with full supplementation of amino acids resulted in a rapid increase in serum thyroxine (T4), triiodothyronine (T3), free T4, and reverse T3, and subsequently, a rapid decrease in TSH in several days after the nutrition was begun. When amino acid solution was changed to that depleted of phenylalanine and tyrosine after the restoration of thyroid functions, serum T4 and T3 showed a gradual decrease, but serum free T4 and TSH remained within normal range. However, resupplementation of phenylalanine and tyrosine after 8 weeks of depletion gave a rapid increase in serum T4, T3, free T4, and reverse T3. These results suggested that the primary hypothyroidism was caused by an impaired T4 production and that the deficiency of amino acids in PCM partly contributed to the impairment of T4 production.
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PMID:Primary hypothyroidism in an adult patient with protein-calorie malnutrition: a study of its mechanism and the effect of amino acid deficiency. 312 81

The responses to TRH and bovine TSH (bTSH) were compared in 19 men with uncontrolled type II diabetes mellitus and eight healthy control subjects. Baseline serum TSH, T3 and T4 were similar in both groups and the rise of serum TSH, T3 and T4 following the intravenous (IV) administration of TRH (500 micrograms) was not significantly different. Diabetic subjects showed a blunted response to the subcutaneous (sc) administration of bTSH (5 U) when their maximal serum T3 and T4 values were compared with controls (T4, 9.4 +/- 0.3 v 12.3 +/- 1.1 micrograms/dL, P less than .005; T3, 185 +/- 9 v 233 +/- 17 ng/dL, P less than .025; diabetic v control). When the response to bTSH was examined in seven patients after 4 to 5 days of strict glycemic control, the maximal T3 response was found to increase in six, and the maximal T4 response in five. These data show that the thyroidal secretory response to large doses of TSH is decreased in uncontrolled diabetes mellitus and that strict glycemic control frequently improves the response.
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PMID:Decreased thyroidal response to thyrotropin in type II diabetes mellitus. 313 39


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