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 aim of the study was the evaluation of growth hormone secretion under physiologic conditions in two groups of type I diabetics: responding and nonresponding to TRH stimulation. Both groups matched for age and metabolic control of diabetes were studied during 24-hours and after GHRH stimulation. The whole diabetic group (n = 18) showed circadian rhythm of GH secretion with mesor value of 4.03 micrograms/l. TRH-responders had lower mesor GH value than TRH-nonresponders: 3.53 vs. 5.32, p < 0.05. GH response to GHRH was almost identical in both groups. C-peptide level was lower in TRH-responders: 0.16 vs. 0.56 microgram/l, p < 0.05. No correlation was found between growth hormone response and HbA1 and C-peptide levels. It is concluded that type I diabetics responding to TRH stimulation are characterized by lower mean 24-hour GH levels and lower C-peptide values.
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PMID:Lower 24-hour growth hormone levels in type I diabetics responding to thyrotropin-releasing hormone (TRH). 134 74

Thyrotropin-releasing hormone (TRH) blunts growth hormone (GH) response to various stimuli in normal subjects. We were interested if similar inhibitory effect of TRH could be demonstrated in diabetes mellitus where GH is abnormally regulated. In this study we compared the effect of TRH on GH response to L-dopa in normal and diabetic subjects. TRH 0.2 mg iv blunted GH response to L-dopa 0.5 g p.o. in normal subjects with peak GH values 13.1 and 7.3 micrograms/l, p < 0.05. In the diabetics no inhibitory effect of TRH was demonstrated and GH was even paradoxically increased after TRH: 14.9 and 21.9 micrograms/l, p = NS. Lack of inhibitory effect of TRH was more pronounced in patients with proliferative retinopathy. It is concluded that TRH has no inhibitory effect on L-dopa-induced GH response in diabetic subjects. This finding provides further evidence for disturbed GH regulation in diabetes mellitus.
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PMID:Thyrotropin-releasing hormone (TRH) does not suppress growth hormone response to L-dopa in insulin-dependent diabetes mellitus. 134 75

Reviews in brief the studies of the effects of some non-glucose regulators of various origins on pancreatic insulin secretion mediated by endocrine, paracrine, and neurocrine mechanisms, carried out in this laboratory. Model experiments with primary monolayer cultures of isolated islet cells have helped demonstrate a direct insulinotropic effect of STH, TRH, C-terminal tetrapeptide cholecystokinin, opioid peptides and blood plasma of patients with insulin-dependent diabetes mellitus. The findings evidence that the insulinotropic effect of the blood serum of patients with type I diabetes may be associated with both stimulation and suppression of the functional activity of the cultivated islet cells. This latter type of effect influences the basal and glucose-stimulated secretion of insulin. The destructive effect of the plasma of patients with insulin-dependent diabetes on the function of islet cell culture is confirmed by the presence of autoantibodies to islet cell surface antigens in the plasma of 53-55% of the examined patients and by a cytotoxic effect in 45% of cases.
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PMID:[Insulinotropic factors in health and disease]. 148 May 83

Thyrotropin-releasing hormone (TRH) is produced in the hypothalamic paraventricular nucleus (PVN) as a 255-amino acid precursor (pro-TRH) with 5 TRH progenitor sequences. Pro-TRH is enzymatically processed to yield TRH and other peptides, which are transported to the median eminence and released into hypophysial portal blood. To elucidate the role of TRH in the control of thyroid function, we studied hypothalamic TRH synthesis and release in many conditions. TRH synthesis and release were assessed by pro-TRH mRNA measurement, and by sampling portal blood or push-pull perfusate, respectively. Destruction of the PVN reduced TRH and TSH secretion dramatically, while electrical stimulation of this nucleus enhanced their release. Hence, the PVN is important for normal TSH secretion. TRH synthesis and release decreased in hyperthyroid rats, but increased in hypothyroid rats. The magnitude of these changes, however, was small compared with alterations in TSH, suggesting that the feedback of thyroid hormones on TSH release is mainly exerted at the pituitary level. TRH synthesis and release increased during cold exposure, and decreased during starvation and diabetes. Thus, altered thyroid function during cold exposure, diabetes and starvation seems due to modified hypothalamic TRH synthesis and release.
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PMID:Regulation of hypothalamic TRH production and release in the rat. 151 60

Diabetes mellitus is frequently associated with reduced levels of TSH, PRL, GH, and gonadotropins. In this study we have wanted to determine whether chemically induced diabetes mellitus is associated with a decreased hypothalamic release of TRH. Male rats were made diabetic with streptozotocin (STZ; 65 mg/kg), whereas controls received vehicle. After 2 weeks, STZ diabetic rats had 25% lower body weights, 3.5-fold higher blood glucose, and 40-60% lower plasma TSH, T3, and T4 levels than controls. The plasma T4 dialyzable fraction had increased 2.5-fold in STZ diabetic rats, and the plasma free T4 concentration was similar to that in controls. Thus, treatment with STZ results in decreased plasma TSH and T4 levels, but does not reduce free T4 concentrations. The content of TRH in hypothalami of 2-week STZ diabetic rats was similar to that in controls, but in vitro these hypothalami released less TRH than those of control rats. In 2-week STZ diabetic rats, TRH in hypophysial stalk blood was 30% lower than that in control rats. The in vitro TRH secretion from hypothalami of untreated rats was dependent on the glucose concentrations in the incubation medium; increasing the glucose concentration from 10 to 30 mM did not alter TRH secretion, but basal TRH release increased in the absence of glucose. In conclusion, STZ-induced diabetes in the rat is associated with reduced hypothalamic secretion of TRH, which, in turn, may be responsible for the reduced plasma TSH and thyroid hormone levels. Furthermore, it is suggested that the inhibitory effect of STZ-induced diabetes on TRH secretion is probably not due to hyperglycemia.
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PMID:Hypothalamo-hypophysial-thyroid axis in streptozotocin-induced diabetes. 153 Jul 81

TRH is synthesized in the islets of Langerhans and was found in the perfusate of isolated rat pancreas. In the present study, designed to determine the role of endogenous TRH, we first characterized chromatographically the identity of immunoreactive TRH with synthetic pGlu-His-Pro-NH2. Since endogenous TRH secretion may mask the effects of exogenous TRH, we performed, in parallel to dose-response studies, immunoneutralization experiments using anti-TRH serum to neutralize the endogenous TRH secretion from isolated perfused rat pancreas. The data indicate that exogenous TRH enhances basal glucagon secretion; inversely, anti-TRH serum inhibits glucose plus arginine-induced glucagon secretion and produces a concomitant slight inhibition of somatostatin secretion. The present study shows a physiological contribution for endogenous TRH as a local modulator of intraislet hormone regulation; from these observations, we postulate a direct effect of pancreatic TRH on glucagon-containing (alpha) cell secretion, which, in turn, may produce the fluctuation in somatostatin secretion. Local TRH secretion provides a model for positive feedback regulation of glucagon secretion, frequently associated with diabetes.
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PMID:Antithyrotropin-releasing hormone serum inhibits secretion of glucagon from isolated perfused rat pancreas: an experimental model for positive feedback regulation of glucagon secretion. 163 22

To investigate endocrinological changes associated with severely uncontrolled type 1 (insulin-dependent) diabetes mellitus 27 patients (19 men, eight women) with ketoacidosis or severe ketonuria (= group 1) were examined on admission and after recovery. For comparison 13 non-ketotic patients (seven men, six women), admitted for adjustment of treatment because of poor diabetic control (= group 2), and 20 healthy controls were studied. On admission, the serum testosterone levels in men were lower in group 1 (15.1 +/- 2.0 nmol l-1) (mean +/- SEM) than in group 2 (27.2 +/- 2.8 nmol l-1) (p less than 0.01) and healthy controls (20.6 +/- 2.0 nmol l-1) (p less than 0.05). During treatment the testosterone levels in group 1 rapidly rose to the control level. The serum oestradiol levels in women were low in group 1 both on admission and discharge. The serum prolactin levels were low in female patients in group 1 (119 +/- 17 mIU l-1) compared with the women in group 2 (315 +/- 75 mIU l-1) (p less than 0.05). On admission the serum cortisol levels were higher and their response to 1 mg of dexamethasone was weaker in group 1 than in group 2 and healthy controls. After recovery the serum cortisol levels fell by 15% (p less than 0.01) and the response to 1 mg of dexamethasone returned to normal in group 1. In group 1 during treatment the serum free T4 and reverse T3 levels fell, and the T3 levels rose, whereas the thyroid stimulating hormone (TSH) levels and their responses to TRH remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal changes in severely uncontrolled type 1 (insulin-dependent) diabetes mellitus. 194 23

Thyroid hormone picture of 28 patients (15 males and 13 females), mean age 56.6 yr (range 45-65 yr), with seriously decompensated type II diabetes mellitus has been studied. In each patient the study was repeated after 3 months of treatment of diabetes. The patients showed significantly lower serum T3 levels and significantly higher serum rT3 levels (P less than 0.001), in comparison with a group of 16 normoglicemic subjects. After 3 months of strict control of diabetes T3 and FT3 significantly increased (P less than 0.01), whereas significant variations of rT3 were not found. Among the whole group of diabetics 5 patients had low levels of serum T4 (P less than 0.01 vs. controls), high levels of serum TSH (P less than 0.001 vs. controls) and an exaggerated responsiveness to exogenous TRH (P less than 0.001 vs. controls). After the 3 months of treatment these patients showed a significant decrease of rT3 (P less than 0.02) and of delta-TSH (P less than 0.01). In the whole group of diabetics significant statistical correlations between glycometabolic and thyroid parameters were not found. The study, on the whole, showed in patients with seriously decompensated type II diabetes, a hormone picture like the low-T3 syndrome, in some cases, however, pituitary TSH secretion suggested the existence of incipient failure of thyroid hormones. A connection between alterations in thyroid hormone picture and glycometabolic imbalance, even statistically labile, is however indicated by improvement of thyroid function when diabetes is carefully controlled.
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PMID:[Changes in the thyroid hormone picture that may be found in severely decompensated type II diabetics]. 200 Jan 80

The plasmatic levels of TSH in 2 group of diabetic patients (7 decompensated and 8 decompensated, but in treatment) were measured at 9:30 and 23:30 hours. The mean glycemia levels were of 280 +/- 45 and 150 +/- 30 mg/dl (p less than 0.0005). There was no significant difference between daily TSH and nocturnal TSH in any of the groups, but there was a tendency for the nocturnal TSH to be higher in decompensated patients. There was no difference when comparing the TSH of the first group to the TSH of the 2nd group. The mean TSH N/TSH D was superior by 1 (1.36 in decompensated and 1,095 in treated patients). The correlation between glycemia and TSH D was negligible in all groups. The data suggests the tendency that the circadian rhythm of TSH in maintained in diabetes decompensation with shorter rhythm registered in treated patients. This shows a certain normality in the suprahypophysary area in charge of the rhythm and is similar to the minor liberation of TSH after TRH stimulus that other authors have described as happening in the decompensation of diabetes mellitus.
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PMID:[Decompensated diabetes mellitus and circadian rhythm of plasma TSH]. 210 38

Thyrotrophin (TSH) secretion was studied in 63 patients with Cushing's syndrome (53 patients with pituitary dependent Cushing's disease, eight with adrenocortical tumours, and two with the ectopic ACTH syndrome). Prior to treatment, TSH response to 200 micrograms of TRH intravenously was significantly decreased compared to controls; TSH response was 'flat' (increment less than 2 mU/l) in 34 patients (54%). Patients with a flat response to TRH had significantly higher morning and midnight cortisol levels than patients with a TSH response of 2 mU/l and more; this was not due to differences in serum thyroid hormone levels. Basal TSH, TSH increment after TRH, and stimulated TSH value, but not serum triiodothyronine, were correlated with cortisol measurements (0800 h serum cortisol, midnight cortisol, and urinary free corticoid excretion). After exclusion of 40 patients with additional disease (severe systemic disease, diabetes mellitus, or goitre), cortisol-TSH correlations were even more pronounced (r = -0.73 for midnight cortisol and stimulated TSH levels), while in the patients with additional complications, these correlations were slight or absent. Successful treatment in 20 patients was associated with a rise in thyroid hormone levels and the TSH response to TRH. These results indicate that (1) the corticoid excess but not serum T3 is the principal factor regulating TSH secretion in Cushing's syndrome, (2) a totally flat response to TRH is rare, and (3) TSH suppression and lower than normal serum thyroid hormone levels are reversible after treatment. Since factors like severe systemic disease, diabetes mellitus and goitre also affect TSH secretion, they tend to obscure the statistically significant correlations between cortisol excess and TSH secretion.
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PMID:TSH secretion in Cushing's syndrome: relation to glucocorticoid excess, diabetes, goitre, and the 'sick euthyroid syndrome'. 212 25


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