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

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

We have evaluated the endocrine changes in 10 male subjects with hemochromatosis. Two subjects initially had aplastic anemia, and the remainder had idiopathic hemochromatosis. Four of the ten patients had diabetes mellitus. Sexual dysfunction (impotence and/or decreased libido) was observed in 8 subjects. Six patients had subnormal testosterone levels; FSH levels were almost uniformly low, but LH concentrations were more variable. Only three patients had normal testosterone responses to hCG. Hypothyroidism, free T4 less than 0.9 ng/dl, was present in 4 subjects, and the etiology was heterogeneous. Basal prolactin levels were elevated in 2 patients and failed to respond adequately to TRH in 2 other patients. Growth hormone reserve was normal in all but 1 patient, and pituitary-adrenal reserve was normal in all but 1 patient. We conclude that disturbances in both pituitary and end-organ function are observed in hemochromatosis. These central and end-organ defects may exist alone or simultaneously. Hypogonadism is almost universal, and is a consequence of defective function of the hypothalamic-pituitary axis and/or primary Leydig cell disturbance. Other evidence of pituitary disturbance are observed but are rather uncommon.
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PMID:The endocrine manifestations of hemochromatosis. 634 90

Gonadotropin responses to GnRH and PRL responses to TRH and metoclopramide (MTC) were investigated in nine consecutive women with amenorrhea and insulin-treated diabetes mellitus. Nine normal menstruating diabetic women, 12 normal women in the early follicular phase, and nine consecutive nondiabetic women with functional amenorrhea served as controls. No significant differences were found in relation to diabetes regulation within the two diabetic groups. Amenorrheic patients with diabetes mellitus had significantly lower basal PRL levels than normal women and estradiol levels compared to the other groups. Basal plasma LH concentrations were significantly lower in women with amenorrhea and diabetes mellitus than in nondiabetics with amenorrhea, whereas plasma FSH levels were similar in all groups. The LH response to GnRH was significantly lower in amenorrheic patients with diabetes mellitus than in normal women, and a significant correlation (r = 0.81, P less than 0.01) was found between the LH response to GnRH and the basal estradiol level in these women. The FSH response to GnRH and the PRL response to TRH were similar in all groups. Amenorrheic diabetics had significantly lower PRL responses to MTC compared to other groups, and nondiabetics with amenorrhea had significantly lower PRL response than normal women. It is concluded that diabetic patients with functional amenorrhea have low basal and MTC-stimulated PRL levels, low basal LH levels, and decreased LH response to GnRH despite low estrogen levels. These hormonal changes may in part be caused by a raised central dopaminergic activity leading to a depression of pituitary ovulatory mechanisms.
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PMID:Gonadotropin responses to gonadotropin-releasing hormone and prolactin responses to thyrotropin-releasing hormone and metoclopramide in women with amenorrhea and insulin-treated diabetes mellitus. 640 66

In two girls (14 and 16 years) and one boy (19 years) with PLW-syndrome and pronounced obesity (240, 210 and 77% overweight) endocrine function tests were carried out. Growth hormone secretion was decreased but normalized after reduction of weight. Thyroxin levels as well as basal and TRH stimulated TSH concentrations were normal. HCG application in the boy induced no rise of the normal basal testosterone levels. Oral glucose tolerance test demonstrated an increased stimulation of insulin in two cases, no other symptoms of diabetes mellitus were found. In the LHRH test an insufficient rise of gonadotropins was found. However, after two weeks of pernasal application of an LHRH analogue (D-Leu6-des-Gly10-EA) the gonadotropin stimulation was distinctly improved and onset of puberty was induced in the male patient. These results are indicative of a hypothalamic disturbance in patients with PLW-syndrome.
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PMID:[Endocrine studies on the Prader-Labhart-Willi syndrome: puberty induction in a 19-year-old boy after long-term treatment with an LHRH analog]. 641 33

Altered thyroid hormone metabolism with decreased serum T3 and increased rT3 concentrations in patients with uncontrolled diabetes mellitus has been well documented. However, data regarding TSH secretion are sparse, especially the influence of glycemic control. Therefore, we examined serum T4, free T4, T3, rT3, T3 resin uptake, and TSH as well as the TSH response to TRH administration [expressed as TSH increment (delta TSH) and area under the curve (theta TSH)] in 29 newly discovered type II diabetic patients (DM) before treatment and in 12 normal subjects. The study was repeated in the DM patients after attainment of euglycemia and normalization of glycosylated hemoglobin (HbA1C) following therapy with diet and tolazamide for 8-12 weeks. Serum T4, free T4, and T3 resin uptake were not significantly different in DM compared to those in normal subjects. Serum T3 was low and rT3 was high in DM before treatment, and both normalized on achieving the euglycemic state. Basal TSH in uncontrolled DM was not significantly different from that in normal subjects and remained unchanged during treatment. However, delta TSH and theta TSH were significantly reduced (P less than 0.01) in uncontrolled DM. Both fasting plasma glucose (FBS) and HbA1C levels correlated inversely with delta TSH as well as theta TSH (FBS vs. delta TSH, r = -0.42; FBS vs. theta TSH, r = -0.38; HbA1C vs. delta TSH, r = -0.40; HbA1C vs. theta TSH, r = -0.42; P less than 0.05 for all correlations). Finally, TSH responses returned to normal on attainment of euglycemia and normal HbA1C concentrations. These studies indicate that regulation of TSH secretion is altered in DM during the decompensated state and normalizes when euglycemia is achieved.
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PMID:Impaired pituitary thyrotroph function in uncontrolled type II diabetes mellitus: normalization on recovery. 643 Sep 48

In order to establish whether cholinergic receptors mediate GH secretion induced by TRH in insulin-dependent diabetes, 10 patients were treated with pirenzepine, an anticholinergic agent, and tested with TRH. Basal concentrations of GH were elevated in these patients and 8 of 10 patients responded to TRH with a significant rise in GH levels. Pretreatment with pirenzepine (40 mg given iv 10 min before TRH) suppressed the TRH-induced GH rise. Pirenzepine had no effect on TRH-induced TSH release. This finding suggests that a cholinergic mechanism is involved in the paradoxical response of GH to TRH in diabetic patients.
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PMID:The growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics involves a cholinergic mechanism. 643 81

Since TRH has been reported to evoke GH secretion in diabetic patients, we have investigated the influences of the enhanced GH secretion normally seen in diabetic patients on this response by measuring serum GH concentrations in 27 non-ketotic, stable, insulin-dependent diabetic (IDD) patients (14 male, 13 female). GH concentrations were measured over periods of 1 hr prior to and 1 hr following IV administration of both 200 micrograms TRH and 2 ml N Saline given on separate days. GH concentrations were not statistically significantly different between males and females during the two 120 min test periods and in individual patients GH concentrations did not differ significantly at any time during the tests. Sixteen of the 27 patients (Group 1) demonstrated elevation of serum GH following TRH, which was not statistically different from 11 of 27 patients who showed increased GH concentrations following saline administration. Seven subjects (4 male, 3 female) had a higher peak GH concentration following TRH than during their own 2 pre-injection test periods or following saline. Eleven patients failed to show any GH rise following IV TRH (Group 2). During the TRH test periods integrated GH concentrations in Group 1 patients were not statistically significantly different from those of Group 2: Group 1, 7.1 (0.7-15.8) (median and range) mU.min.l(-1), Group 2, 2.7 (0.4-25.4) mU.min.l(-1).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res 1984 Jul
PMID:Serum growth hormone (GH) and the responses to thyrotropin-releasing hormone (TRH) in diabetes mellitus: lack of evidence for TRH evoked GH secretion. 644 27

Growth hormone (GH) response was studied in 8 insulin-dependent and 7 non-insulin-dependent diabetics after stimulation with L-Dopa (500 mg orally) and TRH (0.2 mg iv.). L-Dopa induced a clear GH response in insulin-dependent diabetes (IDDM) and in the control group while in non-insulin-dependent diabetes (NIDDM) peak GH levels were lower (P less than 0.05) and 4 of 7 subjects failed to respond to L-Dopa stimulation. TRH had no effect on GH levels in NIDDM and in the controls. Insulin-dependent diabetics responded to TRH stimulation and GH levels at 20 and 30 min were significantly higher as compared with NIDDM and the control group. The degree of hyperglycemia seemed not to influence GH response. The highest GH levels were noted in two patients with proliferative retinopathy. It is suggested that TRH-induced GH release may be a characteristic feature in some patients with IDDM.
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PMID:TRH-induced growth hormone release in insulin-dependent diabetes mellitus. 644 6

We evaluated serum thyroid hormones, TSH, and prolactin before and after induction of TRH and thyroid microsomal autoantibodies in 91 diabetic children and adolescents (mean age 11.11 +/- 4.13 yr), with illness ranging from a few days to 14.25 yr, and in 127 "short-normal" subjects (mean age 10.32 +/- 3.18 yr). All were clinically euthyroid. The control pubertal subjects showed T4, rT3, TBG, and rT3/T3 ratio values that were significantly lower than those of prepubertal subjects. The PRL area was significantly higher in pubertal than in prepubertal females. In diabetic patients, differences between pubertal and prepubertal subjects were similar to those of controls regarding T4 levels and PRL area only. T3, T4, and fT3 appeared to be significantly lower than in controls, while the rT3/T3 ratio was higher. A negative correlation (r = -0.277, P = 0.009) between T3 and HbA1 levels was demonstrated. Furthermore, thyroid function was not different in subjects with or without retinal changes or in subjects with or without residual B-cell function. Microsomal autoantibodies were observed in 6.25% of the subjects examined, though none showed any clinical or humoral sign of impaired thyroid function. In conclusion, the lower T4 and rT3 values detected in pubertal controls suggest an increased efficacy of peripheral thyroid activity in this particular life span. Considering the fact that, in diabetic children, such a decrease in rT3 at puberty is not present and that the T3 value in diabetic children is persistently lower than in controls, it would seem that even diabetic children show a "low T3 syndrome," as in adult diabetic subjects.
Diabetes 1984 Jun
PMID:Thyroid function and prolactin levels in insulin-dependent diabetic children and adolescents. 672 48

During diabetic ketoacidosis, in 17 adult patients, significant decreases in serum TBG and total T4 levels were observed, without significant alteration of the T4 to TBG binding property. In addition, serum free T4 (FT4) was moderately elevated and the TSH response to TRH was markedly blunted. No correlation, however, was found between TSH blunting and FT4 elevation. Correlation of these serum anomalies required at least 5 days of adequate control of the diabetes. Thus, diabetic ketoacidosis in euthyroid patients is characterized by multiple alterations in thyroid function parameters and caution is recommended in the interpretation of thyroid tests during and in the days following this severe metabolic disorder.
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PMID:Alterations in circulating thyroid hormones and thyroxine-binding globulin levels during diabetic ketoacidosis. 676 90


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