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

A 32-year-old man is reported with the Morgagni-Morell-Stewart syndrome with hypertension, diabetes, obesity, emotional lability, irritability and thickening of the internal lamina of the frontal bone in radiogram, which is the phatognomonic sing for the syndrome. The syndrome is rarely observed in men. Hormonal determinations showed increased serum concentrations of prolactin and thyrotropic hormone.
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PMID:[Morgagni-Stewart-Morel syndrome in a young man]. 263 53

A double-blind, partial crossover study on the therapeutic effect of yohimbine hydrochloride on erectile dysfunction was done in 82 sexually impotent patients. All patients underwent a multifactorial evaluation, including determination of penile brachial blood pressure index, cavernosography, sacral evoked response, testosterone and prolactin determination, Derogatis sexual dysfunction inventory and daytime arousal test. After 1 month of treatment with a maximum of 42.0 mg. oral yohimbine hydrochloride daily 14 per cent of the patients experienced restoration of full and sustained erections, 20 per cent reported a partial response to the therapy and 65 per cent reported no improvement. Three patients reported a positive placebo effect. Maximum effect takes 2 to 3 weeks to manifest itself. Yohimbine was active in some patients with arterial insufficiency and a unilateral sacral reflex arc lesion, and in 1 with low serum testosterone levels. The 34 per cent response is encouraging, particularly in a Veterans Administration population presenting with a high incidence of diabetes and vascular pathological conditions not found in regular office patients. Only few and benign side effects were recorded, which makes this medication worth an attempt, often as a first line of treatment even at a dose of 8 tablets.
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PMID:Effect of yohimbine hydrochloride on erectile impotence: a double-blind study. 265 5

Counterregulatory effect following administration of biosynthetic human proinsulin (BHPI) and human insulin (BHI) were compared during hypoglycemia standardized by means of a glucose controlled insulin infusion system (GCIIS). A total of 0.148 +/- 0.010 U/kg of BHPI had to be given by the GCIIS in order to obtain a minimal blood glucose (BG) of 26 +/- 2 mg/dl (means +/- SEM) at 43 +/- 2 min. In contrast, 0.083 +/- 0.004 U/kg of BHI were sufficient to produce a minimal BG of 21 +/- 1 mg/dl (n.s.) at 35 +/- 1 min. (P less than 0.005). Moreover, BHPI infusion resulted in prolonged hypoglycemia and delayed blood glucose recovery. On a molar basis, the acute BG lowering effect of BHPI was about 13% that of BHI (BHPI 3.94 +/- 0.27 vs. BHI 0.51 +/- 0.03 nmol/kg). Serum proinsulin after BHPI reached its maximum of 19.4 +/- 2 pmol/ml at 20 min. and still exceeded basal values markedly at the end of the test period at 240 min. Serum insulin peaked at 10 min. (162 +/- 47 microU/ml) and had already returned to basal values (7.5 +/- 1 microU/ml) after 45 min. No severe side effects were observed and there was no need for glucose administration, but clinical symptoms of hypoglycemia were more pronounced after BHPI. Compared to BHI, BHPI produced a higher cortisol peak (252 +/- 16 vs. 168 +/- 10 ng/ml), a more pronounced secretion of ACTH and GH as well as a stronger decline of serum potassium (3.20 +/- 0.06 vs. 3.58 +/- 0.08 mmol/l). Counterregulatory prolactin secretion did not differ significantly. Urinary epinephrine secretion following hypoglycemia after BHPI exceeded that after BHI (10.3 +/- 4.8 vs. 3.0 +/- 0.5 ng/120 min.). Serum lactate increase after BHPI was more prolonged (1.68 +/- 0.24 vs. 0.37 +/- 0.14 mmol/l at 120 min.). BHPI-induced inhibition of lipolysis, as determined by free fatty acid patterns, was delayed and less pronounced. Our results indicate that the observed more distinct glucose counterregulation is due to prolonged hypoglycemia rather than to any specific BHPI action on the hypothalamic-pituitary axis. We regard this as a consequence of the prolonged circulating and biological half-life. A preferential proinsulin action on the liver may play an additional role. Whether this "depot effect" may be beneficial in the treatment of diabetes mellitus remains to be established.
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PMID:Comparative study of hormonal counterregulation during GCIIS-guided hypoglycemia tests using human proinsulin and human insulin (recombinant DNA). 284 67

Acute insulin-induced hypoglycaemia in humans provokes autonomic neural activation and counterregulatory hormonal secretion mediated in part via hypothalamic stimulation. Many patients with Type 1 (insulin-dependent) diabetes have acquired deficiencies of counterregulatory hormonal release following hypoglycaemia. To study the integrity of the hypothalamic-pituitary and the sympatho-adrenal systems, the responses of pituitary hormones, beta-endorphin, glucagon and adrenaline to acute insulin-induced hypoglycaemia (0.2 units/kg) were examined in 16 patients with Type 1 diabetes who did not have autonomic neuropathy. To examine the effect of duration of diabetes these patients were subdivided into two groups (Group 1: 8 patients less than 5 years duration; Group 2: 8 patients greater than 15 years duration) and were compared with 8 normal volunteers (Group 3). The severity and time of onset of hypoglycaemia were similar in all 3 groups, but mean blood glucose recovery was slower in the diabetic groups (p less than 0.01). The mean responses of glucagon, adrenaline, adrenocorticotrophic hormone, prolactin and beta-endorphin were similar in all 3 groups, but the mean responses of growth hormone were lower in both diabetic groups than in the normal group (p less than 0.05). The mean increments of glucagon and adrenaline in the diabetic groups were lower than the normal group, but these differences did not achieve significance; glucagon secretion was preserved in several diabetic patients irrespective of duration of disease. Various hormonal responses to hypoglycaemia were absent or diminished in individual diabetic patients, and multiple hormonal deficiencies could be implicated in delaying blood glucose recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Counterregulatory hormonal responses to hypoglycaemia in type 1 (insulin-dependent) diabetes: evidence for diminished hypothalamic-pituitary hormonal secretion. 285 69

A comparison was made of the metabolic, hormonal, haemodynamic and symptomatic responses to acute hypoglycaemia induced by short-acting porcine and human insulins in 16 fasting, insulin-dependent diabetic patients, 8 of whom had diabetes for less than 5 years (Group A) and 8 of whom had diabetes for greater than 15 years (Group B). Each patient received an intravenous injection of 0.2 units/kg of insulin on two separate occasions. No differences were found between the groups in the rate of fall of blood glucose or the blood glucose nadir with either insulin, but in Group B, glucose recovery was more rapid after human insulin (p less than 0.01). No differences in the responses of blood lactate, plasma free fatty acids, glucagon or prolactin were observed between the groups. In Group B the rises of growth hormone and cortisol occurred more rapidly following human insulin (p less than 0.01), while the rise in adrenaline was greater following porcine insulin. Haemodynamic changes were identical following each species of insulin in both diabetic groups. A questionnaire was used to score 18 symptoms of hypoglycaemia on a 7 point scale. No significant differences were found in the mean scores of each symptom of hypoglycaemia or in the total symptom score. Thus recovery of blood glucose from hypoglycaemia was slightly more rapid after administration of human insulin to diabetic patients of long duration, but it is unlikely that these marginal differences would confer any clinical advantage in this subgroup.
Diabetes Res 1988 May
PMID:Responses to acute insulin-induced hypoglycaemia in diabetic patients: a comparison of short-acting human and porcine insulins. 285 85

The effect of a new long-acting somatostatin analog SMS 201-995 (SMS) on hormonal mechanisms controlling the glucose metabolism was tested in 8 type I diabetics over a 3-day period. In addition to dietary measures and conventional insulin therapy, the patients received a subcutaneous dose of 50 micrograms SMS three times daily for 3 days. Serum growth hormone (GH) was measured at various intervals throughout the investigational period. Glucagon, somatomedin C (SM-C), triiodothyronine, thyroxine, luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL) were also determined before and at the end of the therapy with SMS. Basal GH and plasma SM-C had decreased significantly (p less than 0.05 and p less than 0.01, respectively) by the 3rd day. In all cases the insulin requirements could be reduced (mean 28%) without deterioration of the metabolic control. Moreover, blood glucose profiles showed a tendency to lower postprandial peaks after SMS treatment. Glucagon, triiodothyronine, thyroxine, LH, FSH and PRL showed no significant changes. No side effects or alterations in laboratory chemistries were recorded. Dampening of glucose oscillations and counterregulatory mechanisms, and reduction of insulin dosage by SMS may enable a better control of unstable diabetes. Its slow plasma clearance and long action compared to the native peptide will warrant the use of this analog as a additive to standard diabetes therapy in more prolonged trials.
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PMID:Suppression of growth hormone and somatomedin C by long-acting somatostatin analog SMS 201-995 in type I diabetes mellitus. 288 4

Because respiratory distress syndrome may result, in part, from a hormonal deficiency in the developing fetus, we investigated the endocrine millieu of 28 infants of women with diabetes who were delivered prematurely (34 to 37 weeks of gestation). The umbilical serum concentrations of estrone, estradiol, estriol, cortisol, and prolactin in infants of women with diabetes who developed respiratory distress syndrome (n = 6) were lower than those in infants of women with diabetes who had normal lung function. Serum hormone levels in age-matched newborns of normal women were higher than those in the infants of women with diabetes with respiratory distress syndrome but were not different than those in the infants of women with diabetes with normal lung function. Plasma glucose levels were highest in women whose neonates developed respiratory distress syndrome. An inverse correlation existed between maternal glucose levels and lecithin-sphingomyelin ratios in amniotic fluid. Thus diabetes occasionally results in significantly delayed maturation of the fetal endocrine milieu. In these instances, delayed fetal lung maturation is a frequent occurrence. Moreover, both phenomena may be related to the extent of diabetic control during pregnancy.
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PMID:Endocrine maturation and lung function in premature neonates of women with diabetes. 292 88

Human insulin (BHI, recombinant DNA) and pork insulin (PI) were compared in 10 healthy volunteers. Using a glucose controlled insulin infusion system for the performance of the insulin hypoglycemia test (IHT), a comparable dosage of both insulins had to be infused (BHI 0.129 +/- 0.007 vs PI 0.115 +/- 0.01 U/kg; mean +/- SEM). Blood glucose slopes and nadirs did not differ significantly (BHI 30 +/- 2 vs PI 29 +/- 2 mg/dl). There was no difference in C-peptide inhibition (minimum for BHI 0.50 +/- 0.08 vs PI 0.42 +/- 0.08 micrograms/l). Maximum hormone responses were identical for ACTH (BHI 78.4 +/- 11.3 vs PI 76.0 +/- 8.7 pg/ml), cortisol (BHI 246 +/- 20 vs PI 252 +/- 15 ng/ml) and GH (BHI 43.8 +/- 7.3 vs PI 49.4 +/- 6.7 ng/ml). Peak levels of prolactin did not differ significantly (BHI 1,335 +/- 315 vs PI 1,766 +/- 614 microU/ml). The urinary excretion pattern of epinephrine in three 120 min periods before, during and after IHT was identical (before IHT: BHI 0.9 +/- 0.2 vs PI 0.6 +/- 0.1 micrograms/120 min; during IHT: BHI 12.6 +/- 2.2 vs PI 13.4 +/- 2.5 micrograms/120 min; after IHT: BHI 2.5 +/- 0.7 vs PI 3.7 +/- 1.3 micrograms/120 min). No differences in the minima of serum potassium levels were observed (BHI 3.38 +/- 0.04 vs PI 3.33 +/- 0.05 mmol/l). We conclude that the biological effects of human insulin and pork insulin are comparable. Our data do not support the assumption of a different hypothalamic handling of human insulin (recombinant DNA) and porcine insulin.
Diabetes Res 1985 May
PMID:Comparative study of hormonal counter-regulation during GCIIS-guided insulin hypoglycemia tests using human insulin (recombinant DNA) and pork insulin. 299 78

Streptozotocin-induced diabetes causes a decrease in growth hormone and prolactin receptors in the livers of female rats, and in the serum concentration of somatomedin-C/insulin-like growth factor-I, concomitantly with an increase in the serum testosterone levels. In this study, a possible role for adrenal androgens in the loss of receptors was examined. Rats were adrenalectomised bilaterally 3 days after the induction of diabetes with streptozotocin (100 mg/kg intravenously), and livers were removed 3 days later. Adrenalectomy had no effect on binding of ovine prolactin or bovine growth hormone to liver microsomal membranes from non-diabetic rats, but in diabetic rats it entirely abolished the 56% decrease in prolactin binding and significantly reversed the 66% decrease in growth hormone binding and the parallel fall in serum levels of somatomedin-C/insulin-like growth factor-I (p less than 0.05). Adrenalectomy also prevented the diabetes-induced rise in serum testosterone. Daily injection of testosterone to normal and diabetic rats for 12 days significantly reduced both prolactin and growth hormone binding (p less than 0.001), with the effect of diabetes being additive upon the testosterone effect. Implantation of testosterone-filled silastic capsules at the time of adrenalectomy (i.e. for 3 days) did not prevent the adrenalectomy-induced restoration of both growth hormone and prolactin receptors. The resulting high serum testosterone level did not reduce binding to growth hormone receptors in control rats over the 3 day period, and caused no further decrease in diabetic rats. However, binding to prolactin receptors was reduced by 47% in control animals with no further loss in diabetic animals (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adrenal involvement in the diabetes-induced loss of growth hormone and prolactin receptors in the livers of female rats. 300 52

Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. Out of 18 insulin dependent diabetic patients who were positive for antibodies to islet cell surface membrane (ICSA), 3 cases (16.7%) were positive for antibodies to GH3 cells and 12 cases (66.7%) were positive for antibodies to AtT-20 cells. Moreover, out of 18 insulin dependent diabetic patients who were negative for ICSA, 2 (11.1%) and 6 cases (33.3%) were positive for antibodies to GH3 cells and AtT-20 cells, respectively. Among 5 adrenocorticotropic hormone (ACTH) deficient patients, all of the sera were positive for antibodies to AtT-20 cells. These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency.
Diabetes Res 1987 Feb
PMID:Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 303 74


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