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

Several studies report increased growth hormone (GH) responses to provocative stimuli in patients with diabetic retinopathy. We studied GH responses to 1 microgram/kg body wt human pancreatic GH-releasing hormone 1-44 (hpGHRH 1-44) in 33 patients with type I diabetes mellitus, 31 patients with type II diabetes mellitus, and 2 control groups (N = 11 and 8). Based on the results of fundoscopy and fluorescein angiography, the diabetic patients were subdivided into patients without diabetic retinopathy, patients with nonproliferative diabetic retinopathy, and patients with proliferative diabetic retinopathy. Growth hormone responses to hpGHRH 1-44 in diabetic patients with proliferative or nonproliferative retinopathy or without retinopathy were not significantly different regardless of the type of diabetes. Remarkably, GH responses to hpGHRH 1-44 in type I diabetic patients without retinopathy were significantly higher than the matched controls. Our data suggest that diabetic retinopathy in type I and in type II diabetes is not associated with increased GH responsiveness to hpGHRH 1-44, whereas in type I diabetes mellitus without diabetic retinopathy, a GH hyperresponsiveness to hpGHRH seems to occur.
Diabetes 1987 Feb
PMID:No evidence for increased growth hormone responses to growth hormone-releasing hormone in patients with diabetic retinopathy. 310 Mar 67

Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. Growth hormone responses in non-obese Type 2 diabetic patients were not statistically different from control subjects. However, obese Type 2 diabetic patients had significantly decreased growth hormone responses to growth hormone releasing hormone when compared with non-obese Type 2 diabetic patients (p less than 0.02). In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. Growth hormone responses before and after insulin treatment were not statistically different. Our data demonstrate that growth hormone responses to growth hormone releasing hormone in non-obese Type 2 diabetic patients do not differ significantly from control subjects; obesity blunts growth hormone responses to growth hormone releasing hormone in Type 2 diabetes mellitus; and growth hormone responses following growth hormone releasing hormone administration in Type 2 diabetes mellitus are not influenced by the state of metabolic control.
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PMID:Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus. 310 23

Hormonal and metabolic changes were compared in five insulin-dependent diabetic men and five control men during a 3-h marathon-training run. Insulin was withheld 16-26 h before the start of the run, and a normal breakfast was finished 2.5 h before the start of the run. Blood glucose concentrations decreased significantly in the diabetic subjects but remained constant in the control subjects. During the run, plasma free fatty acids, beta-hydroxybutyrate, and alanine concentrations behaved similarly in both groups. Only postexercise ketosis was more pronounced in the diabetic subjects. Peripheral serum free-insulin concentrations were slightly lower in the diabetic subjects at the start of the study, but these insulin concentrations became significantly elevated afterward compared with the control subjects. Plasma glucagon levels increased in the diabetic but not in the control subjects. Growth hormone levels increased sharply and to significantly higher levels in the diabetic than in the control subjects, who presented a slow gradual increase. Plasma cortisol levels were slightly, but at some moments significantly, higher in the diabetic subjects. The plasma catecholamine concentrations increased in both groups but to significantly higher levels in the diabetic subjects. There is no evidence from this study for an insufficient secretion of counterregulatory hormones if a hypoglycemic reaction occurs during a long-distance run in reasonably well controlled, well-trained diabetic subjects without long-term complications.
Diabetes Care 1988 Jan
PMID:Metabolic and hormonal changes in IDDM during long-distance run. 327 73

To determine whether children with insulin-dependent diabetes mellitus (IDDM) might have exaggerated hormonal responses to hypoglycemia, the euglycemic-hypoglycemic glucose clamp procedure was used to provide a uniform hypoglycemic stimulus (plasma glucose kept at 90 mg/dL for 2 hours, then reduced to 50 to 55 mg/dL for 1 hour) in children and adults with and without IDDM. The chidren with IDDM showed an exaggerated rise in plasma epinephrine levels (625 +/- 112 pg/mL) compared with adults with IDDM (259 +/- 57 pg/mL, P less than 0.02); the same was true for children and adults without IDDM (811 +/- 100 vs 458 +/- 85 pg/mL, P less than 0.05). Among the children, the increase in epinephrine during hypoglycemia was similar in prepubertal and pubertal patients. Children with IDDM showed a greater rise in plasma norepinephrine than did adults with IDDM (P less than 0.001), and both diabetic groups failed to mount a glucagon response. Growth hormone and cortisol responses were unaffected by either childhood or diabetes. Enhanced secretion of epinephrine, induced by mild reductions in plasma glucose, may contribute to the management difficulties characteristically observed in the young patient with diabetes.
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PMID:Exaggerated epinephrine responses to hypoglycemia in normal and insulin-dependent diabetic children. 358 99

DNA replication and insulin release have been studied in islets isolated, using a tissue culture technique, from rat fetuses of different gestational ages. The islets were cultured for 3 days in media with high and low concentrations of glucose or amino acids. The DNA replication was determined by autoradiography and the insulin secreted into the medium was measured by radioimmunoassay. In islets of 22-day-old fetuses, DNA replication was stimulated by both glucose and amino acids. At gestational days 18 and 20, only amino acids increased DNA replication. However, both high glucose and high amino acid concentrations increased the islet insulin secretion into the culture medium at all ages studied. In an attempt to induce glucose-sensitive DNA replication in vitro, islets obtained from 18- and 20-day-old fetal pancreata were cultured in the presence of either triiodothyronine or human growth hormone. Triiodothyronine failed to influence either DNA replication or insulin release. Growth hormone, however, increased DNA replication and insulin release in both the experimental groups but did not induce a growth response to glucose. It is concluded that the appearance of glucose-stimulated B-cell growth is a late event in the fetal development of the rat, parallelling the late maturation of both insulin biosynthesis and release. This finding may explain the difficulties in producing islet cell hyperplasia and diabetic fetopathy previously shown in rat models of diabetes in pregnancy.
Diabetes 1985 Aug
PMID:Glucose-stimulated DNA replication of the pancreatic islets during the development of the rat fetus. Effects of nutrients, growth hormone, and triiodothyronine. 389 21

In order to investigate the causes underlying metabolic instability in type I diabetes mellitus, we studied 8 unstable (group 1) and 4 well-controlled (group 2) diabetic patients, matched for age and duration of diabetes. Subjects were connected overnight to an artificial pancreas and brought to normoglycemia. On the following morning, insulin administration was discontinued for 6 hours and both metabolic and hormonal studies were carried out during this period. After insulin withdrawal, group 1 showed a faster rise of blood glucose (peak: 324.63 +/- 24.93 vs 175.25 +/- 42.63 mg/dl, p less than 0.01), beta-OH-butyrate (peak: 2,273.25 +/- 415.78 vs 550.50 +/- 158.17 mumol/l, p less than 0.01), and glycerol (164.10 +/- 38.90 vs 28.25 +/- 10.6 mumol/l, p less than 0.01). C-peptide secretion increased in group 2 from 0.09 +/- 0.052 to 0.22 +/- 0.099 pmol/ml whereas it remained almost undetectable in group 1 (p less than 0.01, group 1 vs group 2). Growth hormone, cortisol and immunoreactive glucagon were not significantly different in the two groups at any time after insulin withdrawal. Free insulin, after repeated s.c. or i.m. injection of porcine monocomponent insulin (10 IU), was not different in the two groups. We concluded that type I diabetic patients showing severe metabolic instability produced more glucose, ketone bodies and glycerol after insulin withdrawal than control 'stable' patients. This difference could not be accounted for by an excessive secretion of counterregulatory hormones or by an erratic insulin absorption from the injection sites and may have been related to the degree of B-cell failure, as measured by the absence of C-peptide and/or to the degree of insulin resistance.
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PMID:Metabolic instability in type I diabetic patients. Studies on insulin absorption, hepatic production of metabolites and glucose counterregulation. 390 36

Growth hormone (GH) responses to growth-hormone-releasing hormone (GRH) and thyrotropin-releasing hormone (TRH) were studied in 17 diabetic patients. Ten patients (group 1) had retinopathy corresponding to stage III-V (Scott's classification), and the remaining seven patients (group 2) had no retinopathy despite longer duration of diabetes in comparison with the patients in group 1. There were no differences in age, percent of ideal body weight, and serum HbA1 levels between the two groups. Basal serum GH levels were 1.9 +/- 0.4 ng/ml (mean +/- SEM) in group 1, and not different from the values in group 2 (1.6 +/- 0.7 ng/ml). However, GH responses to synthetic human GRH-44 (1 micrograms/kg body wt, i.v. bolus) were significantly greater in group 1, as judged by the maximal response or integrated GH secretion after the administration of GRH. There were no differences in serum insulin-like growth factor I (IGF-I) levels between group 1 (262 +/- 35 ng/ml) and group 2 (232 +/- 30 ng/ml), and no significant correlation was found between serum IGF-I levels and GH responses to GRH in either of the two groups. Paradoxical GH responses to TRH (500 micrograms, i.v. bolus) were found in only one patient in each group. We have thus demonstrated that GH responses to GRH are more pronounced in diabetic patients with retinopathy than in patients without this complication, although it remains to be determined whether or not greater GH responses to GRH are causally related to the development of diabetic retinopathy.
Diabetes 1985 Jul
PMID:Growth hormone responses to growth-hormone-releasing hormone and thyrotropin-releasing hormone in diabetic patients with and without retinopathy. 392 95

Castrate female rats given weekly applications of DMBA to the genital tract and treated additionally with growth hormone, insulin or alloxan (to induce diabetes) are heavier and have more sarcomatous and epithelial cervico-vaginal neoplasms than intact animals under the same experimental conditions. Promotion of carcinogenesis and gain in body weight are independent phenomena caused by castration in the medicated rats. Growth hormone is most effective in enhancing body weight in all animals, but least as regards tumour formation. It reduces the incidence of sarcomas in intacts, but raises that of epithelial neoplasms, and promotes both types of neoplasms in castrates. The highest incidence of cervico-vaginal epithelial and sarcomatous tumours occurs in spayed diabetics.Squamous celled epitheliomas of the vulva are not affected by castration or additional medication, while basal celled neoplasms tend to be more frequent in intacts than in castrates and particularly numerous in intact failed diabetics. Vulval sarcomas are usually rare but are increased in numbers in diabetic and in insulin treated intacts.Granular myoblastomas of the cervico-vaginal tract occur in intacts only and particularly in diabetics and those medicated with growth hormone or insulin.
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PMID:The effect of growth hormone, insulin and alloxan-induced diabetes on carcinogenesis in the genital tract of intact and castrate female rats. 433 34

Growth hormone release inhibiting hormone (GH-RIH) was infused at a rate of 1.3 mug/min for 28 hours into four patients with acromegaly, two of whom also had clinical diabetes mellitus. Growth hormone and glucagon were suppressed throughout the infusion though delayed secretion of insulin occurred in association with both meals and an oral glucose load. Glucose tolerance was improved in one diabetic patient who was taking chlorpropamide while the other required much less insulin than usual. Secretion of endogenous thyroid-stimulating hormone was lowered in one euthyroid patient on carbimazole. Luteinizing hormone, follicle-stimulating hormone, ACTH, and prolactin were not affected. Serum somatomedin levels were reduced in one patient. There was a rapid rebound of all the suppressed hormones when the infusions stopped. Longer-acting analogues of GH-RIH will be needed before long-term therapy of acromegaly or diabetes mellitus becomes possible, but such preparations should be available soon for clinical trial.
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PMID:Long-term infusion of growth hormone release inhibiting hormone in acromegaly: effects on pituitary and pancreatic hormones. 437 89

Adrenal cortical response in acute medical illness has been studied by measuring the plasma 11-hydroxycorticosteroid (11-OHCS) concentration in 178 patients. Those with unbalanced diabetes, acute infections, and severe myocardial infarction had high levels. The results obtained suggest that in a patient with a severe infection and hypotension a plasma 11-OHCS level of less than 15 mug./100 ml. indicates an inadequate adrenal cortical response, and one patient with septicaemia and temporary adrenal cortical insufficiency is described. Growth hormone levels were increased in patients with severe diabetic ketosis but not in those with hyperosmolar non-ketotic diabetic coma.
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PMID:Plasma 11-hydroxycorticosteroid and growth hormone levels in acute medical illnesses. 579 69


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