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

Growth hormone (hGH) responsiveness to exercise and somatomedin C (SmC) activity were measured in ten children with insulin-deficient diabetes mellitus. Four of the ten children showed a significant degree of growth retardation. Normal SmC activity was found in association with elevated hGH levels. The hypothesis that growth-retarded diabetics have a failure of Sm production despite high hGH levels (analogous to malnutrition and Laron dwarfism) was not substantiated by this study. Chronic deficiency of insulin, itself a somatomedin, may play a major role in diabetic growth failure.
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PMID:Growth failure, somatomedin and growth hormone levels in juvenile diabetes mellitus--a pilot study. 22 35

In labile diabetes mellitus wihout ketoacidosis we have studied plasma prolactin levels and a possible causal connection between fluctuation in blood glucose concentration and plasma prolactin, growth hormone and cortisol levels. The hormone concentrations in plasma and blood glucose concentration were determined at 20 min intervals for a 24 h period in six male patients with insulin treated diabetes mellitus. Prolactin varied within the normal range but without any significant rise in relation to sleep in five out of the six patients. Growth hormone levels were low with superimposed secretory peaks. Plasma cortisol showed a normal diurnal rhythm. Blood glucose fluctuated as expected, but the variations and especially the falls in blood glucose to non-hypoglycaemic levels were not followed by increases in plasma hormone concentrations. No relationship could be demonstrated between the changes in the plasma concentration of prolactin, growth hormone and cortisol.
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PMID:Diurnal variations in plasma prolactin, growth hormone, cortisol and blood glucose in labile diabetes mellitus. 55 82

Growth hormone injected daily in 6 dogs for 6 days caused a 20-fold elevation in fasting serum immunoreactive insulin (IRI) without appreciable change in serum glucose in 1 day. In the somatotrophic diabetes that occurred after 2 days, the hyperinsulinaemia was maintained and the serum IRI/glucose (I/G) ratio declined from the early high level but remained elevated. During this treatment, in response to glucose infusion, the rise in serum IRI above the initially high fasting level was 16 times the normal. In response to glucagon, the rise in IRI was twice the normal and the rise in glucose was more prolonged, resulting in a decline in the I/G ratio. In response to arginine infusion, the rise in serum IRI was 8 times the normal and the rise in the I/G ratio was twice normal. Following a meal, the rise in serum IRI was 8 times the normal. Thus, with growth hormone treatment the insulin secretory responses to these stimulating factors were magnified over the already elevated fasting level of secretion. The insulin content of the pancreas was reduced to less than 10% of normal by growth hormone treatment for 6 days, due apparently to elevation of the rate of secretion over the rae of formation of insulin.
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PMID:Somatotrophic diabetes: insulin release responses to arginine and glucagon in dogs. 70 Feb 82

We report a female small for date neonate, who developed transient diabetes mellitus (TDN) five days after birth and required insulin therapy for five weeks. At the onset of the disease, plasma insulin concentration was extremely low. At four weeks of age, after insulin withdrawal, the patient was still hyperglycemic, and basal insulin values assayed over a period of 24 h were mostly inadequate. Glucagon secretion was not suppressed. Growth hormone levels were lower than those of three small for date infants of the same age. At three months of age, the patient was still intolerant to an oral glucose load, insulin secretion remained inadequate while glucagon paradoxically increased 30 min after glucose challenge. The oral glucose tolerance values were in the normal range at six months of age. We conclude that TDN is caused by a transitory defect of insulin secretion, which would also explain the glucagon response as a consequence of insulin deficiency. We found no evidence associating the insulin antagonists observed in our study with the pathogenesis of this illness.
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PMID:[Transient diabetes mellitus in a dystrophic newborn infant]. 71 99

The secretion of insulin, glucagon and growth hormone was determined in the serum of patients with recently diagnosed juvenile-type diabetes (10 patients) during stimulation by intravenous infusion of L-arginine and was compared with the results found in a group of five healthy persons. The value of the insulinemia was significantly lower in the diabetics as compared with the healthy controls. Serum glucagon levels were higher in all diabetics when fasting and after L-arginine administration as compared with the controls but a significant difference was observed only at the peck of secretion (5 min after L-arginine administration). Growth hormone concentration was slightly higher in the diabetics after secretory stimulation than in the controls, particularly at the peak of secretion (30 and 45 min) but the difference was statistically no significant.
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PMID:Serum insulin, pancreatic glucagon and growth hormone levels in response to intravenous infusion of L-arginine in patients with recently detected juvenile diabetes. 95 42

The state of the blood vessels is normal at the clinical onset of juvenile diabetes. Vascular changes develop slowly and progressively. According to the growth hormone hypothesis, elevated serum growth hormone is one casual factor in the development of diabetic angiopathy. The hypothesis proposes an effect of growth hormone not on blood glucose but directly on blood vessels. This hypothesis is based on serum growth hormone studies and on a controlled clinical trial of the effect of hypophysectomy on small blood vessels. An animal model of large-vessel disease in diabetes is briefly described. There is a large molecule in diabetic serum causing proliferation of aortic myomedial cells in culture. Growth hormone causes a similar proliferation. A short summary is given of the present situation in somatostatin research relating to diabetes mellitus.
Diabetes 1976
PMID:Growth hormone's role in diabetic microangiopathy. 98 6

Earlier studies have shown a stimulatory effect of diabetic serum on the growth of rabbit aortic medial cell cultures. Growth media supplemented with normal serum with added insulin (50-2,000 muU./ml. serum) did not enhance the growth of the medial cell cultures. Control media containing serum from recent diabetics with low insulin concentration stimulated the growth (2p less than 0.01). Supplementation of normal serum with human growth hormone (final concentration 1-5 ng./ml. medium) resulted in a significant enhancement of growth (2p less than 0.005). The growth-promoting effect of growth hormone was not detectable with lower concentrations (0.5 ng. and 0.1 ng./ml. medium). The growth effect of the low concentration of growth hormone could not be augmented by increasing the concentration of glucose in the incubation medium. Growth hormone in an amount of 1 ng./ml. medium increased both the number of 3H-thymidine-labeled cells as identified by autoradiography and the number of mitotic bodies (2p less than 0.005 and 2 p less than 0.025). The present results demonstrate that the growth-stimulating factor(s) in diabetic human serum described earlier is not insulin but may well be growth hormone.
Diabetes 1976 Nov
PMID:Growth hormone stimulating the growth of arterial medial cells in vitro. Absence of effect of insulin. 99 22

To detect abnormalities in the secretion of insulin and growth hormone in monozygotic twin siblings of patients with juvenile-onset diabetes, their responses during oral, cortisone-primed oral, and intravenous, glucose tolerance tests and intravenous tolbutamide tests were compared to those of matched controls. The twins had higher mean serum insulin levels during all tests, but differences reached statistical significance (P less than 0.02) only in the cortisone-primed test. Growth hormone levels were higher in the twins (P less than 0.04) in the intravenous tolbutamide tolerance test. The frequency of abnormal oral glucose tolerance tests among controls, diabetic monozygotic twins and the offspring of two diabetic parents was also compared. Twins and controls had nearly the same frequency of normal tests; however, the diabetic offspring had a significantly higher (P less than 0.001) prevalence of abnormal tests. These data suggest that magnitudes of environmental and genetic factors operating in monozygotic "pre-diabetic" children of diabetic parents.
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PMID:Serum insulin and growth hormone response patterns in monozygotic twin siblings of patients with juvenile-onset diabetes. 112 40

Glucose, insulin, and growth hormone values were studied prospectively in 75 premature infants during the first five days after birth. Intravenous glucose was given at a mean rate of 4.7-4.9 mg./kg./min. (range 3-7). Mean birth weight was 1,394+/-47 gm. (mean+/-S.E.M.). Blood glucose values were significantly higher on days 1 and 2 than on days 3 to 5. Hypoglycemia (blood glucose less than 20 mg./100 ml.) occurred in two SGA and one AGA infants. On the other hand, hyperglycemia (greater than 125 mg./100 ml.) was found in 32 of the 75 (42.7 per cent) infants. A significantly greater number of deaths occurred in infants with hyperglycemia (19/32) than in those with normoglycemia (19/32) than in those with normoglycemia (5/43). Mean plasma insulin values were significantly higher on days 1 and 2 (15+/-3 and 18+/-4 muU./ml.) than on days 3 and 4-5 (6+/-1 and 7+/-2 muU./ml.). In addition, mean insulin levels were significantly higher during hyperglycemic than during normoglycemic glucose levels at similar postnatal age. Growth hormone values were higher during the first three days than subsequently, but the values were similar in normoglycemic and hyperglycemic groups. Significant negative correlations were seen between glucose values on the first two days of postnatal life and birth weight, gestational age, and Apgar scores, whereas positive correlations were found with FiO2 and respiratory distress score (RDS).
Diabetes 1976 May
PMID:Insulin and growth-hormone responses in neonatal hyperglycemia. 126 41

Growth hormone (GH) levels were measured after a 75g oral glucose load (OGTT) in normal adults, patients with impaired glucose tolerance (IGT), insulin-dependent diabetes mellitus (IDDM) and acromegaly. Nadir GH levels at 2-hour post-OGTT in normal subjects ranged from 0.4 to 8.4 mIU/L, the 95% confidence interval being 0.4-4.4 mIU/L. In IGT and IDDM subjects basal fasting GH levels were not significantly different from normal and did not alter during OGTT. The high fasting GH level measured in one each of the IGT and IDDM patients was suppressible at 1-hour after glucose intake. In contrast, acromegalic patients had elevated fasting GH levels (11.8-178 mIU/L) although in 3 patients, the levels were mildly elevated and overlapped with normal. OGTT failed or only partially suppressed GH secretion in all acromegalics. Therefore, elevated fasting GH levels are not diagnostic and OGTT is required for accurate diagnosis and assessment of treatment of acromegalic patients.
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PMID:Evaluation of suppression of growth hormone levels following a 75g oral glucose tolerance test. 149 29


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