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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of a new octapeptide analogue of somatostatin (SMS 201-995) on blood glucose and gut hormone levels was studied in 10 C-peptide-negative, insulin-dependent diabetic (IDDM) subjects. On separate days, either 50 or 100 micrograms SMS or placebo was s.c. injected simultaneously with an identical insulin dose 30 min before a mixed meal. Postprandial blood glucose decreased after 100 micrograms SMS s.c. within 30 min from 8.9 +/- 0.7 to 7.8 +/- 0.6 mmol/L (P less than 0.001) and remained at similar levels during 180 min. In contrast, postprandial blood glucose concentration increased after placebo from 9.9 +/- 0.8 to 13.8 +/- 0.9 mmol/L (SMS versus placebo P less than 0.001). Plasma glucagon decreased rapidly after SMS to the limit of detection (P less than 0.001) and remained lowered during 180 min; in contrast, glucagon levels increased after the meal during the placebo study (SMS versus placebo P less than 0.001). Plasma growth hormone concentrations were significantly lower after SMS than after placebo (P less than 0.05). SMS abolished completely the postprandial increase in plasma gastrin and pancreatic polypeptide (PP) concentrations. Plasma free fatty acid (FFA) and triglyceride concentrations decreased after SMS, reaching significantly lower levels than after placebo (P less than 0.05 and P less than 0.01), respectively). Plasma SMS concentration increased rapidly after s.c. administration of SMS; its appearance preceded that of plasma free insulin after s.c. insulin injection. Fifty micrograms SMS was similarly effective as 100 micrograms in decreasing blood glucose, triglycerides, glucagon, and gut hormone concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduced postprandial hyperglycemia after subcutaneous injection of a somatostatin-analogue (SMS 201-995) in insulin-dependent diabetes mellitus. 286 93

We have recently obtained encouraging short-term results after a single subcutaneous injection of the long-acting somatostatin analogue SMS 201-995 in acromegalic patients. Increased growth hormone (GH) levels may be involved in the pathogenesis of proliferative retinopathy in type I diabetes mellitus. In this study we thus investigated the effect of 3 X 50 micrograms SMS 201-995 daily on the metabolic control and hormone secretion of eight type I diabetics over a 3-day period. GH levels decreased by 32% (p less than 0.05) and somatomedin C levels by 31% (p less than 0.01) on the 3rd day of treatment compared with a control day. The insulin requirements during conventional subcutaneous insulin therapy were reduced by 28% (p less than 0.01) in seven patients without deterioration of metabolic control (mean blood glucose levels, 153.8) versus 154.7 mg/dl). Triiodothyronine, thyroxine, glucagon, prolactin, luteinizing hormone and follicle-stimulating hormone showed no significant changes. We conclude that SMS 201-995 could be an excellent tool for further clinical investigation and therapy of diabetic vascular complications.
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PMID:Somatostatin analogue SMS 201-995 in type I diabetes mellitus. Initial experience after repeated administration. 287 2

Postprandial changes in blood glucose, insulin and glucagon were examined in 7 non-insulin dependent diabetic patients, before and after 3 days' treatment with the somatostatin analogue, octreotide (50 ug injected subcutaneously thricedaily). After octreotide injection, postprandial rises in plasma insulin and glucagon were significantly flattened. The postprandial glycaemic rise was delayed but the area under the glycaemic curve was not increased. Animal studies have suggested that octreotide inhibits growth hormone and glucagon secretion much more powerfully than native somatostatin, while relatively sparing insulin secretion. However, the present findings suggest that this analogue is not sufficiently selective to be therapeutically useful in non-insulin dependent diabetes.
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PMID:Postprandial glycaemic effects of a long-acting somatostatin analogue (octreotide) in non-insulin dependent diabetes mellitus. 289 27

Altogether 54 male patients with insulin-dependent diabetes mellitus participated in the studies. The impact of insulin-induced hypoglycemia on posthypoglycemic insulin sensitivity was evaluated for up to 12 hours following nadir hypoglycemia. The effect on glucose homeostasis following transient elevation of counterregulatory hormones was studied by exogenous administration of adrenaline, adreno-corticotropic hormone and growth hormone and by suppression of the endogenous release of growth hormone in connection with hypoglycemia. The studies were performed in the fasting state preceded by a 24 hour intravenous insulin infusion in order to avoid interference of subcutaneous insulin. Insulin resistance was determined by a constant rate intravenous infusion of somatostatin, insulin and glucose. This test seemed appropriate for the evaluation of total insulin resistance, and its reproducibility was acceptable. By using this method it was demonstrated that insulin resistance occurred for at least 12 hours after a hypoglycemic event in patients with IDDM, and that adrenaline caused immediate insulin resistance which, however, faded out within four to six hours, while GH exerted no immediate effect on insulin sensitivity but caused marked and sustained insulin resistance after a lag period of about four hours. Cortisol had no apparent effect within six hours but enhanced the effect of GH. The magnitude of these diabetogenic effects of hypoglycemia and GH was less pronounced in patients who already were more insulin resistant. These results are compatible with the idea that adrenaline is of major importance for the counterregulation and restoration of blood glucose during the first few hours following hypoglycemia, while GH is responsible for the induction of a long-lasting state of insulin resistance. It is possible that such prolonged insulin resistance may cause posthypoglycemic hyperglycemia in patients with IDDM. These studies therefore indicate that the GH suppressing hormone somatostatin may be of clinical value as an adjunct to insulin in the treatment of patients with insulin-dependent diabetes mellitus and labile blood glucose control.
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PMID:Studies on posthypoglycemic insulin resistance in insulin-dependent diabetes mellitus. 290 16

The effects of an iv thyrotropin releasing hormone (TRH) bolus on serum growth hormone (GH) and cortisol levels were evaluated in 59 children and adolescents with insulin dependent diabetes mellitus (IDDM) and in 24 healthy, age-matched control subjects. In the IDDM group GH baseline levels sharply rose within 30 min after TRH and successively normalized. On the contrary, TRH injection failed to affect GH serum concentrations in the control group. The GH increase after TRH in IDDM patients was positively correlated to age, but unrelated to other variables, such as sex, pubertal stage, duration of disease, glycemia, glycosylated hemoglobin, thyrotropin and T4 concentrations. Twenty-one out of 59 diabetics and only 1/24 controls exhibited a paradoxical GH response to TRH, arbitrarily defined as a precocious increase (within 30 min), of more than 100% with respect to the baseline value, associated with a GH peak greater than 10 ng/ml. Eighteen IDDM patients underwent a second TRH test 12 to 24 months later and substantially exhibited the same GH pattern documented the first time. The mechanism responsible for such anomalous GH responsiveness to TRH in IDDM is unclear. However, it cannot be attributed to a nonspecific stress reaction, as proven by the lack of a concomitant increase of cortisol serum levels in the same subjects.
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PMID:Effects of intravenous TRH on growth hormone and cortisol serum levels in children and adolescents with insulin dependent diabetes mellitus. 309 14

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.
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PMID:No evidence for increased growth hormone responses to growth hormone-releasing hormone in patients with diabetic retinopathy. 310 Mar 67

In cross-sectional studies elevations in growth hormone (GH), factor VIII related antigen (VIIIR:Ag), and plasminogen activator activity (PAA) have been connected with diabetic retinopathy. To evaluate the importance of these factors for the development of retinopathy, we have carried out a prospective study. In a primary study GH, VIIIR:Ag, and PAA were evaluated during a 25 min exercise test in 22 insulin dependent diabetes mellitus (IDDM) patients. After 5-7 years, the patients were re-evaluated and the presence of retinopathy in the follow-up study was correlated to the findings in the primary study. Patients with retinopathy in the primary or the second study (n = 14) showed a significant increase in GH (p less than 0.05) during the first 5 min of exercise compared with patients without retinopathy. Moreover, the 14 retinopathy patients showed further significant elevations in GH (p less than 0.001), VIIIR:Ag (p less than 0.01) and PAA (p less than 0.001) during the remaining 20 min of exercise. In contrast, patients without retinopathy (n = 8) in the follow-up study, did not show significant elevations in GH, VIIIR:Ag, and PAA during exercise. A lack of rise in GH, VIIIR:Ag, and PAA during exercise seems to indicate a resistance to retinopathy in IDDM patients.
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PMID:Absent elevations in growth hormone, factor VIII related antigen, and plasminogen activator activity during exercise in diabetic patients resistant to retinopathy. 313 76

A 24 hour biostator control was carried out on 30 patients with insulin dependent diabetes, mean age 34 years (16-61 years) and mean duration of the disease 7 years (1-33 years). All patients had normal body mass (+/- 10% according to Broka's formula). The plasma levels of glucagon, growth hormone, cortisol and C-peptide were determined at the beginning and at the end of the biostator control. With the decrease of glycemia (from 12.71 +/- 4.3 to 5.75 +/- 1.5 mmol/l, p less than 0.001) only the cortisol level fell reliably (p less than 0.001), the growth hormone and glucagon levels fell statistically insignificantly. There is no reliable correlation between the contra-insulin hormones studied and the glycemia level.
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PMID:[Effect of biostator control on levels of contra-insulin hormones]. 320 5

17 patients with active acromegaly (7 of them had diabetes mellitus, too), 13 patients with type I diabetes mellitus and 20 healthy controls were examined. The residual beta-cell secretion was determined by venous Tolbutamide test and the insulin sensitivity was determined by euglycemic clamp-technique. A positive correlation was found between the growth hormone level and prolactin and the size of the basic insulin secretion. In acromegaly (with or without diabetes) the sensitivity of beta-cell apparatus towards the stimulant Tolbutamide is preserved but the insulin reserves are diminished. There exists a positive correlation between the growth hormone level and the degree of insulin resistance and between the increased prolactin level and the degree of insulin resistance in acromegalic patients.
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PMID:[Insulin secretion and action in acromegaly]. 332 80

The possible involvement of growth hormone (GH) and human placental lactogen (HPL) in the development of diabetic tissue damage during pregnancy was studied in 16 insulin-dependent diabetic patients (IDDM), 8 gestational diabetic patients (GD) and 14 normal pregnant women. GH and HPL were elevated in pregnancies complicated by diabetes but, in contrast to the rise of HPL, GH declined throughout pregnancy in all the groups studied. The concentrations of neither correlated with plasma glucose, insulin requirement or duration of diabetes. HPL was positively correlated with urinary albumin excretion (UAE) in all 3 groups, but with blood pressure only in the IDDM group. There was also a significant and positive correlation in all patients between HPL at the end of pregnancy and placental weight. No evidence of serious tissue damage was found in either diabetic group. The vibration sensory threshold was unaffected by pregnancy and was similar to that of normal women. However, in the IDDM group UAE increased significantly postpartum when compared with second trimester values; they also had higher UAE than the other 2 groups post-delivery. A small but significant rise in diastolic blood pressure (DBP) was found in the 3 groups studied between the second and third trimester and pre-delivery. The same trend in systolic blood pressure (SBP) was seen in the diabetic groups. The IDDM had higher systolic and diastolic blood pressures than the normal women at all stages of gestation.
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PMID:High levels of growth hormone and human placental lactogen in pregnancy complicated by diabetes. 351 44


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