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

Twenty-four hr glucose and hormonal monitoring was conducted in 34 randomly selected children with insulin dependent diabetes. Asymptomatic nocturnal hypoglycemia was present in 18% (6/34). The nocturnal plasma glucose decline of 20-25 mg/dl/hr reached a mean nadir of 50 mg/dl. The mean rebound hyperglycemia of 300 mg/dl over the subsequent 6.4 hrs. was significantly greater than any glucose excursion in diabetic children with daytime, symptomatic hypoglycemia (n = 5) or in those with non-hypoglycemic profiles (n = 23). Coincident with the nocturnal decline, but preceding the glucose nadir, was a marked release of growth hormone which was significantly greater (p less than .05) than that observed in the other diabetic groups. This release of growth hormone, and the nocturnal hypoglycemia, were reflected in the ratio of awake/sleep mean concentrations of glucose and growth hormone. These data support the speculation that growth hormone release contribute to the hyperglycemic rebound observed. Mean 24 hr growth hormone concentrations varied considerably from patient to patient such that a generalization for growth hormone concentrations in insulin dependent diabetes cannot be made. Asymptomatic nocturnal hypoglycemia is a frequent complication of the therapy of insulin dependent diabetes. Subsequent hyperglycemic rebound (the "Somogyi Effect") is associated with exuberant counterregulatory release of growth hormone. The precise pathophysiological role of this growth hormone release is unclear.
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PMID:Profiles of metabolic control in diabetic children-frequency of asymptomatic nocturnal hypoglycemia. 701 41

Insulin-dependent diabetes mellitus (IDDM) with onset below 35 years of age was studied in 52 Black and 38 Indian patients. IDDM accounted for approximately 10.4% and 1.1% of diabetes in the respective racial groups. The mean age and body weight in the Black and Indian diabetics were 27.6 years and 24.7 years, and 60.2 kg and 54.7 kg, respectively. The duration of diabetes in the majority of Blacks was 1-4 years, and that in Indians 5-9 years. The initial presentation in more than 80% of the patients was acute, with severe keto-acidosis in 15%. A positive family history of diabetes was obtained in more than 50% of Indians and in less than 6% of Blacks. Complications were present in 33% of Indian patients and were related to the duration of illness and dose of insulin required. Basal growth hormone, cortisol, cholesterol and triglyceride concentrations in serum were higher in Indians than in Blacks, but the differences were not significant. The disease was unrelated to excess alcohol intake or to pancreatic calcification.
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PMID:Insulin-dependent diabetes mellitus with early onset in blacks and Indians. 725 49

Insulin-dependent diabetes mellitus (IDDM) during adolescence is associated with complex derangements of the growth hormone (GH)/insulin-like growth factor (IGF) axis. Despite GH hypersecretion, IGF-I levels and IGF bioactivity are reduced. The diabetogenic effects of GH are well established, and GH hypersecretion has been implicated in the deterioration in glycemic control during adolescence and in the development of microangiopathy. Insulin deficiency or reduced portal delivery of insulin plays a central role in the development of these abnormalities, and although continuous subcutaneous insulin delivery may improve plasma IGF-I levels, it does not necessarily suppress GH levels. Recombinant IGF-I has been proposed as an adjunct to conventional insulin therapy, as restoring circulating IGF-I levels might lead to GH suppression. Placebo-controlled studies have shown a consistent reduction in GH secretion and related improvements in insulin sensitivity following a single subcutaneous IGF-I injection (40 micrograms/kg). Repeated daily subcutaneous IGF-I administration for 1 month resulted in a sustained increase in IGF-I levels, as well as a reduction in GH secretion and insulin requirements. There was no increase in hypoglycemia or other adverse effects. Recombinant IGF-I used in conjunction with insulin may therefore provide an additional approach to the management of IDDM during adolescence, allowing correction of abnormalities in the GH/IGF axis and leading to improved control and, hence, reduced risk of long-term complications. However, this hypothesis needs to be rigorously tested in long-term placebo-controlled studies.
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PMID:Insulin-like growth factors (IGFs) and IGF-I treatment in the adolescent with insulin-dependent diabetes mellitus. 747 4

Type 1 diabetes mellitus is associated with decreased insulin-like growth factor-1 (IGF-1) levels, enhanced values of growth hormone (GH) and IGF-binding protein 1 (IGFBP-1). Since the liver is the major source of IGF and IGFBP production, we have therefore examined whether levels of IGFs (IGF-1 and IGF-11) and IGFBPs (IGFBP-1 and IGFBP-3) differ when insulin is infused into the portal or peripheral vascular system. IGF, IGFBP, and GH levels were determined within 1-3 weeks of diagnosis in 36 patients (ranging in age from 18 to 22 years) with Type 1 diabetes mellitus. IGF-1 levels were low before insulin therapy administration (0.49 +/- 0.05 vs. 1.11 +/- 0.04 U/ml in controls, P < 0.01). With insulin treatment, IGF-1 levels rose to the normal range and IGF-1 normalisation depended on diabetes control and the route of insulin infusion. Diabetic patients with conventional insulin therapy (CIT; n = 12) had low IGF-1 (0.57 +/- 0.07 U/ml) compared with patients with continuous subcutaneous insulin infusion (CSII; n = 12; 0.75 +/- 0.08 U/ml; P < 0.05) and intraportal insulin infusion (IPII; n = 12; 1.07 +/- 10.05 U/ml; P < 0.05). Significant correlations were found between IGF-1 and parameters of glycemic control: HbA1c (r = -0.64; P < 0.01) and glycemia (r = -0.56; P < 0.05). The pattern of changes in IGF-11 levels was not significantly different from that of controls and was not altered by insulin therapy (0.98 +/- 0.08 and 1.01 +/- 0.04 U/ml in controls). Measured fasting 08:00 h IGFBP-1 levels were elevated 3-fold and IGFGP-3 levels were 2-fold lower in diabetic patients than in controls. Elevated IGFBP-1 levels were significantly correlated with metabolic control (glycemia, r = 0.64, P < 0.01; HbA1c, r = 0.71, P < 0.01). The mean elevated GH level before insulin administration (13.4 +/- 0.9 mg/l) was decreased by intensified insulin therapy (CSII, 8.8 +/- 0.6, P < 0.05; IPII, 5.6 +/- 0.9 mg/l, P < 0.001). There was a negative correlation between GH and IGF-1 (r = -0.72, P < 0.01). These results show the role of glycemic control and the route of insulin administration in the normalisation of IGF-1, IGFBP-1 and GH up to non-diabetic controls in patients with recent-onset Type 1 diabetes mellitus.
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PMID:Insulin-like growth factors and binding proteins in patients with recent-onset type 1 (insulin-dependent) diabetes mellitus: influence of diabetes control and intraportal insulin infusion. 753 Jun 21

Diabetes mellitus is a frequent manifestation in patients with acromegaly and it can show up even before the latter manifests. Typically, the diabetes mellitus in these patients does not tend to develop ketosis. We present the case of a patient hospitalized due to diabetic ketoacidosis associated to a perianal abscess. Diabetes mellitus type I was rejected and the presence of insulin-resistance was verified. She required insulin therapy just for three months. The clinical, hormonal and radiological evaluation showed, three years latter, the presence of a hypophyseal tumor producing growth hormone. After performing a trans-sphenoidal adenomectomy, the insulin-therapy could be removed with a normal glycemic profile. This case of acromegaly demonstrates the relationship between growth hormone and glucose metabolism. It can be considered that the ketoacidosis was the first manifestation of the acromegaly, which is exceptional.
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PMID:[Diabetic ketoacidosis as the first manifestation of acromegaly]. 774 14

Children with IDDM have diminished glucagon responses to hypoglycemia. We evaluated possible mechanisms in 60 children and adolescents with IDDM (age 15.4 +/- 2.6 years, duration 7.8 +/- 3.5 years [mean +/- SD]) and without diabetic complications. These were: 1) suppression by hyperinsulinism, 2) autonomic neuropathy, 3) a pan-islet cell defect, and 4) a glucotoxic effect. Glucagon and pancreatic polypeptide responses to hypoglycemia (insulin bolus 0.15-0.75 U/kg) were studied after insulin withdrawal and 3 days of intensive insulin therapy. Responses to arginine and mixed meal were also studied. The control group consisted of children with non-growth hormone deficient short stature. IDDM children had lower glucagon responses to hypoglycemia than controls (p < 0.001), the response to arginine did not differ from controls, and was greater than the response to hypoglycemia (p < 0.001). Responses to hypoglycemia after insulin withdrawal and intensive therapy did not differ. Basal pancreatic polypeptide levels were lower in IDDM than in controls (p < 0.05) but responses to hypoglycemia did not differ between groups. Thus the diminished glucagon response to hypoglycemia reflects a defect in hypoglycemic recognition or response by the alpha cells.
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PMID:Abnormal alpha cell hypoglycemic recognition in children with insulin dependent diabetes mellitus (IDDM). 782 Feb 17

We have compared intraoperative glycaemic control, insulin requirements and metabolic and endocrine variables in 40 non-insulin-dependent diabetic patients (NIDDM) and 40 insulin-dependent diabetic patients (IDDM) undergoing general anaesthesia for elective procedures. Two i.v. insulin regimens were used: continuous i.v. infusion (group A: 1.25 u.h-1) and repeated i.v. boluses (10 u./2 h). Blood concentrations of glucose were measured every 15 min from just before induction of anaesthesia until 2 h after surgery. Plasma lactate and pyruvate concentrations, ketone bodies, C-peptide and counter-regulatory hormones were also measured. Glycaemia did not differ significantly in the two types of diabetes, regardless of the insulin therapy used. The amounts of insulin administered were similar in NIDDM and IDDM. There was no significant difference for other metabolic variables. Plasma concentrations of growth hormone (GH) increased significantly during surgery, especially in IDDM patients, but this change did not alter intraoperative glycaemic control. We conclude that mean glycaemic control, insulin requirements and development of ketone bodies in NIDDM and IDDM patients did not differ during the operative period, regardless of the insulin regimen used. Therefore, during the operative period, it is not necessary to modify the insulin regimen according to the type of diabetes. The consequences of increased plasma GH concentrations on glycaemic control in IDDM patients after operation are unknown.
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PMID:Intraoperative glycaemic control in non-insulin-dependent and insulin-dependent diabetes. 799 82

Insulin stimulates glucose uptake and non-oxidative glucose metabolism (predominantly glycogen synthesis) in skeletal muscle. Among other things, insulin resistance is characterized by a subnormal insulin-stimulated glucose disposal, and it appears to be associated with an increased risk for development of non-insulin-dependent diabetes mellitus (NIDDM). The aim of the present investigation has been to elucidate the mechanism of action of insulin on non-oxidative glucose metabolism both during conditions of insulin resistance and during physiological modification of glucose metabolism. To do so, the effect of insulin was investigated both with respect to its initial activation of the insulin receptor kinase and the terminal step of the signal pathway, namely stimulation of the glycogen synthase. From needle biopsies of human skeletal muscle (vastus lateralis) cellular membranes were solubilized and the insulin receptors were partially purified by affinity chromatography using wheat germ agglutinin. Subsequently insulin binding and the insulin-stimulated tyrosine kinase activity were characterized. The insulin receptor kinase activity did not change during physiological modification of the glucose metabolism (exercise training, acute exercise, growth hormone exposure or experimental hyperglycemia). No specific abnormalities of the insulin receptor kinase activity were revealed in insulin-dependent diabetes (IDDM) or in common NIDDM. In addition, insulin receptor kinase activity did not change during dietary or sulphonylurea treatment of NIDDM. Glucose deposition as glycogen in muscle is regulated by glycogen synthase (GS), which during insulin stimulation undergoes dephosphorylation and becomes more active at physiological concentrations of glucose-6-phosphate. Recently, insulin was shown to stimulate a cascade of phosphorylation-dependent kinases which ultimately activate a glycogen-bound subunit of a phosphatase (G-subunit of phosphatase-1) which promotes dephosphorylation GS by the catalytic subunit. The quantity of the GS enzyme (GStot) in muscle may be reduced in the diabetes disease. However, it may increase during physical training of insulin-dependent diabetic patients. GStot is not altered during acute exposure to insulin, hyperglycemia or muscle contraction. The insulin stimulation of GS is reduced in insulin resistant NIDDM patients. However, once the hyperglycemia and the insulin resistance is ameliorated during treatment with diet or sulphonylurea drugs the activation of GS improves. Growth hormone-induced transient insulin resistance in non-diabetic subjects, is accompanied by a reduced insulin stimulation of GS. Experimentally induced hyperglycemia in normal subjects has no influence on GS activation by insulin. After an acute exercise bout the GS in muscle becomes activated. The mechanism of this post-exercise GS activation is still unknown.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insulin receptor function and glycogen synthase activity in human skeletal muscle. Physiology and pathophysiology. 803 33

Fasting serum growth hormone (GH) levels of different groups of diabetic patients were measured and compared to age-matched normal subjects. Insulin-dependent diabetes mellitus (IDDM) children (aged 12-17 years) were found to have significantly lower fasting GH levels than age-matched normal children (p < 0.001). In the adult age groups of 18-44 and 45-76 years, the IDDM patients showed increased fasting GH levels compared to age-matched normal subjects (p < 0.06 and p < 0.001 respectively) and non-insulin-dependent diabetes mellitus (NIDDM) patients (p < 0.05 and p < 0.001 respectively). The fasting GH levels of IDDM patients of the age group 18-44 years also showed significant correlations with glycated haemoglobin (r = 0.510, p = 0.002) and fasting blood sugar levels (r = 0.571, p = 0.01).
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PMID:Fasting growth hormone levels in diabetes mellitus. 812 44

The stimulatory effects of growth hormone (GH) and glucagon on renal function are well known, but it is uncertain whether these hormones are involved in the increase in renal function, characteristic of type 1 (insulin-dependent) diabetes mellitus. Therefore, the circulatory levels of GH and glucagon were measured in 10 type 1 diabetic patients with an elevated glomerular filtration rate (GFR > 130 ml min-1 1.73 m-2) and in 20 age and sex matched normofiltering patients (GFR ranging from 90-130 ml min-1 1.73 m-2). In the patients, fasting glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were determined using 125I-iothalamate and 131I-hippuran, respectively, during near-normoglycaemia. On a separate day, the levels of glucagon and GH were determined in the fasting basal state and after exercise. Multiple regression analysis disclosed that GFR was positively correlated with HbA1 (r2 = 0.18, p < 0.01), glucagon (r2 = 0.14, p < 0.03) as well as exercise-stimulated GH (r2 = 0.10, p < 0.05). ERPF was independently associated with HbA1 (r2 = 0.24, p < 0.005) and glucagon (r2 = 0.18, p < 0.01), whereas renal vascular resistance (RVR) was negatively correlated with stimulated GH (r2 = 0.18, p < 0.02). Kidney volume was positively correlated with HbA1 (r2 = 0.26, p < 0.001) and inversely with RVR (r2 = 0.16, p < 0.01), but not with glucagon or stimulated GH. The present study suggests that circulatory GH and glucagon play a contributory role in the renal haemodynamic changes in type 1 diabetes mellitus.
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PMID:Contributory roles of circulatory glucagon and growth hormone to increased renal haemodynamics in type 1 (insulin-dependent) diabetes mellitus. 814 Mar 92


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