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

Previous reports concerning insulin-like growth factor-I (IGF-I) in diabetics are conflicting. This study describes IGF-I in children with insulin-dependent diabetes mellitus (IDDM) and healthy controls in relation to pubertal development. Sixty-six children participated (34 girls and 32 boys) of which 33 had IDDM. The mean age in the study population was 14.3 years, (range 7.1 to 19.7). Serum IGF-I was significantly decreased in diabetics. Diabetic girls had a mean IGF-I of 28.3 (14.4; = SD) nmol/l compared with 42.8 (15.0) nmol/l in controls. In diabetic boys the result was 30.0 (16.0) nmol/l compared with 44.1 (23.4) in controls. Growth hormone was measured in only one fasting morning serum sample from each individual. There was no difference between girls, but diabetic boys had higher mean serum concentration of growth hormone than controls (3.5 (4.8) vs. 1.8 (1.5) micrograms/l respectively). Diabetic girls had delayed menarche, corresponding to a slightly delayed bone maturation.
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PMID:Decreased serum insulin-like growth factor I during puberty in children with insulin dependent diabetes mellitus (IDDM). 771 26

Insulin-like growth factor I (IGF I) is an endocrine hormone that mediates most of the effects of pituitary growth hormone. Other important regulatory factors of serum IGF I levels are insulin and nutrition. Most of the circulating IGF I is bound to three IGF binding proteins (BP), mostly IGFBP-3, BP-2 and BP-1. IGF I is also produced by many cells in the body where it exerts autocrine and/or paracrine effects. IGF I has a specific receptor on most cells, the so-called type 1 IGF receptor. When IGF I is administered intravenously as a bolus it leads to acute hypoglycaemia in a similar way to insulin and mainly with the insulin receptor. Chronic administration of IGF I to hypophysectomized or diabetic rats leads to prominent anabolic effects and growth. In this manuscript, metabolic and endocrine effects of recombinant IGF I are discussed. Recombinant IGF I therapy increases energy expenditure and lipid oxidation and decreases proteolysis and protein oxidation. These effects occur despite a partial inhibition of insulin and growth hormone secretion. The therapeutic spectrum of recombinant IGF I, consisting of inhibition of catabolism, stimulation of anabolism, decreases of triglyceride and cholesterol levels and a striking increase in insulin sensitivity, renders IGF I a very interesting, powerful tool for insulin-resistant states such as non-insulin-dependent diabetes mellitus.
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PMID:Recombinant human insulin-like growth factor-I: a therapeutic challenge for diabetes mellitus. 782 34

Growth hormone (GH) hypersecretion has been described in diabetes mellitus and seems to be involved in the pathogenesis of diabetes complications. As pirenzepine (PZ), a cholinergic muscarinic antagonist, is able to inhibit GH hypersecretion in insulin-dependent diabetes mellitus (IDDM), we investigated whether PZ is also able to inhibit spontaneous and stimulated GH-release in non-insulin-dependent diabetes mellitus (NIDDM). Ten non-obese well-controlled patients with NIDDM underwent in random order the following three double-blind one week treatments: placebo (PL), PZ at low dose (PL in the morning plus PZ 50 mg at 22 h) or high dose (PZ 50 mg at 8 h plus 100 mg at 22 h). Pirenzepine administration significantly (p < 0.05) decreased nocturnal GH release after both low and high dose (AUC, PL vs PZ: 107.3 +/- 26.5 vs 48.3 +/- 10.5 and 57.6 +/- 9.6 micrograms/L/h, respectively). The GH response to arginine infusion was significantly inhibited by PZ at high dose (AUC, 147.1 +/- 48.8 vs 444.7 +/- 194.3 micrograms/L/h, p < 0.01), but not at low dose. Glucose, insulin, glucagon and somatostatin responses to arginine infusion were not changed by pirenzepine treatment. In conclusion, the muscarinic blockade by PZ is able to inhibit the spontaneous and stimulated GH secretion also in NIDDM without affecting insulin secretion.
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PMID:Pirenzepine decreases basal and stimulated GH secretion in patients with type 2 (non-insulin-dependent) diabetes mellitus. 800 63

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

Throughout gestation, maternal insulin-like growth factor I (IGF-I) increases progressively despite suppressed pituitary growth hormone (GH) secretion. We have previously shown that in normal pregnancy, a specific placental GH variant, rather than human placental lactogen (hPL), substitutes for pituitary GH in the regulation of maternal IGF-I. We studied the maternal IGF-I secretion in a cohort of 286 normal and abnormal pregnancies (617 blood samples). Regardless of pathology and gestational age, IGF-I values correlated with corresponding placental GH but not with hPL values. Similar correlations were evidenced for each 2-wk gestational period between 32 and 39 wk. In pathological pregnancies, when only those hormonal results that are obtained before any treatment are considered and diabetes is excluded, IGF-I levels were closely related to corresponding placental GH, but not to hPL. In women with a fetoplacental unit disorder, low placental GH levels resulted in low IGF-I and in a secondary pituitary GH increase, whereas in patients without detectable impairment of the fetoplacental unit normal placental GH corresponded to normal IGF-I. These results suggest that in pathological as well as in normal pregnancy, placental GH, and not hPL, substitutes for pituitary GH to regulate the maternal IGF-I secretion.
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PMID:Regulation of maternal IGF-I by placental GH in normal and abnormal human pregnancies. 823 32

The changes in normal endocrine physiology which accompany pregnancy result in changes in normal ranges of hormone levels and in specific changes in the course and management of endocrine diseases. This review presents information about the various endocrine diseases and their management in pregnant adolescents. Normal pituitary function during pregnancy is described as is the effect of pregnancy on pituitary tumors such as microadenomas and prolactinomas. The effects of bromocriptine therapy in cases where tumor enlargement occurs during pregnancy are tabulated. Methods of distinguishing placental growth hormone secretion and pituitary growth hormone secretion in patients with acromegaly are presented (with the note that acromegalic patients rarely become pregnant). TSH-secreting, gonadotropin, and nonsecreting tumors are rare in this age group, and there is no evidence that they enlarge during pregnancy. The discussion of the pituitary covers chronic hypopituitarism, Sheehan's Syndrome, lymphocytic hypophysitis, and diabetes insipidus. After reviewing normal changes in thyroid physiology during pregnancy, hyperthyroidism (usually due to Graves' disease), thyroid storm, and hypothyroidism are considered. The adrenal is the next subject, with a brief description of normal changes during pregnancy followed by comments on Cushing's Syndrome, adrenal insufficiency, congenital adrenal hyperplasia, and primary hyperaldosteronism. The symptoms, diagnosis, and treatment of pheochromocytomas, which are uncommon during pregnancy but are associated with high fetal and maternal mortality, are the next topics. After a review of changes in calcium metabolism during pregnancy and hypercalcemia, this report ends with a consideration of diabetes mellitus which includes alterations in maternal carbohydrate metabolism during pregnancy, effects of diabetes on the fetus, and management of insulin-dependent diabetes mellitus during pregnancy (the most likely type to be present in adolescents).
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PMID:Endocrine problems of adolescent pregnancy. 824 53

Growth hormone (GH) and insulin have both mitogenic and metabolic actions. The growth-promoting effects of GH in vivo are thought to be mediated by insulin-like growth factor-I (IGF-I), whereas the metabolic effects of GH are thought to be either direct or mediated by factors other than IGF-I. In previous studies using HTLV-II-transformed T-lymphoblast cell lines established from normal individuals, we have shown that GH preincubation induces resistance to the growth-promoting (mitogenic) action of insulin. In this study, using T-cell lines from 3 American control subjects, 1 African control subject, and 1 African Pygmy (the latter previously shown to be resistant to the growth-promoting actions of both IGF-I and GH), we examined the role of local IGF-I in the mediation of GH-induced resistance to the mitogenic action of insulin. In these studies, we quantified the stimulation of T-cell colony formation in response to insulin in the presence and absence of either GH or IGF-I.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1994 Jan
PMID:Growth hormone induces resistance to the mitogenic action of insulin through local IGF-I. Studies in normal and Pygmy T-cell lines. 826 19

In order to determine whether acromegaly is still associated with increased mortality, a hospital case note review of all patients with acromegaly followed up in Stoke-on-Trent since 1967 was carried out. Of 79 subjects identified, 51 are alive and being monitored and 28 have died. Mortality was compared to the general population by life table analysis. Secretion of growth hormone was assessed and compared in dead and alive patients. The effect of diabetes, hypertension, and growth hormone secretion on long-term outcome was assessed. Acromegaly is still associated with increased mortality, with an overall ratio of observed to expected deaths equal to 2.68 (95% C.I. 1.8-3.9; p < 0.001), but the survival of 31 (39%) patients whose growth hormone level had been reduced to below 5 mU/l was equal to that of the general population (O/E = 1.42; 95% C.I. 0.46-3.31: p > 0.05). The dead patients had had significantly higher growth hormone levels than those still alive, but mortality did not appear to be influenced by diabetes or hypertension. The cause of death was vascular in 57% of cases. Growth hormone hypersecretion is still associated with excess mortality in acromegaly. The present study suggests that the therapeutic objective should be to lower average daytime growth hormone levels to less than 5 mU/l. There is need for a large study to compare different modes of treatment in terms of their effect on growth hormone secretion and on long-term outcome.
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PMID:An audit of outcome of treatment in acromegaly. 832 47

Growth hormone (GH), insulin-like growth factor-1 (IGF-1) and prolactin (PRL) in blood and urine were observed in 20 patients with acromegaly in a double-blind placebo-controlled 14-day clinical trial with the somatostatin analog octreotide. Hormones were determined by the same radioimmunoassays in blood and urine. Significant reduction of GH and IGF-1 during octreotide treatment compared to placebo was seen in blood but not in urine. Patients with diabetes mellitus, 2 of the 20 patients, showed notably increased urinary GH and IGF-1 in relation to blood levels. Therefore, results without the two diabetic patients were calculated, showing significant reduction of urinary GH and IGF-I during treatment on some, but not all observation days. The intraindividual variations of GH and IGF-1 were greater in urine than in blood. PRL levels were not significantly affected by octreotide either with or without the two diabetic patients. In conclusion, this study indicates, that GH and IGF-1 in blood are preferable to urinary GH and IGF-1 as response markers during treatment of acromegaly with octreotide. One disadvantage with urinary assessments of GH and IGF-1 in acromegaly seems to be the relatively higher excretion in patients with diabetes mellitus.
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PMID:Growth hormone and insulin-like growth factor-1 in blood and urine as response markers during treatment of acromegaly with octreotide: a double-blind placebo-controlled study. 851 80

The present study focuses on the pathogenesis of increased frequency of large-vessel disease in diabetes. The diabetic arterial wall displays characteristic alterations of the extracellular matrix secreted by arterial smooth-muscle cells. The effects of insulin and growth hormone on the synthesis of sulphate-labelled proteoglycans and heparan sulphate proteoglycan were studied. Proteoglycans and heparan sulphate proteoglycan were obtained from the medium and the cell layer of cultured human arterial smooth-muscle cells grown in 5% human serum. Heparan sulphate proteoglycan was quantified using ethanol precipitation combined with specific enzyme degradation. Addition of insulin (0.01, 0.05 and 0.10 mU/ml) induced a significant accumulation of 35S-labelled proteoglycans in the cell layer (2p < 0.005 and 2p < 0.001). The relative amount of cell-associated heparan sulphate proteoglycan increased during insulin stimulation (2p < 0.05). Growth hormone stimulation (5.0 and 10.0 ng/ml) caused a significant decrease in the ratio between heparan sulphate proteoglycan and proteoglycan in the cell layer (2p < 0.02 and 2p < 0.01), whereas the distribution of proteoglycans between the cell layer and the medium was unaltered.
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PMID:Effect of insulin and growth hormone on the synthesis of radiolabelled proteoglycans from cultured human arterial smooth-muscle cells. 861 30


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