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

We report the results of indirect immunofluorescent (IFI) detection of IgA and IgG antireticulin antibodies (IgA-ARA and IgG-ARA, respectively) in 283 serum samples from pediatric patients with coeliac disease (with and without gluten containing diets), patients with non-coeliac gastrointestinal disease, patients without gastrointestinal disease (control group) and patients with an increased risk for coeliac disease (diabetes mellitus, dermatitis herpetiformis or first grade relatives of coeliac patients). Our results indicate that IgA-ARA is a reproducible marker, with high positive (99-100%) and negative (100%) prediction values, when it is applied to children who have been on gluten containing diets for a long time (more than six months). The IgA-ARA measurement is not applicable in cases of selective IgA deficiency. Although IgG-ARA has a high predictive positive value, its low predictive negative value makes it a poor diagnostic tool. In the risk groups, our results suggest that these antibodies are useful in patient selection for intestinal biopsy.
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PMID:[Iga and IgG antireticuline in celiac disease. Their application as diagnostic markers of the disease]. 148 14

Poorly controlled insulin-dependent diabetes mellitus (IDDM) is associated with elevated basal plasma growth hormone (GH), disproportionally low insulin-like growth factor I (IGF-I) levels, and impaired somatic growth. These derangements in the GH-IGF axis imply a state of GH resistance. The mechanism of GH resistance is unknown; it may involve a defect at the level of the GH receptor, unresponsiveness due to a postreceptor defect in GH action, or both. To investigate a potential receptor involvement, we measured plasma high-affinity GH-binding protein (GHBP), which represents a truncated GH receptor and may reflect GH receptor levels in tissues, in patients with IDDM, patients with non-insulin-dependent diabetes (NIDDM), and nondiabetic control subjects. Patients with IDDM had significantly lower plasma GHBP levels than either patients with NIDDM or nondiabetic control subjects (mean value 18.2 vs. 24.6 and 23.8% GH bound/ml plasma, respectively, P less than 0.001). This difference persisted when only lean patients (less than 115% ideal body wt) were included in the analysis. Basal plasma GH levels were significantly elevated in IDDM compared with either patients with NIDDM or nondiabetic control subjects (mean 6.9 vs. 2.1 and 2.0 micrograms/L, respectively, P less than 0.001), whereas IFG-I levels were not significantly different in IDDM and NIDDM. No correlations were found between levels of GHBP and HbA1, duration of diabetes, or plasma GH. GHBP and IGF-I levels were significantly correlated in NIDDM but not in IDDM. We conclude that IDDM is associated with low GHBP levels and that GH resistance found in this disorder may be mediated, at least in part, by a decrease in GH receptor levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1992 May
PMID:Low plasma growth hormone binding protein in IDDM. 156 30

A 58-year-old man, with primary hemochromatosis, cirrhosis, and diabetes mellitus treated with insulin developed hepatoma. As the tumor grew, he lost his dependence on insulin therapy and experienced episodes of hypoglycemia. His response to infuse insulin was studied using the euglycemic clamp technique. Insulin was infused at rates of 1 and 10 mu/kg/min. The insulin dose response curve was shifted to the left and at plasma insulin levels of 72 microU/ml, steady-state glucose consumption was 9.6 mg/kg/min, 50% more than in normals, and nearly three times greater than that in other cirrhotics. The insulin clearance rate was 4417 m1/m2/min, almost five and six times more than in normals and cirrhotics, respectively. Basal hepatic glucose production was 3.6 mg/kg/min, two and three times higher than in normal and in cirrhotic subjects, respectively. The decrease in amino acid during hyperinsulinemia was more than 30% higher than in normal and other cirrhotics. IFG-I and II levels were not elevated in this patient. Increased insulin sensitivity and increased insulin clearance and serum amino acid decrease in response to insulin in vivo, suggest that insulin responsive tissues are at last partially responsible for tumor hypoglycemia. The increased glucose disposal rate probably accounted for the disappearance of the diabetes.
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PMID:Case report: increased insulin sensitivity in tumor hypoglycemia in a diabetic patient: glucose metabolism in tumor hypoglycemia. 165 53

Insulinopenic diabetes mellitus in the rat is associated with reduced circulating levels of insulin-like growth factor-I (IGF-I), resulting primarily from decreased IGF-I synthesis in liver and extrahepatic sites. Plasma GH levels in these animals are also suppressed, with loss of episodic secretion and decreased pituitary synthesis. Intrapituitary IGF-I has been postulated to exert local autocrine/paracrine negative feedback regulation on GH synthesis and secretion. The present studies were designed to examine regulation of pituitary IGF-I peptide content and gene expression in insulinopenic streptozotocin (STZ)-diabetic rats compared to that in liver and testis. Serum IGF-I levels were reduced by 86% in STZ-diabetic rats together with reduction of IGF-I content in liver (53%) and testis (74%; all P less than 0.001 vs. control). Concomitantly, liver and testicular IGF-I mRNA levels were reduced by 90% (P less than 0.001 vs. control). Insulin treatment restored IGF-I peptide levels in serum, liver, and testis toward normal, with a partial but significant increase in liver IGF-I mRNA. In contrast, pituitary IFG-I peptide content increased by 69% in STZ-diabetic rats (P less than 0.001 vs. control), with no change in IGF-I gene expression. Insulin treatment completely reversed the rise of pituitary IGF-I peptide content. These results demonstrate a novel discordance in the regulation of IGF-I gene expression and peptide content between pituitary and other tissues in STZ-induced diabetic rats. Elevated IGF-I levels in the pituitaries of these animals may partly explain the suppressed GH synthesis and secretion seen in STZ-diabetic rats and provide further evidence for a potential autocrine or paracrine role of pituitary IGF-I in GH regulation.
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PMID:Pituitary insulin-like growth factor-I content and gene expression in the streptozotocin-diabetic rat: evidence for tissue-specific regulation. 198 70

The effects of insulin and insulin-like growth factor I (IFG-I) on protein synthesis were compared in muscle isolated from lean and goldthioglucose (GTG)-obese mice. Two types of skeletal muscles, the red soleus and the white extensor digitorum longus (EDL) muscles, were studied. In muscles from lean mice, 6.7 nM insulin and 50 nM IGF-I caused a similar maximal stimulation of tyrosine incorporation in total proteins (40% increase). However, the potency of IGF-I was only 5-10% that of insulin both in soleus and in EDL muscles (EC50 approximately equal to 6 nM for IGF-I and 0.5 nM for insulin). Basal rate of protein synthesis was identical in muscles from GTG-obese and lean mice. Similarly, a comparable increase in the rate of protein synthesis was obtained using maximally effective concentrations of insulin and IGF-I in both lean and GTG-obese animals. SDS-polyacrylamide gel electrophoresis analysis of proteins labeled with 35S-methionine confirmed that, in muscles from lean and GTG-obese animals, insulin and IGF-I increased overall protein synthesis in a similar manner. These results suggest that the protein synthesis machinery is not impaired in GTG-induced obesity, which is therefore not associated with resistance to insulin for its effect on protein metabolism.
Diabetes 1983 May
PMID:Insulin and insulin-like growth factor I. Effects on protein synthesis in isolated muscles from lean and goldthioglucose-obese mice. 640 79

Infants with transient neonatal diabetes mellitus are small for gestational age and fail to thrive postnatally unless insulin is administered. We have measured the concentrations of insulin-related growth factors in an infant girl with this condition to learn if deficiencies in one or more of these factors could be responsible for the impaired growth. Cord blood serum radioimmunoassayable insulin and somatomedin C/insulin-like growth factor I (SMC/IGF-I) were low, but insulin-like growth factor II (IGF-II) measured by a specific radioreceptor assay was normal. Insulin therapy begun on the fourth day of life resulted in a prompt increase in weight and a delayed rise in SMC/IFG-I. No significant changes in IGF-II were observed. After 2.5 months, insulin treatment was discontinued. At that time, endogenous insulin secretion was documented by increased urinary C-peptide. Normal growth and SMC/IFG-I levels persisted. We conclude that growth failure in this condition may be related not only to a lack of insulin but also to SMC/IGF-I deficiency. A deficiency in IGF-II is not involved.
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PMID:Plasma somatomedins, endogenous insulin secretion, and growth in transient neonatal diabetes mellitus. 700 55

Recombinant DNA technology has made large amounts of insulin-like growth factor-I (IGF-I) available for studies in animal models and humans. It has been shown that treatment with IGF-I is associated with increased insulin sensitivity in normal subjects as well as in patients with growth hormone deficiency, Type 1 and Type 2 diabetes mellitus and type A insulin-resistance. The metabolic effects of IFG-I appear to be beneficial in these conditions. The reported side effects of IGF-I, which may be largely due to overdosage, have limited its use to small and mostly short-term clinical studies.
Diabetes Metab 1996 Jul
PMID:Insulin-like growth factor-I in the therapy of non-insulin-dependent diabetes mellitus and insulin resistance. 876 73

Subjects at increased risk for developing non-insulin-dependent diabetes mellitus (NIDDM) were encouraged via a public awareness campaign, general practitioners, or a direct approach (in the case of women with previous gestational diabetes) to attend one of three English and two French centers for fasting plasma glucose (FPG) measurement. Of 1,580 subjects (mean +/- SD age, 47 +/- 10 years), 29% were male, 56% had a diabetic relative, 20% had a history of elevated blood glucose or glycosuria, and 9% previously had gestational diabetes. Thirty-one percent (493) had an initial increased fasting glucose ([IFG] 5.5 to 7.7 mmol.L-1), 3% (41) a diabetic fasting glucose ([DFG] > or = 7.8 mmol.L-1), and 66% (1,046) a normal fasting glucose ([NFG] < 5.5 mmol.L-1). Four hundred forty-one of the 493 returned for a second FPG measurement, and 67% (293) of these had a similar value on repeat testing 2 weeks later. A 75-g, 2-hour oral glucose tolerance test (OGTT) in 223 of these subjects showed that 37% (83) had impaired glucose tolerance (IGT), 26% (58) diabetes mellitus (DM), and 37% (82) normal glucose tolerance (NGT). Seven percent of self-referred patients had NIDDM by World Health Organization (WHO) criteria. Eighty-eight percent of those with an initial DFG had an increased glycated hemoglobin (> 6.2%), and 75% an increased fructosamine (> 282 mumol.L-1). While these two glycemic measures provided good discrimination for diabetes, neither were reliable in detecting those with increased but not diabetic FPG values. In conclusion, 293 (19%) of 1,580 self-referred subjects were identified as having persistently increased FPG, and 227 have been entered into a randomized NIDDM prevention trial evaluating healthy-living advice and sulfonylurea therapy.
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PMID:The Fasting Hyperglycaemia Study: I. Subject identification and recruitment for a non-insulin-dependent diabetes prevention trial. 943 59

Japan Diabetes Society organized a committee for the revision of diagnostic criteria of diabetes mellitus in 1995. Like ADA and WHO reports, this committee adopts a classification based on etiologies, and presents a two-dimensional figure with etiologies and the state of insulin deficiency on different axis. The words IDDM and NIDDM will be retained as terms representing the different degree of insulin deficiency. On the basis of glycemia, diabetic type is defined when fasting plasma glucose exceeded 126 mg/dl and/or 2-hour plasma glucose by 75 g GTT exceeded 200 mg/dl. The diagnosis of diabetes in an individual can be made by confirming sustained diabetic type on repeated tests or co-existance of characteristic clinical features of diabetes. Normal type is defined by FPG < 110 mg/dl and 2hPG < 140 mg/dl. The borderline type, defined as neither normal nor diabetic types, corresponds to IFG plus IGT according to ADA and WHO reports. The application of HbA1c for diagnosis of diabetes and the criteria for gestational diabetes mellitus are also discussed.
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PMID:[Outline of revision of classification and diagnostic criteria of diabetes mellitus in Japan]. 1019 34

The objective of this study was to compare the results between two diagnostic criteria by ADA (1997) and WHO (1985) among those with fasting plasma glucose (FPG) level 5.6-7.8 mmol/l from a community-based survey in Kin-Hu and Kin-Chen, Kinmen conducted in 1991-94. According to official household registry, 10,797 residents aged over 30 were eligible for screening. 7580 had completed FPG screening and 1855 with FPG 5.6-7.8 mmol/l were invited to receive a 75-g oral glucose tolerance test (OGTT). 78.5% (1456/1855) had completed OGTT. The prevalence of impaired fasting glucose (IFG, by ADA) was 15.7%; the prevalence of impaired glucose tolerance (IGT, by WHO) was 22.7%; the prevalence of undiagnosed diabetes was 7.4% by ADA criteria and 10.9% by WHO criteria. It should be noticed that, among subjects with FPG 5.6-7.8 mmol/l, 50.3% of individuals with undiagnosed diabetes and 67.6% of individuals with IGT by WHO criteria would be missed by ADA criteria. Based on the above findings, the two-step screening strategy using FPG as the first line screening and OGTT for high-risk group (FPG 5.6-7.8 mmol/l) only was recommended in epidemiological study and case finding in consideration of feasibility and validity.
Diabetes Res Clin Pract 1999 Aug
PMID:Comparison of the results between two diagnostic criteria by ADA and WHO among subjects with FPG 5.6-7.8 mmol/l in Kin-Hu and Kin-Chen, Kinmen, 1991-94. 1049 85


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