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  • 1
    ISSN: 1432-0428
    Schlagwort(e): Islet amyloid polypeptide ; amylin ; amidation ; invivo effect ; insulin resistance ; diabetes mellitus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Islet amyloid polypeptide is a 37 amino acid hormone-like peptide which is the major protein component of islet amyloid deposits commonly found in patients with Type 2 (non-insulin-dependent) diabetes mellitus. Recent studies indicate that a physiologically active form of this peptide appears to be carboxyamidated and secreted from the insulin-producing beta cell. In order to clarify the possible in vivo actions of islet amyloid polypeptide, we have studied the effects of synthesized islet amyloid polypeptide-amide on peripheral glucose utilization by performing hyperinsulinaemic euglycaemic glucose clamp studies on dogs. Exogenously administered islet amyloid polypeptide-amide (an infusion from 1.0 to 100 μg·kg−1·h−1, over 2 h) inhibited the insulin-stimulated glucose disposal rate in a dose dependent manner. Twenty-five μg·kg−1·h−1 of islet amyloid polypeptide-amide infused via a peripheral vein significantly lowered the glucose disposal rate by 20% (from 17.4±1.7 to 14.4±1.7 mg·kg−1·min−1, n = 5, p〈0.01). These findings suggest that islet amyloid polypeptide-amide causes peripheral insulin resistance in vivo.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0428
    Schlagwort(e): Islet amyloid polypeptide ; amylin ; diabetes mellitus ; fasting concentration ; oral glucose tolerance test
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Fasting plasma islet amyloid polypeptide concentrations and their responses to an oral glucose load were determined in non-diabetic control subjects and patients with abnormal glucose tolerance in relation to the responses of insulin or C-peptide. Plasma islet amyloid polypeptide was measured by radioimmunoassay. In the non-diabetic control subjects, fasting plasma islet amyloid polypeptide was 6.4±0.5 fmol/ml (mean ± SEM) and was about 1/7 less in molar basis than in insulin. The fasting islet amyloid polypeptide level rose in obese patients and fell in patients with Type 1 (insulin-dependent) diabetes mellitus. In non-obese patients with impaired glucose tolerance and Type 2 (non-insulin-dependent) diabetic patients without insulin therapy, the level was equal to that of the control subjects, but a low concentration of islet amyloid polypeptide relative to insulin or C-peptide was observed in the non-obese Type 2 diabetic group. The patterns of plasma islet amyloid polypeptide responses after oral glucose were similar to those of insulin or C-peptide. However, compared to non-obese patients, a hyper-response of islet amyloid polypeptide relative to C-peptide was noted in obese patients who had a hyper-response of insulin relative to C-peptide. This study suggests that basal hypo-secretion of islet amyloid polypeptide relative to insulin exists in non-obese Type 2 diabetes and that circulating islet amyloid polypeptide may act physiologically with insulin to modulate the glucose metabolism.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-0428
    Schlagwort(e): Key words NIDDM, glycogen synthase, DNA polymorphism, genetics, hypertension.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary We investigated the possible association between alleles of a simple tandem repeat DNA polymorphism in the human glycogen synthase gene and non-obese non-insulin-dependent diabetes (NIDDM) in Japanese subjects. Nine alleles (−4G, −3G, −2G, −1G, 0G, 1G, 2G, 3G, and 4G) were identified in the study group of 164 patients with NIDDM and 115 non-diabetic subjects. The overall frequency distribution of the glycogen synthase gene alleles was significantly different between the two groups (p =0.0316). The 2G allele was found more frequently in patients with NIDDM than in non-diabetic subjects (17.7 % vs 8.7 %, p =0.0016). These results suggest that the 2G allele could be a genetic marker of NIDDM in Japanese subjects. [Diabetologia (1994) 37: 536–539]
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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