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  • 1
    Electronic Resource
    Electronic Resource
    Circulating insulin-like growth factor I in Type 1 (insulin-dependent) diabetic patients with retinopathy (1989)
    Springer
    Diabetologia 32 (1989), S. 753-758 
    Details
    ISSN: 1432-0428
    Keywords: Somatomedin ; carrier protein ; diabetes complications
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The relationship between insulin-like growth factor I (IGF I) and diabetic retinopathy was investigated. This somatomedin circulates bound to at least two large carrier proteins with molecular weights of approximately 150,000 and 35,000. Total and protein binding profiles of insulin-like growth factor I were determined in the serum of 18 patients who had had Type 1 (insulin-dependent) diabetes for 15–20 years, but had no signs of nephropathy and a similar degree of mild subclinical neuropathy. Nine had preproliferative or proliferative retinopathy and 9 had little or no background retinopathy but there was no difference in diabetes duration, insulin doses or glycaemic control between the two groups. In the latter group, the amounts of the somatomedin I and the serum profiles were similar to those in 9 healthy control subjects. In patients with advanced retinopathy, however, binding of insulin-like growth factor I to the carrier proteins was significantly altered. Binding to the low molecular weight protein increased to 140% whereas binding to the large molecular weight protein decreased to 70% of the normal level. In the latter Type 1 diabetic patients total serum insulin-like growth factor I was decreased to 60% of the normal level (p〈0.02). When the alteration in serum profile was adjusted for, the level of somatomedin associated with the small carrier complex was normal whereas that associated with the large carrier complex was reduced by almost 60% in Type 1 diabetic patients with retinopathy. It is proposed that the total circulating somatomedin level is low in advanced diabetic retinopathy. Furthermore, changes in. the carrier binding of insulin-like growth factor I rather than in the total circulating level of the somatomedin may be involved in diabetic retinopathy.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00274537
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Renal and splanchnic exchange of human biosynthetic C-peptide in Type 1 (insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 423-428 
    Details
    ISSN: 1432-0428
    Keywords: Glucose utilization ; Type 1 (insulin-dependent) diabetes mellitus ; human C-peptide ; glucagon ; renal uptake ; hepatic uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Biosynthetic human C-peptide or NaCl (154 mmol·l−1) was given intravenously to 13 Type 1 (insulin-dependent) diabetic patients to determine the renal and splanchnic exchange of C-peptide. Catheters were inserted percutaneously into an artery and a renal and hepatic vein. Infusions of C-peptide were given for 60 min at two dose levels (5 and 30 pmol·kg−1·min−1). Insulin was infused throughout the study (0.5 mU·kg−1·min−1) and plasma glucose was kept constant by a variable glucose infusion. The regional blood flows were measured by indicator dilution techniques. In 11 of the 13 patients basal C-peptide levels were not detectable. The arterial steady-state C-peptide concentration was 0.81±0.10 nmol·l−1 and 2.33±0.30 nmol·l−1 at the low and high rate infusions, respectively. Renal uptake was 124±18 pmol·min−1 at the low infusion corresponding to 39% of the infused amount. At the higher dose C-peptide infusion renal uptake increased to 155±21 pmol·min−1 (p〈0.05). Urinary excretion of C-peptide was 7±2 pmol·min−1 at the low dose infusion and increased to 34±6 pmol·min−1 at the high dose infusion (p〈0.01). The proportions of infused amount excreted were fairly constant and between 2% and 3%. No net exchange of C-peptide was found across the splanchnic vascular bed. The rate of glucose infusion had to be increased by 35% during the low dose C-peptide, but not during NaCl infusion in order to maintain a constant plasma glucose concentration. Arterial plasma concentrations of noradrenaline increased by 15–25% during both C-peptide and NaCl infusions. It is concluded that in patients with Type 1 diabetes (a) the kidney is the primary site of C-peptide removal, (b) renal metabolism rather than urinary excretion is the dominating process for C-peptide elimination (c) the excreted proportions of an infused amount of C-peptide were fairly constant between 2% and 3% and (d) no hepatic C-peptide catabolism could be detected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403181
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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