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  • 1
    Electronic Resource
    Electronic Resource
    Decreased hepatic glucagon responses in Type 1 (insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 521-526 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 diabetes mellitus ; Glucagon ; Hepatic glucose production
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of glucagon infusion on hepatic glucose production during euglycaemia was evaluated in seven Type 1 (insulin-dependent) diabetic patients and in ten control subjects. In the diabetic subjects normoglycaemia was maintained during the night preceding the study by a variable intravenous insulin and glucose infusion. During the study endogenous insulin secretion was suppressed by somatostatin (450 μg/h) and replaced by insulin infusion (0.15 mU·kg−1·min−1). 3H-glucose was infused for isotopic determination of glucose turnover. Plasma glucose was clamped at 5 mmol/1 for 2 h 30 min and glucagon (1.5 ng· kg−1·min−1) was then infused for the following 3 h. Hepatic glucose production and glucose utilisation were measured during the first, second and third hour of the glucagon infusion. Basal hepatic glucose production (just prior to glucagon infusion) was similar in diabetic (1.2±0.3 mg·kg−1·min−1) and control (1.6±0.1 mg·kg−1·min−1) subjects. In diabetic patients hepatic glucose production rose slowly to 2.1±0.5 mg·kg−1·min−1 during the first hours of glucagon infusion and stabilized at this level (2.4±0.5 mg·kg−1·min−1) in the third hour. In control subjects hepatic glucose production increased sharply to higher levels than in the diabetic subjects (3.4±0.3 mg·kg−1·min−1) during the first and second hour of glucagon infusion (p〈0.05) and then gradually fell (2.9±0.4 mg·kg−1·min−1) during the third hour. In conclusion, when stimulated with glucagon at a physiologic plasma concentration diabetic patients had 1) an overall reduced hepatic glucose production response and 2) an abnormal sluggish response pattern. These abnormalities may imply inappropriate counter-regulation following a hypoglycaemic episode.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403290
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Basal and insulin stimulated substrate metabolism in tumour induced hypoglycaemia; evidence for increased muscle glucose uptake (1991)
    Springer
    Diabetologia 34 (1991), S. 17-20 
    Details
    ISSN: 1432-0428
    Keywords: Glucose turnover ; forearm technique ; intermediary metabolites ; euglycaemic and hypoglycaemic glucose clamp ; indirect calorimetry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary While it has very recently been reported that tumour induced hypoglycaemia is characterised by elevated production of insulin-like growth factor 2, the tissues responsible for induction of hypoglycaemia are largely unknown. We have investigated a patient with a large retroperitoneal mass and spontaneous hypoglycaemia. When compared to a reference population the patient displayed: (1) An increased glucose disposal rate and a five-fold elevation of forearm glucose uptake. (2) A decreased endogenous glucose production rate. (3) Decreased circulating levels of lipid intermediates. (4) Increased glucose oxidation and decreased lipid oxidation. (5) Low circulating levels of insulin-like growth factor 2 and insulin-like growth factor-binding protein-3 and normal levels of insulin-like growth factor 1. (6) Normal insulin sensitivity (euglycaemic glucose clamp). Blood concentrations of insulin, C-peptide, proinsulin, glucagon, growth hormone and catecholamines were within normal range, but the growth hormone response to hypoglycaemia was blunted. The data suggest that the mechanisms behind tumour induced hypoglycaemia are of systemic nature and that the tissue most prominently affected is striated muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404019
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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