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  • 1
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; B cell function ; C-peptide ; glycaemic control
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Within 24h of diagnosis, 15 consecutive Type 1 (insulin-dependent) diabetic patients were allocated at random to one of two treatment groups: group A (n=9, mean age: 28 years, range: 17–35 years) was treated conventionally with one or two daily doses of insulin; group B (n=6, mean age: 27 years, range: 21–37 years) was treated with nine daily injections of fast-acting insulin for ten days and thereafter conventionally as for group A. The mean diurnal blood glucose concentration during the initial ten days of insulin treatment was 11.7±0.5mmol/l (mean±SEM) in group A and 6.4±0.3 mmol/l in group B (p〈0.01). Pancreatic B cell function was evaluated 1, 7, 14, 90, and 180 days after the start of insulin treatment from the C-peptide response to a standard meal. At one and seven days after diagnosis, no difference was found in B cell function between the two groups. After 14 days, the amount of C-peptide secreted during the test meal was 18.0±2.6 nmol (mean±SEM) in group A compared with 29.0+3.6 nmol in group B (p〈0.05). After 90 and 180 days, no difference was demonstrated in B cell function. The maximal B cell function observed was similar in the two groups, but occurred earlier in group B (at 14 days) than in group A (at 90 days) (p〈0.05). This study indicates that strict initial glycaemic control may lead to an earlier improvement in B cell function, but that this improvement is of short duration.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Type 1 diabetes ; hypoglycaemia ; B cell function ; glucagon ; glucose recovery ; lipolysis ; ketogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Hormonal, metabolic and cardiovascular responses to insulin induced hypoglycaemia were investigated in seven Type 1 (insulin-dependent) diabetic patients with residual B cell function, eight Type 1 diabetic patients without B cell function and six healthy subjects. No differences were found between the diabetic groups regarding nadir of glucose and rate of recovery to normoglycaemia. The patients with residual B cell function had a glucagon response to hypoglycaemia which was close to that of normal subjects. In patients without B cell function, the glucagon response to hypoglycaemia was present, albeit significantly smaller than in the patients with preserved B cell function (0.025 ng/ml, range 0.007–0.042 versus 0.054 ng/ml, range 0.029–0.087). The group without B cell function had signs of an exaggerated rate of lipolysis and ketogenesis compared with the patients with B cell function and the normal subjects.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Chronic pancreatitis ; B cell function ; exocrine pancreatic function ; C-peptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Exocrine pancreatic function was evaluated by a Lundh meal test and a secretin-cholecystokinin test in 16 patients with chronic pancreatitis. B cell function was assessed by measuring the concentration of C-peptide after stimulation with oral glucose and intravenous glucagon. The C-peptide response to intravenous glucagon and oral glucose was closely correlated (r = 0.88,p 〈 0.01). Plasma C-peptide after glucagon was significantly correlated to the post-prandial concentration of lipase (r = 0.72,p 〈 0.001), amylase (r=0.64,p 〈 0.05) and to amylase output (r = 0.64,p 〈 0.05). Eight out of nine patients treated with insulin had residual B cell function, but it diminished significantly with increasing duration of diabetes. We conclude that B cell function is correlated to pancreatic enzyme secretion and that patients with insulin-treated diabetes secondary to chronic pancreatitis have a residual insulin secretion similar to that of patients with Type 1 (insulin-dependent) diabetes.
    Type of Medium: Electronic Resource
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