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  • 1
    ISSN: 1432-1440
    Keywords: Lipoprotein(a) ; Hyperthyroidism ; Cholesterol ; Apolipoproteins ; Lipoprotein receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Lipoprotein(a) [Lp(a)] is a low-density lipoprotein (LDL) particle in which apolipoprotein B-100 (apoB) is attached to a glycoprotein called apolipoprotein(a) [apo(a)]. Apo(a) has several genetically determined phenotypes differing in molecular weight, to which Lp(a) concentrations in plasma are inversely correlated. High plasma levels of Lp(a) are associated with atherosclerotic diseases. It is therefore of interest to study whether factors other than the apo(a) gene locus are involved in the regulation of Lp(a) concentrations. We measured plasma concentrations of Lp(a) and other lipoproteins and determined apo(a) phenotypes in 31 patients with hyperthyroidism, before and after the patients had become euthyroid by treatment. The mean concentration of LDL cholesterol rose from 2.67 to 3.88 mmol/l (P〈0.01), apoB rose from 0.79 to 1.03 g/l (P〈0.01), and the median Lp(a) concentration increased from 9.74 to 18.97 mg/dl (P〈0.01) on treatment. Lp(a) concentrations were inversely associated to the size of the apo(a) molecule both before (P〈 0.01) and after treatment (P〈0.01). The increase in Lp(a) was significant patients with high molecular weight apo(a) phenotypes (n = 9; P〈0.01) and in patients with low molecular weight apo(a) phenotypes (n=16; P〈 0.01), but not in those with apo(a) “null types” (n = 6; P = 0.5). The low levels LDL cholesterol and apoB in untreated hyperthyroidism may result from increased LDL receptor activity. The increase in Lp(a) levels were not correlated with the increase in LDL cholesterol or apoB. Most other clinical evidence indicates that the LDL receptor is not important in Lp(a) catabolism, and we suggest that the low Lp(a) levels seen in thyroid hormone excess are caused by an inhibition of Lp(a) synthesis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Key words IDDM ; insulin analogues ; metabolic control.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Recombinant DNA technology allows the production of insulin analogues with faster absorption rates from subcutaneous tissue as compared to soluble human insulin. The human insulin analogue B10Asp (mono/dimeric) is absorbed twice as fast as soluble human insulin (hexameric). A double blind, randomised crossover study with a 1-month run-in period and two 2-month treatment periods was performed in 21 male insulin-dependent diabetic (IDDM) patients aged 18–40 years in order to compare the metabolic control obtained with equimolar doses of the analogue B10Asp vs soluble human insulin (Actrapid) given as mealtime insulin and intermediate acting isophane insulin (Protaphane) at bedtime. At the end of each 2-month study period, the patients were admitted to the metabolic ward. We found significantly higher plasma insulin/analogue levels after breakfast, lunch and dinner with B10Asp as compared to Actrapid (p 〈 0.05). The plasma insulin/analogue levels were significantly lower before lunch and dinner with B10Asp as compared to Actrapid (p 〈 0.05). Also, the plasma insulin/analogue level tended to be lower at bedtime when comparing B10Asp to Actrapid. The 24-h blood glucose profiles showed identical fasting blood glucose, significantly lower blood glucose after breakfast with the analogue (p 〈 0.05), no differences in blood glucose after lunch and dinner but a significantly higher blood glucose at midnight using the analogue (p 〈 0.05). The overall 24-h mean blood glucose concentrations, the daily insulin dose, HbA1 c, diet, home blood glucose monitoring and frequency of hypoglycaemia were almost identical in the two treatment periods. In conclusion, the overall glycaemic control remained unchanged and quite good when Actrapid was exchanged dose for dose with the insulin analogue B10Asp in IDDM patients treated with a basal bolus regime. [Diabetologia (1995) 38: 592–598]
    Type of Medium: Electronic Resource
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