Biomedical subjects
Erik Hägg
Publications and source records attributed to Erik Hägg.
Hemoglobin A1c can be analyzed in blood kept frozen at -80 degrees C and is not commonly affected by hemolysis in the general population.
The ability of glycated hemoglobin A(1c) (HbA(1c)) to predict diabetes is unknown, but could be evaluated by analyses on samples stored in biobanks. The stability of HbA(1c) in long-term stored samples is, however, unknown. Moreover, the effect of hemolysis on HbA(1c) in the general population is not assessed. To explore these questions HbA(1c) was determined in 3 groups (n = 717) of samples with storage times at -80 degrees C differing between 10 years and 2 months. The results were compared with HbA(1c) analyzed in fresh blood samples (n = 174). The subjects were free from diabetes and aged 40 to 60 years. HbA(1c) was analyzed by cation exchange high-performance liquid chromatography (HPLC). The mean HbA(1c) results for the fresh and long-term stored samples were 4.25% +/- 0.39 and 4.19% +/- 0.43, respectively (P = not significant [NS]). The HbA(1c) levels in fresh and 2-month stored samples were essentially equal. There was no correlation between HbA(1c) in the fresh samples and the hemolysis parameters reticulocytes, haptoglobin, or bilirubin. HbA(1c) is apparently stable in samples long-term stored at -80 degrees C and is not commonly affected by hemolysis in the general population. HbA(1c) analyzed on biobank samples could be used to assess the predictive value for future diabetes and relationship to other morbidity and mortality.
The effects of GH replacement therapy on cardiac morphology and function, exercise capacity and serum lipids in elderly patients with GH deficiency.
OBJECTIVES: To assess effects of GH replacement therapy on cardiac structure and function, exercise capacity as well as serum lipids in elderly patients with GH deficiency (GHD). PATIENTS AND METHODS: Thirty-one patients (six females, 25 males), aged 60-79 years (mean 68 years) with GHD on stable cortisone and thyroxine substitution were studied. All men with gonadotropin deficiency had testosterone and one woman had oestrogen replacement. They were randomized in a double-blind manner to GH or placebo treatment for 6 months, followed by another 12 months GH (Humatrope, Eli Lilly & Co, Uppsala, Sweden). GH dose was 0.017 mg/kg/week for 1 month and then 0.033 mg/kg/week divided into daily subcutaneous injections at bedtime. Echocardiography, exercise capacity tests and serum lipid measurements were performed at 0, 6, 12 and 18 months. RESULTS: During the 6-month placebo-controlled period there were no significant changes in the placebo group, but in the GH-treated group there was a significant increase in IGF-I to normal levels for age, with median IGF-I from 6.9 to 18.5 nmol/l, increase in resting heart rate and maximal working capacity. During the open GH study, IGF-I increased from 8.7 to 19.2 nmol/l at 6 months and 18.8 nmol/l at 12 months (P </= 0.001). At 6 months, in the open GH study group, a minor decrease in aortic outflow tract integral (VTI) from 21.8 to 20.7 cm (P = 0.031) and an increase in heart rate at rest from 63 to 67 bpm (P = 0.017), heart rate at maximum exercise from 138 to 144 bpm (P = 0.005) and maximum load at exercise from 142 to 151 Watts (P = 0.014) were seen. These changes were temporary and returned at 12 months with no significant difference from baseline values. Left ventricular dimensions and blood pressure showed no significant changes. At 6 months, in the open GH study group, there was a significant decrease in serum low-density lipoprotein (LDL) cholesterol from 3.7 to 3.4 mmol/l (P = 0.006), a decrease in LDL/HDL ratio from 3.4 to 3.1 (P = 0.036) and a decrease in serum total cholesterol from 5.6 to 5.3 mmol/l (P = 0.036). At 12 months, serum lipids showed same changes with a significant decrease in serum LDL cholesterol (P = 0.0008), in LDL/HDL ratio (P = 0.0005) and in serum total cholesterol (P = 0.049). Serum HDL cholesterol showed no significant change at 6 months, at 12 months a significant increase was seen from 1.2 to 1.4 mmol/l (P = 0.007). There were no significant changes in serum triglycerides. CONCLUSIONS: GH substitution to elderly patients with GHD caused only a transient increase in heart rate. At the end of the 12 months there were no significant changes on cardiac noninvasive structural and functional parameters. Maximal working capacity transiently improved. Thus, the therapy was safe without negative effects on cardiac structural and functional noninvasive parameters. Lipid profiles improved with reduction of serum LDL cholesterol accompanied by significant improvement of LDL/HDL ratio and serum HDL cholesterol after 12 months treatment.
[Placebo--something to believe in?].
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Chronic infusion of a melanocortin receptor agonist modulates dopamine receptor binding in the rat brain.
Previous studies have shown that melanocortin peptides have facilitatory effects on dopaminergic neurotransmission. In the present study we tested the hypothesis that chronic exposure to melanocortin receptor agonists causes a prolonged release of dopamine resulting in changes in the expression of dopamine receptor subtypes. Using an autoradiographic approach we found that a 2 week intracerebroventricular infusion of the melanocortin receptor agonist melanotan-II induced changes in dopamine D(1)-like and D(2)-like receptor binding in several regions of the rat brain. D(1)-like receptor binding was increased in the nucleus accumbens and the caudate putamen, but reduced in the substantia nigra (reticular part), whereas D(2)-like receptor binding was reduced in the caudate putamen, but increased in the periaqueductal grey, substantia nigra (compact part) and the ventral tegmental area. These data suggest that chronic infusion of a melanocortin receptor agonist alters the activity of dopaminergic neurons in the ventral tegmental area and substantia nigra, and support the hypothesis that melanocortin peptides may regulate the activity of central dopamine neurons.