Search Results

You are looking at 1 - 4 of 4 items for

  • Author: Henning Grønbæk x
  • All content x
Clear All Modify Search
Restricted access

Marcus Howell, Hans Ørskov, Jan Frystyk, Allan Flyvbjerg, Henning Grønbæk, and Marie Foegh

Howell M, Ørskov H, Frystyk J. Flyvbjerg A, Grønbæk H, Foegh M. Lanreotide, a somatostatin analogue, reduces insulin-like growth factor I accumulation in proliferating aortic tissue in rabbits in vivo. A preliminary study. Eur J Endocrinol 1994;130:422–5. ISSN 0804–4643

Coronary artery restenosis following percutaneous transluminal angioplasty occurs with a very high incidence. Major efforts have been aimed at revealing the mechanisms and at developing therapies that might prevent or delay the myointimal proliferation. Most clinical trials have been unsuccessful. Endothelial denudation was induced in 30 rabbits using balloon catheterization of iliac arteries and aorta. Immunoreactive insulin-like growth factor I (IGF-I) was measured in arterial tissue samples obtained 1, 2 and 4 days postoperatively using a double extraction procedure to remove IGF-I binding proteins. Half of the animals were treated with subcutaneous injections of lanreotide, 10 μg/kg twice daily, and the other half served as controls. In the latter group, arterial IGF-I was unaltered from baseline at day 1 and increased by 300 and 400% at days 2 and 4. No increase was observed in the rabbits treated with lanreotide. The results indicate that initial local accumulation of IGF-I may be one of the mechanisms involved in myointimal proliferation after experimental arterial injury. The reduction of local IGF-I accumulation by lanreotide may be involved in the previously observed reduction in myointimal proliferation.

Hans Ørskov, Institute of Experimental Clinical Research, University Hospital, DK-8000 Aarhus C, Denmark

Free access

Peter Holland-Fischer, Hendrik Vilstrup, Jan Frystyk, Dennis Tønner Nielsen, Allan Flyvbjerg, and Henning Grønbæk

Objective

Insertion of a transjugular intrahepatic porto-systemic shunt (TIPS) into patients with liver cirrhosis usually induces a gain in body cell mass. Changes in the IGF system in favor of anabolism may be involved. We, therefore measured blood concentrations of the components of the IGF system in cirrhosis patients before and after elective TIPS.

Design and methods

The study comprised 17 patients and 11 healthy controls. Patients were examined before and 1, 4, 12, and 52 weeks after TIPS. Biochemical analyses of the IGF system were compared with changes in body composition (bioimpedance analysis), glucose and insulin, and metabolic liver function (galactose elimination capacity).

Results

After TIPS, body cell mass rose by 3.2 kg (95% confidence interval (CI): 1.0–5.5) at 52 weeks, in correlation with baseline liver function (r 2=0.22; P=0.03). Peripheral blood concentrations of total IGF1 and 2, bioactive IGF1, and the IGF-binding proteins (IGFBP-1, -2, and -3) remained unchanged throughout the study period. There was no change in fasting glucose, whereas fasting insulin rose by 40% (CI: 11–77%) and glucagon by 58% (CI: 11–132%) from baseline to 52 weeks after TIPS.

Conclusion

Our data confirm that TIPS was associated with an increase in body cell mass in patients with liver cirrhosis, but without any change in the circulating IGF system. Thus, the results do not support the notion that effects on the circulating IGF system are involved in the anabolic effects of TIPS insertion.

Restricted access

Liv Bjørn-Hansen Gøtzsche, Ninna Rosenqvist, Henning Grønbæk, Allan Flyvbjerg, and Ole Gøtzsche

Gøtzsche LB-H, Rosenqvist N. Grønbœk H, Flyvbjerg A, Gøtzsche O. Increased number of myocardial voltage-gated Ca2+ channels and unchanged total β-receptor number in long-term streptozotocin-diabetic rats. Eur J Endocrinol 1996;134:107–13. ISSN 0804–4643.

In order to elucidate further the abnormal myocardial Ca+ metabolism in diabetes mellitus, voltage-gated Ca2+ channels and β-receptors were quantified in myocardial membranes of short- and long-term diabetic rats. Diabetes was induced by an injection of streptozotocin (STZ). Animals were killed 2, 4, 7, 90 and 200 days after STZ. A group of diabetic animals were treated with insulin for 20 days following 180 days of untreated diabetes. Diabetic animals developed low triiodothyronine syndrome. During short-term diabetes, the maximum binding capacity (MBC) for Ca+ channels was reduced by 25% at day 4 p<0.05) and the β-receptor MBC was reduced by 48% p<0.05). A normalizing tendency was observed at day 7 for both receptor types; insulin-treated rats did not differ from controls at that time. After 90 and 200 days of untreated diabetes the Ca+ channel MBC had increased by 36% and 27%, respectively (p < 0.05). Twenty days of strictly regulated blood glucose following 180 days of untreated diabetes totally normalized the Ca+ channel MBC. This is in contrast to a previous report where insulin treatment did not normalize the Ca+ channel MBC. Total β-receptor MBCs did not differ from control values 90 and 200 days after STZ. In conclusion, an increase in rat myocardial Ca2+ channel MBC during long-term diabetes was fully normalized by short-term insulin treatment. The increase in sarcolemmal Ca2+ channels could serve to compensate for a defect coupling of the β-receptor to adenylate cyclase. An elevated Ca+ channel number may, at least theoretically, lead to increased Ca2+ flow across the cardiac sarcolemma and in this way contribute to the diabetic cardiomyopathy by increasing the intracellular Ca2+ concentration.

Liv Bjørn-Hansen Gøtzsche, Dept. of Internal Medicine M, (Diabetes and Endocrinology), Aarhus Kommunehospital, University Hospital of Aarhus, DK-8000 Aarhus C, Denmark.

Restricted access

Mia Demant, Malte Palm Suppli, Signe Foghsgaard, Lise Gether, Magnus Frederik Gluud Grøndahl, Niels Bjørn Dalsgaard, Sigrid S Bergmann, Amalie Rasmussen Lanng, Lærke S Gasbjerg, Martin Thomasen, Jonatan Ising Bagger, Charlotte Strandberg, Merete Juhl Kønig, Henning Grønbæk, Ulrik Becker, Jens J Holst, Joachim Knop, Matthew Paul Gillum, Tina Vilsbøll, and Filip K. Knop

Aims/hypothesis. Metabolic effects of intermittent unhealthy lifestyle in young adults are poorly studied. We investigated the gluco-metabolic and hepatic effects of participation in Roskilde Festival (one week of binge drinking and junk food consumption) in young, healthy males.

Methods. Fourteen festival participants (FP) were studied before, during and after one week’s participation in Roskilde Festival. Fourteen matched controls (CTRL) who did not participate in Roskilde Festival or change their lifestyle in other ways were investigated along a similar timeline.

Results. The FP group consumed more alcohol compared to their standard living conditions (2.0±3.9 vs 16.3±8.3 units/day, p<0.001). CTRLs did not change their alcohol consumption. AUC for glucose during OGTT did not change in either group. C-peptide responses increased in the FP group (320±31 vs 376±25 nmol/l×min, p=0.055) and the Matsuda index of insulin sensitivity decreased (6.2±2.4 vs 4.7±1.4, p = 0.054). AUC for glucagon during OGTT increased in the FP group (1,115±114 vs 1,599±183 pmol/l×min, p=0.003) together with fasting fibroblast growth factor 21 (FGF21) (62±30 vs 132±72 pmol/L, p<0.001), growth differentiation factor 15 (GDF5) (276±78 vs 330±83 pg/mL, p=0.009) and aspartate aminotransferase (AST) levels (37.6±6.8 vs 42.4±11 U/l, p=0.043). Four participants (29%) developed ultrasound-detectable steatosis and mean strain elastography-assessed liver stiffness increased (p=0.026) in the FP group.

Conclusions/interpretation. Participation in Roskilde Festival did not affect oral glucose tolerance, but was associated with a reduction in insulin sensitivity, increases in glucagon, FGF21, GDF15 and AST and lead to increased liver stiffness and, in 29% of the participants, ultrasound-detectable hepatic steatosis.