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Biomedical subjects

K I Birkeland

Publications and source records attributed to K I Birkeland.

At least 19 recordsLinked to original sources
PubMed2006

Blood glucose lowering by means of lifestyle intervention has different effects on adipokines as compared with insulin treatment in subjects with type 2 diabetes.

AIMS/HYPOTHESIS: Adipokines may be important in mediating signals from adipocytes to insulin-sensitive tissue and vasculature. We studied the effect of different glucose-lowering therapies on serum levels of plasminogen activator inhibitor-1 (PAI-1), high-sensitivity C-reactive protein (hs-CRP), TNF-alpha, leptin, adiponectin and ghrelin in patients with type 2 diabetes. SUBJECTS AND METHODS: Twenty-eight patients with poorly controlled type 2 diabetes who were receiving oral hypoglycaemic agents were allocated to one of the following groups, and treated for 1 year: (1) lifestyle intervention (L); (2) insulin treatment (I); and (3) combined treatment (L+I). RESULTS: Similar improvements in glycaemic control occurred in all three groups. There was a reduction in body weight of 3.0 kg (median) (95% CI -5.9 to -2.0) in group L, whereas in groups L+I and I body weight increased by 3.5 kg (95% CI 1.5-4.9) and 4.9 kg (95% CI -3.1 to 8.2), respectively. By trend analyses, group L had reduced levels of PAI-1 (p=0.002), hs-CRP (p<0.0001) and TNF-alpha (p=0.006), while no significant changes were observed in the levels of leptin or adiponectin. In group I, the median levels of PAI-1 (p=0.008), TNF-alpha (p=0.058) and leptin (p=0.004) increased. In the L+I group there was a reduction in PAI-1 levels (p=0.014) and an increase in levels of leptin (p<0.001). The differences in changes in the levels of PAI-1, hs-CRP, TNF-alpha and leptin between groups were also significant (all p<0.01). CONCLUSIONS/INTERPRETATION: Improvement of glycaemic control through lifestyle intervention in type 2 diabetes had more beneficial effects on adipokine levels than when the same lowering of HbA(1c) was achieved with insulin treatment.

Aged↗
PubMed2006

Undiagnosed dysglycaemia and inflammation in cardiovascular disease.

BACKGROUND: Cardiovascular (CV) disease is associated with increased levels of glucose, but the prevalence of dysglycaemia in CV diseases is not fully known. The study examined the prevalence of unknown dysglycaemia and its association with inflammation in Caucasian patients with ischaemic vascular complications, i.e. coronary artery disease (CAD), cerebrovascular disease (CVD) and peripheral artery disease (PAD). MATERIALS AND METHODS: This case-controlled study involved 149 patients (mean age 68 years) hospitalized for CAD, PAD or CVD and 59 control-subjects (CTR) free from CV-disease. The prevalence of dysglycaemia according to WHO/ADA criteria (impaired fasting glycaemia, impaired glucose tolerance or diabetes mellitus) was assessed by a 75-g oral glucose tolerance test. Inflammatory parameters were analyzed in fasting samples. RESULTS: Dysglycaemia was found in 49%, 55% and 57% of patients with CAD, CVD and PAD, respectively; all were significantly higher than among the controls (29%). The odds ratio (95% CI) for being dysglycaemic were 1.7 (1.04-2.77), 1.9 (1.19-3.06) and 2.0 (1.25-3.19) for CAD, CVD and PAD, respectively. Inflammatory markers (the total leucocyte count, soluble tumour necrosis factor-receptor type I, C-reactive protein) were elevated in patient groups and tended to increase with increasing blood glucose levels in all groups. The levels of the anti-inflammatory cytokine transforming growth factor-beta1 and insulin-like growth factor binding protein 3 were lowered in patients with CAD and, in patients with PAD, the former was inversely related to the levels of the blood glucose. CONCLUSIONS: Undiagnosed dysglycaemia was common in patients with ischaemic CV manifestations regardless of vascular bed involved. Inflammation was associated in a dosage-related manner to glucose levels.

Adult↗
PubMed2005

Ethnicity and sex are strong determinants of diabetes in an urban Western society: implications for prevention.

AIMS/HYPOTHESIS: This study was conducted to investigate the prevalence of diabetes and its association with ethnicity and sex, to identify subgroups at special risk. METHODS: We performed a population-based cross-sectional survey of 30- to 67-year-olds in an area of Oslo with low socio-economic status, and collected data using questionnaires, physical examinations and serum analyses for the 2,513 participants (attendance rate 49.3%). RESULTS: In the age group 30-59 years, mean BMI was 28.5 (95% CI: 27.5-29.6) for South Asian women, 26.1 (25.9-26.4) for Western women, 26.7 (26.1-27.4) for South Asian men and 27.2 (26.9-27.5) for Western men. The diabetes prevalence rates were 27.5% (18.1-36.9) for South Asian women, 2.9% (1.9-3.4) for Western women, 14.3% (8.0-20.7) for South Asian men and 5.9% (4.2-7.5) for Western men. The age-adjusted odds ratio (OR) for diabetes for women vs men was 1.9 (0.9-4.1) for South Asians, and 0.4 (0.3-0.6) for the Western population (p<0.001). The age-adjusted OR for diabetes for South Asians vs Westerners was 11.0 (5.8-21.1) for women and 3.0 (1.6-5.4) for men, and after adjustment for WHR the ORs were 7.7 (3.9-15.3) for women and 2.6 (1.4-4.9) for men. After additional adjustments for physical activity, education, body height and fertility for women, the OR was 6.0 (2.3-15.4) for women and 1.9 (0.9-4.0) for men. CONCLUSIONS/INTERPRETATION: The alarmingly high prevalence of diabetes among South Asian women in Norway needs further investigation, as it has considerable public health implications. Ethnic differences in OR for diabetes persisted after adjustment for age, adiposity, physical activity and education. These differences were still present for women after additional adjustment for body height and fertility.

Adolescent↗
PubMed2005

Insulin gene variable number of tandem repeats is associated with increased fat mass during adolescence in non-obese girls.

Obesity and related disorders have become a major health problem. Understanding the interaction between genetic and environmental factors influencing the susceptibility to develop obesity is important when pinpointing people at risk. In a longitudinal study of 256 non-obese adolescents, the influence of the insulin gene (INS) variable number of tandem repeats (VNTR) on anthropometric measures and fat mass was investigated. The adolescents were examined at the age of 12.4 (2.3) (mean, SD) and 16.2 (2.3) years, and at follow-up with dual x-ray absorptiometry (DXA) for measurement of body composition. INS VNTR classes I and III alleles were investigated using the -23T/A single nucleotide polymorphism as a surrogate marker. There was a non-significant trend towards increased body mass index (BMI) and fat mass with the class III allele in girls. Homozygotes for the INS VNTR class III allele had a greater increase in BMI compared with those that were homozygous or heterozygous for the class I allele (3.8 (1.6) versus 2.4 (1.9) kg/m2, p = 0.03), and they had higher fat mass (36.4 (3.9) versus 31.3 (6.8)%, p = 0.02) at follow-up. Our finding that homozygosity of the INS VNTR class III allele seems to predispose to increased weight gain and fat mass raises the possibility that this genotype may be one of the important factors in the gene-environment interaction that eventually results in overweight and insulin resistance.

Absorptiometry, Photon↗
PubMed2005

An intensified lifestyle intervention programme may be superior to insulin treatment in poorly controlled Type 2 diabetic patients on oral hypoglycaemic agents: results of a feasibility study.

AIMS: The aims of this study were to assess whether, in Type 2 diabetic patients with inadequate glycaemic control on oral hypoglycaemic agents (OHA), a lifestyle intervention programme based on exercise and diet counselling (i) was as effective as insulin treatment in controlling blood glucose, and (ii) could prevent the weight gain usually accompanying the introduction of insulin treatment. METHODS: Thirty-eight Type 2 diabetic subjects treated with OHA, HbA(1c) 8-10.5% and body mass index (BMI) 26-40 kg/m2, were randomized to the following treatments: (i) lifestyle intervention (L), (ii) lifestyle intervention + insulin treatment (L+I) and (iii) insulin treatment alone (I). RESULTS: There was a reduction in HbA(1c) of -1.2 (interquartile range 1.0), -1.0 (1.7) and -1.5 (2.5)% in group L, L+I and I, respectively, and all treatment groups achieved beneficial changes in blood lipid variables. There was no significant difference between the groups in the change observed in levels of HbA(1c) between start and 12 months of treatment (P = 0.74). There was a significant difference in weight changes between groups (P < 0.01): group L reduced weight by median -3.0 (4.0) kg, groups L+I and I increased weight by 3.5 (3.4) and 4.9 (6.9) kg, respectively. CONCLUSIONS: Lifestyle intervention was as effective as insulin treatment in improving glycaemic control in poorly controlled subjects with Type 2 diabetes, and resulted in weight loss during the intervention year. However, glycaemic control deteriorated and body weight increased in the lifestyle intervention group 1 year after the intervention stopped.

Administration, Oral↗
PubMed2003

The relationships between dehydroepiandrosterone sulphate (DHEAS), the intensity of Schistosoma mansoni infection and parasite-specific antibody responses. A cross-sectional study in residents of endemic communities in north-east Ethiopia.

There are speculations that the puberty-related hormone dehydroepiandrosterone sulphate (DHEAS) might influence the intensity of infection and immune responses during Schistosoma infections. We studied the relationships between DHEAS, intensity of Schistosoma mansoni infection and humoral immune responses in 135 residents of Ethiopia. Serum levels of eight antibody isotypes against worm and egg antigens were determined by ELISA. DHEAS was measured with an immunoluminometric assay. There was a significant negative correlation between serum levels of DHEAS and intensity of S. mansoni infection. A significant increase in serum levels of DHEAS in the age group 15-19 years was accompanied by a progressive decline in the intensity of infection. Peak level of DHEAS coincided with the lowest intensity of infection in the age group 20-29 years. Multiple regression analysis showed that DHEAS alone had a significant (p<0.0001) negative effect when the effect of age was removed. Age also had a significant (p<0.0001) negative effect on the intensity of infection, after removing the effect of DHEAS. The two predictive variables accounted for 34.4% of the decline in the intensity of infection. Age accounted for 24.9%, whereas DHEAS accounted for 15.2% when the effect of each of the variables was removed. DHEAS had significant negative effects on AWA-specific IgG (p=0.02) and IgG1 (p=0.018) and SEA-specific IgG1 (p=0.009), after adjusting for the effect of age.

Adolescent↗
PubMed2003

Heterogeneity of non-insulin-dependent diabetes expressed as variability in insulin sensitivity, beta-cell function and cardiovascular risk profile.

AIMS: The present study investigated the variability in insulin sensitivity and beta-cell function and their relationship to anti-glutamic acid decarboxylase (GAD) positivity and the metabolic syndrome in a group of patients with non-insulin-dependent diabetes mellitus (NIDDM). METHODS: Fifty-four subjects aged 59.5 +/- 6.1 (mean +/- SD) years with NIDDM for 7.9 +/- 3.9 years referred to hospital due to poor glycaemic control, were investigated. Insulin sensitivity was determined by the euglycaemic hyperinsulinaemic glucose clamp technique as the glucose disposal rate relative to the insulin level obtained (GDRI), and also estimated with the homeostasis model assessment (HOMA-S). beta-cell function was measured by assaying the fasting and glucagon-stimulated C-peptide levels and with the HOMA-B. RESULTS: The insulin sensitivity varied 18-fold between subjects when estimated with the clamp and six-fold when estimated with HOMA-S, and was lower the more criteria for the metabolic syndrome present (P = 0.0001 by anova). The beta-cell function varied four-fold when measured as stimulated C-peptide, and eight-fold when estimated with the HOMA-B. The levels of fasting C-peptide and HOMA-B values tended to be lower in anti-GAD+ (n = 11) than in anti-GAD-subjects (P = 0.06 and P = 0.08, respectively). From previously published coronary risk charts, we estimated the 10-year risk of a coronary heart disease (CHD) event to be > 20% in 17 of 39 patients free from cardiovascular disease at the time of study, 16 of whom qualified for a diagnosis of the metabolic syndrome. CONCLUSIONS: The wide variations in insulin sensitivity and beta-cell function found among subjects with NIDDM support the notion that the disorder is highly heterogeneous. Reduced insulin sensitivity was clearly related to the metabolic syndrome and an increased risk for CHD.

Adult↗
PubMed2003

Increased serum levels of the specific AGE-compound methylglyoxal-derived hydroimidazolone in patients with type 2 diabetes.

A time-delayed fluorescence immunoassay was developed for the determination of serum levels of methylglyoxal (MG)-derived hydroimidazolone using a monoclonal antiserum raised against Nalpha-acetyl-Ndelta-(5-hydro-5-methyl)-4-imidazolone, Europium-labeled anti-mouse IgG antiserum as indicator, and MG modified bovine serum albumin (BSA) as standard. Serum levels of hydroimidazolone were measured in 45 patients with type 2 diabetes aged 59.4 +/- 6.1 (mean +/- SD) years and with duration of diabetes of 7.3 +/- 3.1 years, and in 19 nondiabetic controls aged 56.3 +/- 4.3 years. The serum levels of hydroimidazolone were significantly higher in patients compared to controls: median, 3.0 (5-95 percentile, 1.6 to 5.4) U/mg protein versus 1.9 (1.2 to 2.8) U/mg protein (P =.0005). Significant positive correlations were observed between the serum levels of hydroimidazolone and serum levels of advanced glycation end products (AGEs), measured with a polyclonal anti-AGE antibody: r = 0.59 for patients (P <.0001), and r = 0.65 for controls (P =.002). Similarly, significant correlations were also found between serum levels of hydroimidazolone and N(epsilon)-(carboxymethyl)-lysine (CML): r = 0.36 in patients and r = 0.55 for controls (both P =.02). Serum hydroimidazolone levels did not correlate with fasting plasma glucose or hemoglobin A(1c) (HbA(1c)) levels. The observed differences between patients with diabetes and nondiabetic controls seem to be comparable to differences measured for other AGE compounds.

Diabetes Mellitus, Type 2↗
PubMed2000

[Prevention of cardiovascular disease in type 2 diabetes].

BACKGROUND: Patients with type 2 diabetes have a high risk of morbidity and premature mortality from cardiovascular disease. Epidemiological studies show that many of the risk factors are the same as in non-diabetic subjects. At present there are sufficient data in the literature to recommend prophylactic measures to be initiated in diabetic patients. MATERIAL AND METHODS: We review major studies relevant for prophylactic measures against cardiovascular disease in patients with type 2 diabetes, and suggest Norwegian recommendations. RESULTS: All patients should be advised to adhere to a healthy life style including an appropriate diet, physical exercise and no smoking. Treatment of hyperglycaemia is primarily indicated in order to improve quality of life and reduce the risk of microvascular complications, as it still remains to be proven if glucose lowering therapy may protect against macrovascular disease. Pharmacological prophylactic therapy with acetylsalicylic acid, anti-hypertensive agents and lipid lowering drugs are indicated in high-risk patients. IMPLICATIONS: Several pharmacological and non-pharmacological interventions may protect type 2 diabetic patients from premature cardiovascular morbidity and mortality. Anti-hypertensive treatment may protect diabetic patients both from microvascular and macrovascular disease and premature death.

Antihypertensive Agents↗
PubMed2000

[Hypoglycemic treatment of type 2 diabetes].

BACKGROUND: Hyperglycaemia in type 2 diabetes results from reduced beta-cell function and insulin resistance. The treatment of type 2 diabetes must be targeted against both conditions to reduce symptoms of hyperglycaemia and the risk of diabetic late complications. MATERIAL AND METHODS: In this review we cover the recent scientific documentation from long term studies on treatment effects. We also discuss the different treatments available. RESULTS: Recent clinical trials have shown that lowering blood glucose levels over time significantly reduces development of microvascular complications in type 2 diabetes. There are several treatment options available which make adequate blood glucose control possible in patients with type 2 diabetes. INTERPRETATION: A reduction in the development of microvascular complications in type 2 diabetes is an achievable goal.

Blood Glucose↗
PubMed2000

[The obesity epidemics--do diet pills have a place in the treatment?].

BACKGROUND: Many experts consider obesity a chronic disease that may require long-term therapy. A loss of 5-15% of body weight is associated with improvements in cardiovascular risk factors and morbidity. However, most studies show that the majority of patients who lose weight relapse. Patients may be unable to maintain a low energy intake when confronted with an almost limitless supply of food. Moreover, a number of physiological mechanisms favour a set point for body weight, that may be altered with anti-obesity drugs. MATERIAL AND RESULTS: In the current paper we describe actions and effects of current anti-obesity drugs. The centrally acting drug, sibutramine, is an adrenaline and serotonine re-uptake inhibitor which was recently approved in the USA for obesity. The USA, the European Union and Norway have approved orlistat, a pancreatic lipase inhibitor for weight reduction for up to two years. Patients must maintain a low fat intake in order to avoid gastrointestinal discomfort. In recent studies, orlistat and diet reduced body weight by 9% versus 6% on placebo and diet. No studies have documented long-term safety of anti-obesity drugs. INTERPRETATION: Treatment of a lifestyle-related disease like obesity with medications is controversial, however, such treatment may not differ substantially from treatment of type II diabetes, hyperlipidaemia or hypertension.

Anti-Obesity Agents↗
PubMed2000

Effect of rhEPO administration on serum levels of sTfR and cycling performance.

PURPOSE: We assessed the possibility of using soluble transferrin receptor (sTfR) as an indicator of doping with recombinant erythropoietin (rhEPO). METHODS: A double-blind, placebo-controlled study was conducted with the administration of 5,000 U of rhEPO (N = 10) or placebo (N = 10) three times weekly (181-232 U x kg(-1) x wk-1) for 4 wk to male athletes. We measured hematocrit and the concentration of hemoglobin, sTfR, ferritin, EPO, and quantified the effects on performance by measuring time to exhaustion and maximal oxygen uptake (VO2max) on a cycle ergometer. RESULTS: Hematocrit increased from 42.7 +/- 1.6% to 50.8 +/- 2.0% in the EPO group, and peaked 1 d after treatment was stopped. In the EPO group, there was an increase in sTfR (from 3.1 +/- 0.9 to 6.3 +/- 2.3 mg x L(-1) , P < 0.001) and in the ratio between sTfR and ferritin (sTfR-ferritin(-1)) (from 3.2 +/- 1.6 to 11.8 +/- 5.1, P < 0.001). The sTfR increase was significant after 1 wk of treatment and remained so for 1 wk posttreatment. Individual values for sTfR throughout the study period showed that 8 of 10 subjects receiving rhEPO, but none receiving placebo, had sTfR levels that exceeded the 95% confidence interval for all subjects at baseline (= 4.6 mg x L(-1)). VO2max increased from 63.6 +/- 4.5 mL x kg(-1) x min(-1) before to 68.1 +/- 5.4 mL x kg(-1) x min(-1) 2 d post rhEPO administration (7% increase, P = 0.001) in the EPO group. Hematocrit, sTfR, sTfR-ferritin(-1), and VO2max did not change in the placebo group. CONCLUSION: Serum levels of sTfR may be used as an indirect marker of supranormal erythropoiesis up to 1 wk after the administration of rhEPO, but the effects on endurance performance outlast the increase in sTfR.

Adult↗
PubMed1999

The future of doping control in athletes. Issues related to blood sampling.

When current antidoping programmes were developed, the most frequently used doping agents were xenobiotics, such as stimulants and anabolic steroids, that are readily detectable in urine with the use of gas chromatography and mass spectrometry. As control of traditional doping agents became effective, some athletes turned to other means to improve performance, including blood doping and the application of recombinant peptide hormones such as erythropoietin and growth hormone. Doping with these agents is not easily detected in urine samples, and therefore new strategies must be developed as a supplement to those already in use. Such strategies will probably include analysing blood samples, as several of the most promising methods that are able to detect modern doping agents use blood as the analytical matrix. Non-autologous blood doping results in an admixture of self and foreign red blood cells that can be detected in a blood sample with the methods available. Methods to indicate doping with erythropoietin include the indirect finding of an elevated level of soluble transferrin receptor in serum, or a direct demonstration of a shift from the normal to an abnormal spectrum of erythropoietin isoforms. To indicate doping with growth hormone, a set of serum parameters including insulin growth factors and their binding proteins are under investigation as indirect evidence. A direct method using isotopic differences between endogenous and recombinant growth hormones is being investigated. A similar method has been established to detect the administration of testosterone esters. Several legal and ethical questions must be solved before blood sampling can become a part of routine doping control, but the major ethical question is whether sport can continue as today without proper methods to detect many modern doping agents.

Adult↗
PubMed1999

Serum levels of advanced glycation end products are increased in patients with type 2 diabetes and coronary heart disease.

OBJECTIVE: To investigate whether serum levels of advanced glycation end products (AGEs) and the glycoxidation product Nepsilon-(carboxymethyl)lysine (CML) are increased in patients with type 2 diabetes compared with nondiabetic control subjects and whether levels of AGEs and/or CML differ in patients with type 2 diabetes with or without coronary heart disease (CHD). RESEARCH DESIGN AND METHODS: Serum levels of AGEs and CML were measured with an immunoassay in 32 men and 21 women aged 59.3+/-6.2 years (means +/- SD) with type 2 diabetes for 7.3 + 3.1 years and in 17 men and 17 women aged 56.2+/-4.2 years without diabetes. Of the patients with diabetes, 18 had CHD. RESULTS: The serum levels of AGEs and CML were significantly increased in patients with type 2 diabetes compared with nondiabetic control subjects (median [5th-95th percentile]: AGEs 7.4 [4.4-10.9] vs. 4.2 [1.6-6.4] U/ml, P < 0.0001; CML 15.6 [5.6-29.9] vs. 8.6 [4.4-25.9] U/ml, P < 0.0001). The median level of AGEs but not CML was significantly increased in patients with type 2 diabetes and CHD compared with patients without CHD (8.1 [6.4-10.9] vs. 7.1 [3.5-9.8] U/ml, P = 0.03). There were significant positive correlations between serum levels of AGEs and CML in both patients and control subjects. CONCLUSIONS: Levels of AGEs and CML were significantly increased in patients with type 2 diabetes compared with nondiabetic control subjects, and levels of AGEs but not CML were significantly higher in patients with type 2 diabetes and CHD than in patients without diabetes. These results may indicate a role for non-CML AGEs in the development of macrovascular disease in patients with type 2 diabetes.

Aged↗
PubMed1998

[Diabetes mellitus--a complex interaction between heredity and environment].

Genetic factors play an important and probably necessary role, in the development of most forms for diabetes mellitus, but are not the sole cause of the disease. The disease seems to be caused by an interaction between polygenic inheritance and environmental factors. In type I diabetes, more than ten different genetic markers have been found to be associated with the disease. Genes in the HLA-region, on and near the insulin gene, are the most important ones. In the common form of type II diabetes, a series of candidate genes which are code for important steps in insulin secretion or action have been investigated. So far, none have been identified that contribute significantly to the development of the disease in the majority of cases. The most significant breakthrough in research in recent years has been in the study of maturity-onset diabetes of the young (MODY). Until now, mutations in five different genes, which are code for glucokinase and various transcription factors, have been found to be associated with this form of diabetes. Knowledge of the genetic heterogeneity of diabetes has led to a need for a more pathophysiologically correct classification of the disease.

Diabetes Mellitus↗