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Biomedical subjects

J P Berg

Publications and source records attributed to J P Berg.

At least 19 recordsLinked to original sources
PubMed2000

Leptin levels in relation to body composition and insulin concentration in patients with endogenous Cushing's syndrome compared to controls matched for body mass index.

Cushing's syndrome (CS) is associated with weight gain and visceral obesity. We examined the relationship between regional fat distribution and serum levels of leptin, cortisol and insulin. Twenty-three consecutive patients with recently diagnosed CS (18 with pituitary adenoma, 5 with adrenal tumor), where compared to obese controls, matched for age, sex and Body Mass Index (BMI). Serum insulin, leptin, cortisol, C-peptide and body composition determined by DEXA were measured. Serum leptin levels were significantly increased in patients with CS (36.9+/-3.8 vs 18.9+/-2.4 ng/ml, p<0.001; women: 40.1+/-4.6 vs 21.7+/-2.9 ng/ml, p<0.01; men: 27.9+/-5.7 vs 10.9+/-2.3 ng/ml; p<0.05), the same were fasting insulin levels (178+/-30 vs 81+/-10 pmol/l; p<0.01) and C-peptide (1.51+/-0.12 vs 0.77+/-0.07 nmol/l; p<0.001). In a subgroup of 12 patients, truncal fat mass was significantly elevated when compared to obese controls (19.2 kg vs 14.7 kg, p<0.01, and 42% vs 36% in percentage of truncal body tissue, p<0.05), whereas total fat mass was insignificantly increased. Serum leptin correlated positively to total body fat (%) as in patients with CS (r=0.94, p<0.001) as in controls (r=0.68, p<0.01). The correlation to truncal body fat (%) was also significant in both groups (CS: r=0.84, p<0.001; controls: r=0.63, p<0.01). Multiple regression showed that percent total body fat was the predictor of leptin concentrations among patients with CS (r2=0.88, p<0.001) whereas insulin did not contribute significantly to the variance in leptin concentrations. In controls, both leptin and insulin (r2=0.65, p<0.001) contributed significantly to the variations in leptin levels. Controlled for the differences in total body fat, patients with endogenous CS have significantly increased serum leptin levels, compared to BMI-matched obese controls. This suggests that hyperleptinemia in CS not primarily reflects changes in body composition, but is the result of different hormonal influences on adipose tissue.

Adipose Tissue↗
PubMed2000

Hormones and metabolites of arctic foxes (Alopex lagopus) in response to season, starvation and re-feeding.

Svalbard's arctic foxes experience large seasonal variations in light, temperature and food supply throughout the year, which may result in periods of starvation. The aim of this work is to investigate if there are seasonal variations in post-absorptive plasma thyroid hormones (free thyroxin (fT(4)), free triiodothyronine (fT(3)) and reverse triiodothyronine (rT(3))) and metabolites (free fatty-acids (FFA) and beta-hydroxybutyrate (beta-OHB)) with season and their response to starvation and re-feeding. The concentrations of post-absorptive free triiodothyronine were significantly higher in November than May, while those of thyroxin, reverse triiodothyronine, free fatty-acids and beta-hydroxybutyrate remained unchanged. Possible explanations for the seasonal variations in free triiodothyronine are discussed. There were no significant changes from post-absorptive concentrations of thyroxin and reverse triiodothyronine in starved and re-fed foxes. However, free triiodothyronine concentrations decreased during starvation and increased again with re-feeding both in May and November. Starvation induced high levels of free fatty acids in both May and November, indicating increased lipolysis. There was a significant increase in beta-hydroxybutyrate in November only, indicating that arctic foxes are capable of protein conservation during starvation.

3-Hydroxybutyric Acid↗
PubMed2000

HFE gene mutation (C282Y) and phenotypic expression among a hospitalised population in a high prevalence area of haemochromatosis.

BACKGROUND: Previous studies have shown that up to 0.5% of the Caucasian population is homozygous for the HFE gene C282Y mutation. High prevalence values have been reported in Northern Europe. To what extent the presence of this mutation is associated with overt clinical haemochromatosis is unclear. AIM: To determine the prevalence of the C282Y allele in a hospitalised population of an acute medical department, and study the phenotypic expression in the homozygotes. METHODS: Blood samples were obtained from 2027 hospitalised patients; 1900 Caucasians and 127 non-Caucasians. Serum iron, transferrin, and ferritin were measured at admission. The presence of the HFE gene mutation was determined by polymerase chain reaction based analysis. Follow up fasting blood samples were obtained from patients homozygous for the mutation. RESULTS: Fourteen of the 1900 Caucasian subjects (0.74%) were homozygous and 224 (11.8%) were heterozygous for the C282Y mutation, including 32 subjects (1.7%) who were compound heterozygous for the C282Y and H63D mutations. Ten of 14 (71%) homozygous patients displayed mild to moderate biochemical expression of haemochromatosis with a serum ferritin level <550 microg/l, two (14%) patients were "non expressing", and two of five in whom liver biopsies were carried out had cirrhosis, including one with advanced hepatocellular carcinoma. CONCLUSIONS: The prevalence of C282Y homozygosity in a hospitalised population was 0.74%. However, the majority of homozygous patients displayed mild to moderate biochemical expression. C282Y mutation screening may detect individuals that do not develop haemochromatosis. Transferrin saturation and ferritin, which are used as first line screening in haemochromatosis, may be highly unreliable in the presence of an inflammatory process.

Acute-Phase Reaction↗
PubMed2000

The Sp1 binding site polymorphism in the collagen type I alpha 1 (COLIA1) gene is not associated with bone mineral density in healthy children, adolescents, and young adults.

Up to 85% of the variance in bone mineral density (BMD) is genetically determined. A putative candidate gene involved in the regulation of bone mass is the COLIA1 gene encoding type I collagen, which is the major protein of bone. We examined possible allelic influences of a G to T COLIA1 gene polymorphism in a recognition site for the transcription factor Sp1 on: (i) gain of forearm BMD using single photon absorptiometry (SPA); and (ii), BMD of the forearm, spine, hip, and whole body with dual X-ray absorptiometry (DXA). At baseline, 269 healthy boys and girls aged 8.2-16.5 years were eligible for the study. Forearm BMD measurements obtained at baseline and after 3.8+/-0.1 years (+/-s.d.) were used to calculate the annual percentage change in BMD. Calcium intake and physical activity were determined by a detailed questionnaire at baseline and after 1 year. Essentially no significant differences in forearm BMD gain or in BMD assessed at the forearm, spine, and whole body were observed among the three COLIA1 genotypes. In conclusion, the data indicate that the polymorphism at the Sp1 site in the COLIA1 gene is not associated with BMD or gain of forearm BMD in healthy boys and girls.

Adolescent↗
PubMed1999

High prevalence of the hemochromatosis-associated Cys282Tyr HFE gene mutation in a healthy Norwegian population in the city of Oslo, and its phenotypic expression.

BACKGROUND: Previous studies have shown that 5%-10% of white subjects are heterozygous for the HFE gene C282Y mutation, which is associated with hemochromatosis. The aim of our study was to determine the prevalence of heterozygosity and homozygosity for the C282Y HFE gene mutation and its phenotypic expression in a group of healthy Norwegians. METHODS: Fasting blood samples were obtained from 505 unrelated hospital employees. Serum iron, transferrin, and serum ferritin were measured. Transferrin saturation was calculated. The presence of HFE gene mutation was determined with a polymerase chain reaction-based analysis. RESULTS: Two of the 505 subjects (0.4%) were homozygous and 75 (14.9%) were heterozygous for the C282Y mutation. Median serum ferritin among the heterozygotes was 59 microg/l, compared with 47 microg/l among individuals without the C282Y mutation (P = 0.12). Median transferrin saturation among the heterozygotes was 31%, compared with 24% among individuals without C282Y mutation (P < 0.001). Twenty-three individuals (4.6%) had a serum ferritin level > 200 microg/l. Eight of these (35%) had the C282Y mutation: two homozygotes and six heterozygotes. Transferrin saturation > 50% was observed in 25 individuals (5.0%). Twelve of these (48%) had the C282Y mutation; two were homozygotes and 10 heterozygotes. Only eight individuals (1.6%) had a transferrin saturation > 60%: one homozygote, five heterozygotes, and two individuals without mutation. CONCLUSIONS: Fifteen per cent of a healthy Norwegian population is heterozygous for the HFE gene mutation C282Y. This is among the highest reported prevalence values among healthy individuals. Half of the subjects with transferrin saturation greater than 50% were carriers of the C282Y mutation.

Adult↗
PubMed1999

Vitamin D: a hormonal regulator of the cAMP signaling pathway.

In the rat thyroid FRTL-5 cell line calcitriol, the biologically most active of the naturally occurring vitamin D metabolites, attenuates both TSH-stimulated cAMP production and the effects of cAMP. Calcitriol treatment abolishes the upregulation of the TSHR number occurring in cells cultivated in the absence of TSH. In addition, the level of G(i-2)alpha increases, which may further attenuate the transmembrane signaling of TSH and facilitate the effects of IGFs. The effect of cAMP on PKAI stimulation is inhibited by increasing the level of the PKA subunit RIIbeta. Regulation of TSHR, G(i-2)alpha and RIIbeta is associated with altered cell proliferation and differentiation in several cells and tissues. Effects of calcitriol on these proteins indicate how the vitamin D endocrine system may regulate cAMP signaling in both classical and nonclassical target tissues.

Animals↗
PubMed1999

Serum dehydroepiandrosterone sulfate concentration and thyroid cancer risk: a matched case control study.

In animal models of carcinogenesis, pharmacological doses of dehydroepiandrosterone (DHEA) treatment appear to reduce the incidence of chemically induced thyroid cancers. DHEA and its sulfate (DHEA-S) are secreted in approximately equal amounts, but serum levels of DHEA-S are 300-500 times higher and have no diurnal variation when compared to DHEA. The hypothesis that serum concentrations of DHEA-S may be associated with thyroid cancer risk was tested in a population-based prospective case control study. Data from the practically complete nationwide Cancer Registry of Norway were linked to the data file of a serum bank comprising blood samples from 300,000 Norwegian men and women obtained through national health surveys. A total of 113 donors, who during the years after blood sampling received a diagnosis of thyroid cancer, were identified in the serum bank and were eligible for the study. Each case was matched with 3 controls. Serum levels of DHEA-S were determined blindly. Controls were divided into tertiles, and odds ratios between cases and controls were determined relative to the group with the lowest serum DHEA-S level. The risk of developing thyroid cancer was determined in women 50 years of age or older, in women below age 50, in men, and in the subgroup of 77 cases who had morphologically verified papillary thyroid cancer. No significant association between prediagnostic serum DHEA-S concentrations and thyroid cancer risk was observed. These data indicate that DHEA-S within physiological concentrations does not reduce the risk of thyroid cancer.

Adult↗
PubMed1999

Low levels of serum calcidiol in an African population compared to a North European population.

OBJECTIVE: To compare vitamin D status in an African population living at 10 degrees N with a Norwegian population living at 60 degrees N. DESIGN: Serum samples from 30 healthy young Ethiopians and 31 full term pregnant women from Addis Ababa were collected in September, and from 24 healthy Norwegians in March and 23 pregnant women from Oslo in February to June. METHODS: Serum (s) levels of calcidiol and intact parathyroid hormone (iPTH) were measured. RESULTS: The median values for s-calcidiol were significantly lower in Ethiopians compared with Norwegians (young Ethiopians 23.5nmol/l vs young Norwegians 81nmol/l, P<0.001; pregnant Ethiopians 25nmol/l vs pregnant Norwegians 36nmol/l, P<0.05) while those for s-iPTH were significantly higher (young Ethiopians 5.7pmol/l vs young Norwegians 2.4pmol/l, P<0.001; pregnant Ethiopians 4.8pmol/l vs pregnant Norwegians 2.8pmol/l, P<0.02). CONCLUSION: In spite of abundant availability of ultraviolet radiation, the population from Addis Ababa had a high rate of biochemical vitamin D deficiency compared with the Norwegian group.

Adult↗
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↗
PubMed1998

[Thyroid hormone resistance. Clinical, biochemical and genetic study of a family].

We here present a family where three individuals in three generations had varying degrees of goiter, tachycardia, fatigue, hyperactivity, and learning disability. Serum T3 and free T4 were elevated, whereas TSH was normal or slightly increased. The clinical findings in combination with the hormone values led to several supplementary investigations and therapies being carried out, but they had no beneficial influence on the patients' symptoms. The commonest form of thyroid hormone resistance (RTH) is an autosomal dominantly inherited disorder with varying degrees of hypo- and hyperthyroidism, including the hormonal changes described above. Several mutations, particularly in exons 9 and 10 of the thyroid hormone receptor beta gene, have been described and shown to be responsible for RTH. Exons 7, 8, 9, and 10 in the thyroid hormone receptor beta gene were amplified by polymerase chain reaction and analyzed by DNA sequencing. A heterozygous point mutation in nucleotide 1244 in exon 9 was demonstrated in the two patients with RTH that were available for the study. The guanidine to thymidine point mutation changed the codon for arginine in position 320 in the receptor protein to leucine. This mutation has previously been shown to decrease receptor affinity for T3; it has been demonstrated in some patients with RTH, and it is probably the cause of RTH in the family described in this study.

Adult↗