Changes in BMI-distribution from 1966–69 to 1995–97 in adolescents. The Young-HUNT study, Norway

Background The aim of this study was to explore changes in the BMI-distribution over time among Norwegian adolescents. Methods Height and weight were measured in standardised ways and BMI computed in 6774 adolescents 14–18 years who participated in the Young-HUNT study, the youth part of the Health-study of Nord-Trondelag County, Norway in 1995–97. The results were compared to data from 8378 adolescents, in the same age group and living in the same geographical region, collected by the National Health Screening Service in 1966–69. Results From 1966–69 to 1995–97 there was an increased dispersion and a two-sided change in the BMI-distribution. Mean BMI did not increase in girls aged 14–17, but increased significantly in 18 year old girls and in boys of all ages. In both sexes and all ages there was a significant increase in the upper percentiles, but also a trend towards a decrease in the lowest percentiles. Height and weight increased significantly in both sexes and all ages. Conclusion The increased dispersion of the BMI-distribution with a substantial increase in upper BMI-percentiles followed the same pattern seen in other European countries and the United States. The lack of increase in mean BMI among girls, and the decrease in the lowest percentiles has not been acknowledged in previous studies, and may call for attention

Modulation of β-Catenin Signaling by Glucagon Receptor Activation

The glucagon receptor (GCGR) is a member of the class B G protein–coupled receptor family. Activation of GCGR by glucagon leads to increased glucose production by the liver. Thus, glucagon is a key component of glucose homeostasis by counteracting the effect of insulin. In this report, we found that in addition to activation of the classic cAMP/protein kinase A (PKA) pathway, activation of GCGR also induced β-catenin stabilization and activated β-catenin–mediated transcription. Activation of β-catenin signaling was PKA-dependent, consistent with previous reports on the parathyroid hormone receptor type 1 (PTH1R) and glucagon-like peptide 1 (GLP-1R) receptors. Since low-density-lipoprotein receptor–related protein 5 (Lrp5) is an essential co-receptor required for Wnt protein mediated β-catenin signaling, we examined the role of Lrp5 in glucagon-induced β-catenin signaling. Cotransfection with Lrp5 enhanced the glucagon-induced β-catenin stabilization and TCF promoter–mediated transcription. Inhibiting Lrp5/6 function using Dickkopf-1(DKK1) or by expression of the Lrp5 extracellular domain blocked glucagon-induced β-catenin signaling. Furthermore, we showed that Lrp5 physically interacted with GCGR by immunoprecipitation and bioluminescence resonance energy transfer assays. Together, these results reveal an unexpected crosstalk between glucagon and β-catenin signaling, and may help to explain the metabolic phenotypes of Lrp5/6 mutations

Gender differences in health care use among the elderly population in areas of Norway and Finland. A cross-sectional analysis based on the HUNT study and the FINRISK Senior Survey

BACKGROUND: The aim of the study was to examine gender differences in the self-reported use of health care services by the elderly in rural and metropolitan areas of two Nordic countries with slightly different health care systems: Finland and Norway. METHODS: Population based, cross-sectional surveys conducted in Nord-Tröndelag Norway (1995–97) and in rural and metropolitan areas of Finland (1997) were employed. In the Norwegian data, a total of 7,919 individuals, aged 65–74 years old were included, and the Finnish data included 1,500 individuals. The outcome variables comprised whether participants had visited a general practitioner or a specialist, or had received hospital care or physiotherapy during the past 12 months. Gender differences in the use of health care services were analysed by multiple logistic regression, controlling for health status and socio-demographic characteristics. RESULTS: In Norway, elderly women visited a specialist or were hospitalised less often than men. In Finland, elderly women used all health care services except hospital care more often than men. In Norway, less frequent use of specialist care by women was not associated with self-reported health or chronic diseases. CONCLUSION: The findings revealed differences in self-reported use of secondary care among different genders in areas of Norway and Finland

The Use of Flow-Injection Analysis with Chemiluminescence Detection of Aqueous Ferrous Iron in Waters Containing High Concentrations of Organic Compounds

An evaluation of flow-injection analysis with chemiluminescence detection (FIA-CL) to quantify Fe2+(aq) in freshwaters was performed. Iron-coordinating and/or iron-reducing compounds, dissolved organic matter (DOM), and samples from two natural water systems were used to amend standard solutions of Fe2+(aq). Slopes of the response curves from ferrous iron standards (1 – 100 nM) were compared to the response curves of iron standards containing the amendments. Results suggest that FIA-CL is not suitable for systems containing ascorbate, hydroxylamine, cysteine or DOM. Little or no change in sensitivity occurred in solutions of oxalate and glycine or in natural waters with little organic matter

Prostaglandin E2 Signals Through PTGER2 to Regulate Sclerostin Expression

The Wnt signaling pathway is a robust regulator of skeletal homeostasis. Gain-of-function mutations promote high bone mass, whereas loss of Lrp5 or Lrp6 co-receptors decrease bone mass. Similarly, mutations in antagonists of Wnt signaling influence skeletal integrity, in an inverse relation to Lrp receptor mutations. Loss of the Wnt antagonist Sclerostin (Sost) produces the generalized skeletal hyperostotic condition of sclerosteosis, which is characterized by increased bone mass and density due to hyperactive osteoblast function. Here we demonstrate that prostaglandin E2 (PGE2), a paracrine factor with pleiotropic effects on osteoblasts and osteoclasts, decreases Sclerostin expression in osteoblastic UMR106.01 cells. Decreased Sost expression correlates with increased expression of Wnt/TCF target genes Axin2 and Tcf3. We also show that the suppressive effect of PGE2 is mediated through a cyclic AMP/PKA pathway. Furthermore, selective agonists for the PGE2 receptor EP2 mimic the effect of PGE2 upon Sost, and siRNA reduction in Ptger2 prevents PGE2-induced Sost repression. These results indicate a functional relationship between prostaglandins and the Wnt/β-catenin signaling pathway in bone