Dydrogesterone and norethisterone regulate expression of lipoprotein lipase and hormones-sensitive lipase in human subcutaneous abdominal adipocytes

Aim: In premenopausal women, hyper-androgenicity is associated with central obesity and an increased cardiovascular risk. We investigated the effects of dydrogesterone (DYD)(a non-androgenic progestogen) and norethisterone (NET)(an androgenic progestogen) on lipoprotein lipase (LPL), hormone-sensitive lipase (HSL) and glycerol release in adipocytes isolated from subcutaneous abdominal adipose tissue. Methods: Adipose tissue was obtained from 12 non-diabetic women, mean age 51 years (range 37-78) and mean BMI 25.4kg/m2 (range 20.3-26.4). Adipocytes were treated with increasing doses of DYD and NET for 48 hours prior to protein extraction. Effects on lipogenesis and lipolysis were assessed using western blotting to determine the expression of key enzymes, LPL (56kDa) and HSL (84kDa) respectively. Measurement of glycerol release into the medium provided an assessment of lipolytic activity. Results: Expression of LPL was increased by DYD and NET (mean protein expression relative to control ± SEM); with greatest effect at 10-8M for DYD: 2.32±0.51(p0.05). Conclusions: DYD and NET significantly increased LPL expression relative to control whilst significantly reducing HSL expression. At the concentrations studied, similar effects were observed with the androgenic NET and the non-androgenic DYD despite differing effects on the lipid profile when taken in combination with estrogen. Further work in this area may improve knowledge about the effects of different progestogens on body fat distribution and enable progestogen use to be tailored to the individual to achieve maximal benefits

The Effect of a Placebo on the ROTC APFT Test and Performance Perception

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HIV infection significantly reduces lipoprotein lipase which remains low after 6 months of antiretroviral therapy

Purpose of the study Fractional clearance rate of apolipoprotein B100-containing lipoproteins is reduced in HIV infection before and after antiretroviral (ARV) treatment [1]. We compared lipoprotein lipase (LPL) activity and gene expression in HIV-positive subjects before and 6 months after ARV with HIV-negative controls. Methods Fasting blood post heparin total and hepatic lipase activity,adiponectin, leptin, insulin, glucose, and lipid measurementswere made in 32 HIV-infected and 15 HIVnegative controls. LPL was estimated by subtractinghepatic lipase from total lipase. Adiponectin, LPL andhormone sensitive lipase (HSL) gene expression weremeasured from iliac crest subcutaneous fat biopsies.Patients were tested before, and 6 months after randomisation to AZT/3TC (n = 15) or TDF/FTC (n = 17) with EFV.Between-group comparison was by Mann-Whitney andpaired samples by the Wilcoxon signed rank tests. Summary of results There were no differences in gender, ethnicity, baseline BMI, regional fat distribution (whole body DEXA) and visceral (VAT) and subcutaneous fat (SAT) measured by abdominal CT scans between controls and patients. Trunk fat/BMI ratio, VAT and VAT:SAT ratio significantly increased after 6-month ARV therapy (p = 0.01). There were no differences between groups in serum NEFA,HOMA and leptin levels. Selected other results are shown in Table 1. Conclusion Post heparin lipoprotein lipase activity is reduced in HIV and does not return to control levels after 6 months of ARV therapy. AZT-containing regimens are associated with a greater increase in LPL, LPL gene expression and plasma adiponectin than TDF

GASP II. A MUSE view of extreme ram-pressure stripping along the line of sight: kinematics of the jellyfish galaxy JO201

This paper presents a spatially-resolved kinematic study of the jellyfish galaxy JO201, one of the most spectacular cases of ram-pressure stripping (RPS) in the GASP (GAs Stripping Phenomena in Galaxies with MUSE) survey. By studying the environment of JO201, we find that it is moving through the dense intra-cluster medium of Abell 85 at supersonic speeds along our line of sight, and that it is likely accompanied by a small group of galaxies. Given the density of the intra-cluster medium and the galaxy's mass, projected position and velocity within the cluster, we estimate that JO201 must so far have lost ~50% of its gas during infall via RPS. The MUSE data indeed reveal a smooth stellar disk, accompanied by large projected tails of ionised (Halpha) gas, composed of kinematically cold (velocity dispersion <40km/s) star-forming knots and very warm (>100km/s) diffuse emission which extend out to at least ~50 kpc from the galaxy centre. The ionised Halpha-emitting gas in the disk rotates with the stars out to ~6 kpc but in the disk outskirts becomes increasingly redshifted with respect to the (undisturbed) stellar disk. The observed disturbances are consistent with the presence of gas trailing behind the stellar component, resulting from intense face-on RPS happening along the line of sight. Our kinematic analysis is consistent with the estimated fraction of lost gas, and reveals that stripping of the disk happens outside-in, causing shock heating and gas compression in the stripped tails.Comment: ApJ, revised version after referee comments, 15 pages, 16 figures. The interactive version of Figure 9 can be viewed at web.oapd.inaf.it/gasp/publications.htm

Rotational Dynamics of Vortices in Confined Bose-Einstein Condensates

We derive the frequency of precession and conditions for stability for a quantized vortex in a single-component and a two-component Bose-Einstein condensate. The frequency of precession is proportional to the gradient of the free energy with respect to displacement of the vortex core. In a two-component system, it is possible to achieve a local minimum in the free energy at the center of the trap. The presence of such a minimum implies the existence of a region of energetic stability where the vortex cannot escape and where one may be able to generate a persistent current.Comment: 6 Pages, 6 Figure

Epigenetics and obesity: the devil is in the details

Obesity is a complex disease with multiple well-defined risk factors. Nevertheless, susceptibility to obesity and its sequelae within obesogenic environments varies greatly from one person to the next, suggesting a role for gene × environment interactions in the etiology of the disorder. Epigenetic regulation of the human genome provides a putative mechanism by which specific environmental exposures convey risk for obesity and other human diseases and is one possible mechanism that underlies the gene × environment/treatment interactions observed in epidemiological studies and clinical trials. A study published in BMC Medicine this month by Wang et al. reports on an examination of DNA methylation in peripheral blood leukocytes of lean and obese adolescents, comparing methylation patterns between the two groups. The authors identified two genes that were differentially methylated, both of which have roles in immune function. Here we overview the findings from this study in the context of those emerging from other recent genetic and epigenetic studies, discuss the strengths and weaknesses of the study and speculate on the future of epigenetics in chronic disease research