197 research outputs found

    Monetary policy and commodity price shocks

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    This paper analyses the effects of commodity price shocks in a new Keynesian model. The focus is on the central bank's choice of inflation target and the degree of real wage rigidity. It turns out that using core inflation rather than headline inflation is the superior strategy. Targeting expected headline inflation, as practiced by most central banks, is a viable practical alternative to the core inflation target. Simulations illustrate these points. The introduction of real wage rigidity into the model does not change these conclusions. Real wage rigidity does, however, imply second-round effects, making the monetary policy response, the inflation peak and the output drop more pronounced. Although in practice many of the assumptions of the model, such as full information, do not hold, lessons can be drawn for monetary policy. In case of a commodity supply shock, central banks would do well to focus on some measure of core inflation rather than headline inflation so as to reduce the volatility of both inflation and output. A communication strategy that places greater emphasis on underlying and expected inflation could serve to anchor inflation expectations.

    Osteocalcin is independently associated with C-reactive protein during lifestyle-induced weight loss in metabolic syndrome

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    Bone-derived osteocalcin has been suggested to be a metabolic regulator, potentially improving insulin sensitivity. To scrutinize the relation between osteocalcin and peripheral insulin sensitivity, I analyzed changes of serum osteocalcin relative to changes in insulin sensitivity, low-grade inflammation and bone mineral density following lifestyle-induced weight loss in individuals with metabolic syndrome (MetS). 74 nonsmoking men (45–55 yr) with MetS were randomized to a lifestyle-induced weight loss program (supervision via telemonitoring) or to a control group. Before and after the 6 months intervention period clinical and laboratory parameters and serum osteocalcin levels were determined in fasting blood samples. Lifestyle-induced changes of body composition were analyzed by Dual Energy X Ray-Absorptiometry (DXA). 30 participants in the control and 33 participants in the intervention group completed the study and were included in the data analysis. In participants of the intervention group, weight loss resulted in markedly improved insulin sensitivity and amelioration of low-grade inflammation. Increased serum levels of osteocalcin correlated inversely with BMI (r= -0.63; p< 0.001), total fat mass (r= -0.58, p< 0.001), total lean mass (r= -0.45, p< 0.001), C-reactive protein (CRP) (r= -0.37; p< 0.01), insulin (r= -0.4; p< 0.001), leptin (r= -0.53; p< 0.001), triglycerides (r= -0.42; p< 0.001) and alanine aminotransferase (ALAT) (r=-0.52; p< 0.001). Regression analysis revealed that osteocalcin was associated with changes in CRP but not with changes in insulin concentration, adipose tissue mass or bone mineral density. These results illustrate that the weight loss-induced higher serum osteocalcin is primarily associated with reduced inflammation.:List of abbreviations ................................................................................................................................ 4 Short summary ........................................................................................................................................ 5 Graphical abstract ................................................................................................................................... 6 2 Introduction ......................................................................................................................................... 7 2a The metabolic syndrome ............................................................................................................... 8 2b C-reactive protein (CRP) and its role in MetS .............................................................................. 12 2c Bone-derived osteocalcin and inflammation ............................................................................... 14 2d Study design ................................................................................................................................. 17 3 Original peer-reviewed publication: “Osteocalcin Is Independently Associated with C-Reactive Protein during Lifestyle-Induced Weight Loss in Metabolic Syndrome” .............................................. 19 4 Summary ............................................................................................................................................ 32 5 References ......................................................................................................................................... 36 6 Supplementary data ........................................................................................................................... 45 7 Declaration about the independent preparation of the work ........................................................... 48 8 Presentation of own contribution ..................................................................................................... 49 9 Curriculum vitae ................................................................................................................................. 51 10 Publications ...................................................................................................................................... 57 11 Acknowledgments ............................................................................................................................ 5

    Osteocalcin Is Independently Associated with C-Reactive Protein during Lifestyle-Induced Weight Loss in Metabolic Syndrome

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    Bone-derived osteocalcin has been suggested to be a metabolic regulator. To scrutinize the relation between osteocalcin and peripheral insulin sensitivity, we analyzed changes in serum osteocalcin relative to changes in insulin sensitivity, low-grade inflammation, and bone mineral density following lifestyle-induced weight loss in individuals with metabolic syndrome (MetS). Participants with MetS were randomized to a weight loss program or to a control group. Before and after the 6-month intervention period, clinical and laboratory parameters and serum osteocalcin levels were determined. Changes in body composition were analyzed by dual-energy X-ray absorptiometry (DXA). In participants of the intervention group, weight loss resulted in improved insulin sensitivity and amelioration of inflammation. Increased serum levels of osteocalcin correlated inversely with BMI (r = −0.63; p < 0.001), total fat mass (r = −0.58, p < 0.001), total lean mass (r = −0.45, p < 0.001), C-reactive protein (CRP) (r = −0.37; p < 0.01), insulin (r = −0.4; p < 0.001), leptin (r = −0.53; p < 0.001), triglycerides (r = −0.42; p < 0.001), and alanine aminotransferase (ALAT) (r = −0.52; p < 0.001). Regression analysis revealed that osteocalcin was independently associated with changes in CRP but not with changes in insulin concentration, fat mass, or bone mineral density, suggesting that weight loss-induced higher serum osteocalcin is primarily associated with reduced inflammation

    Mistargeting of aggregation prone mitochondrial proteins activates a nucleus-mediated posttranscriptional quality control pathway in trypanosomes.

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    Mitochondrial protein import in the parasitic protozoan Trypanosoma brucei is mediated by the atypical outer membrane translocase, ATOM. It consists of seven subunits including ATOM69, the import receptor for hydrophobic proteins. Ablation of ATOM69, but not of any other subunit, triggers a unique quality control pathway resulting in the proteasomal degradation of non-imported mitochondrial proteins. The process requires a protein of unknown function, an E3 ubiquitin ligase and the ubiquitin-like protein (TbUbL1), which all are recruited to the mitochondrion upon ATOM69 depletion. TbUbL1 is a nuclear protein, a fraction of which is released to the cytosol upon triggering of the pathway. Nuclear release is essential as cytosolic TbUbL1 can bind mislocalised mitochondrial proteins and likely transfers them to the proteasome. Mitochondrial quality control has previously been studied in yeast and metazoans. Finding such a pathway in the highly diverged trypanosomes suggests such pathways are an obligate feature of all eukaryotes

    Plant Sterol-Poor Diet Is Associated with Pro-Inflammatory Lipid Mediators in the Murine Brain

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    Plant sterols (PSs) cannot be synthesized in mammals and are exclusively diet-derived. PSs cross the blood-brain barrier and may have anti-neuroinflammatory effects. Obesity is linked to lower intestinal uptake and blood levels of PSs, but its effects in terms of neuroinflammation—if any—remain unknown. We investigated the effect of high-fat diet-induced obesity on PSs in the brain and the effects of the PSs campesterol and -sitosterol on in vitro microglia activation. Sterols (cholesterol, precursors, PSs) and polyunsaturated fatty acid-derived lipid mediators were measured in the food, blood, liver and brain of C57BL/6J mice. Under a PSs-poor high-fat diet, PSs levels decreased in the blood, liver and brain (>50%). This effect was reversible after 2 weeks upon changing back to a chow diet. Inflammatory thromboxane B2 and prostaglandin D2 were inversely correlated to campesterol and -sitosterol levels in all brain regions. PSs content was determined post mortem in human cortex samples as well. In vitro, PSs accumulate in lipid rafts isolated from SIM-A9 microglia cell membranes. In summary, PSs levels in the blood, liver and brain were associated directly with PSs food content and inversely with BMI. PSs dampen pro-inflammatory lipid mediators in the brain. The identification of PSs in the human cortex in comparable concentration ranges implies the relevance of our findings for humans
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