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      Correlation of metabolic characteristics with maternal, fetal and placental asprosin in human pregnancy

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          Abstract

          Objective

          Asprosin is a recently discovered hormone associated with obesity and diabetes mellitus. Little is known about asprosin’s role during pregnancy, but a contribution of asprosin to pregnancy complications resulting from maternal obesity and gestational diabetes mellitus (GDM) is conceivable. We assessed the potential effects of obesity, GDM and other clinical parameters on maternal and fetal umbilical plasma asprosin concentrations and placental asprosin expression.

          Design

          The Cologne-Placenta Cohort Study comprises 247 female patients, from whom blood and placentas were collected at the University Hospital Cologne.

          Methods

          We studied the maternal and fetal umbilical plasma and placentas of pregnant women with an elective, primary section. Sandwich ELISA measurements of maternal and fetal umbilical plasma and immunohistochemical stainings of placental tissue were performed to determine the asprosin levels. Also, the relation between asprosin levels and clinical blood parameters was studied.

          Results

          There was a strong correlation between the maternal and fetal plasma asprosin levels and both increased with GDM in normal-weight and obese women. Asprosin immunoreactivity was measured in cultivated placental cells and placental tissue. BMI and GDM were not but pre-pregnancy exercise and smoking were correlated with maternal and/or fetal asprosin levels. Placental asprosin levels were associated with maternal but not with fetal plasma asprosin levels and with BMI but not with GDM. Placental asprosin was related to maternal insulin levels and increased upon insulin treatment in GDM patients.

          Conclusions

          Asprosin could potentially act as a biomarker and contribute to the clinical manifestation of pregnancy complications associated with maternal obesity.

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          Most cited references37

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          Asprosin, a Fasting-Induced Glucogenic Protein Hormone.

          Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome.
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            Physiology of the endothelium.

            In the past, the endothelium was considered to be inert, described as a 'layer of nucleated cellophane', with only non-reactive barrier properties, such as presentation of a non-thrombogenic surface for blood flow and guarding against pro-inflammatory insults. However, it is now becoming clear that endothelial cells actively and reactively participate in haemostasis and immune and inflammatory reactions. They regulate vascular tone via production of nitric oxide, endothelin and prostaglandins and are involved in the manifestations of atherogenesis, autoimmune diseases and infectious processes. They produce and react to various cytokines and adhesion molecules and it is now clear that they can mount anti- and pro-inflammatory and protective responses depending on environmental conditions and are key immunoreactive cells. Endothelial dysfunction or activation also contributes to a variety of disease states.
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              Is Open Access

              An evolving new paradigm: endothelial cells – conditional innate immune cells

              Endothelial cells (ECs) are a heterogeneous population that fulfills many physiological processes. ECs also actively participate in both innate and adaptive immune responses. ECs are one of the first cell types to detect foreign pathogens and endogenous metabolite-related danger signals in the bloodstream, in which ECs function as danger signal sensors. Treatment with lipopolysaccharide activates ECs, causing the production of pro-inflammatory cytokines and chemokines, which amplify the immune response by recruiting immune cells. Thus, ECs function as immune/inflammation effectors and immune cell mobilizers. ECs also induce cytokine production by immune cells, in which ECs function as immune regulators either by activating or suppressing immune cell function. In addition, under certain conditions, ECs can serve as antigen presenting cells (antigen presenters) by expressing both MHC I and II molecules and presenting endothelial antigens to T cells. These facts along with the new concept of endothelial plasticity suggest that ECs are dynamic cells that respond to extracellular environmental changes and play a meaningful role in immune system function. Based on these novel EC functions, we propose a new paradigm that ECs are conditional innate immune cells. This paradigm provides a novel insight into the functions of ECs in inflammatory/immune pathologies.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                11 February 2022
                01 March 2022
                : 11
                : 3
                : e220069
                Affiliations
                [1 ]Department of Pediatrics , and Adolescent Medicine, Faculty of Medicine and University Hospital of Cologne, University of Cologne, Cologne, Germany
                [2 ]Center for Biochemistry , Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany
                [3 ]Center for Pediatric Pathology at the University Hospital Cologne , Cologne, Germany
                [4 ]Center for Molecular Medicine Cologne (CMMC) , University of Cologne, Cologne, Germany
                [5 ]Cologne Center for Musculoskeletal Biomechanics (CCMB) , Cologne, Germany
                Author notes
                Correspondence should be addressed to E Hucklenbruch-Rother: eva.rother@ 123456uni-koeln.de
                Author information
                http://orcid.org/0000-0001-5532-6153
                http://orcid.org/0000-0002-8876-3533
                Article
                EC-22-0069
                10.1530/EC-22-0069
                8942321
                35148275
                cad6a9f4-09ee-4364-9dd6-02e4cf203ea5
                © The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 04 February 2022
                : 11 February 2022
                Categories
                Research

                obesity,gdm,asprosin,insulin,placenta,smoking,exercise
                obesity, gdm, asprosin, insulin, placenta, smoking, exercise

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