The Experts below are selected from a list of 13188 Experts worldwide ranked by ideXlab platform
Ruth Frikkeschmidt - One of the best experts on this subject based on the ideXlab platform.
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early life exposures to perfluoroalkyl substances in relation to Adipokine hormone levels at birth and during childhood
The Journal of Clinical Endocrinology and Metabolism, 2019Co-Authors: Philippe Grandjean, Colleen Shelly, Youssef Oulhote, Peter Plomgaard, Ruth FrikkeschmidtAbstract:BACKGROUND Birth cohort studies have linked exposure to perfluoroalkyl substances (PFASs) with child anthropometry. Metabolic hormone dysregulation needs to be considered as a potential adverse outcome pathway. We examined the associations between PFAS exposures and concentrations of Adipokine hormones from birth to adolescence. METHODS We studied 80 mother-child pairs from a Faroese cohort born in 1997 to 2000. Five PFASs were measured in maternal pregnancy serum and in child serum at ages 5, 7, and 13 years. Leptin, adiponectin, and resistin were analyzed in cord serum and child serum at the same ages. We fitted multivariable-adjusted generalized estimating equations to assess the associations of PFASs at each age with repeated Adipokine concentrations at concurrent and subsequent ages. RESULTS We observed tendencies of inverse associations between PFASs and Adipokine hormones specific to particular ages and sex. Significant associations with all Adipokines were observed for maternal and child 5-year serum PFAS concentrations, whereas associations for PFASs measured at ages 7 to 13 years were mostly null. The inverse associations with leptin and adiponectin were seen mainly in females, whereas the inverse PFAS associations with resistin levels were seen mainly in males. Estimates for significant associations (P value <0.05) suggested mean decreases in hormone levels (range) by 38% to 89% for leptin, 16% to 70% for adiponectin, and 33% to 62% for resistin for each twofold increase in serum PFAS concentration. CONCLUSIONS These findings suggest Adipokine hormone dysregulation in early life as a potential pathway underlying PFAS-related health outcomes and underscore the need to further account for susceptibility windows and sex-dimorphic effects in future investigations.
Christopher J Sinal - One of the best experts on this subject based on the ideXlab platform.
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chemerin a potential endocrine link between obesity and type 2 diabetes
Endocrine, 2012Co-Authors: Alexandra A Roman, Sebastian D Parlee, Christopher J SinalAbstract:Obesity and type 2 diabetes have reached epidemic levels and account for a substantial portion of the annual health expenditures of developed nations. While there is an abundance of epidemiological evidence demonstrating that obesity is a primary risk factor for developing type 2 diabetes, the mechanism(s) underlying this linkage are not completely understood. Given the enormous impact of these disorders on global health, considerable research effort has been devoted to elucidate the pathophysiological relationship between these two disorders. Two factors believed to contribute to the causal link between obesity and type 2 diabetes are chronic inflammation and altered secretion of adipose-derived signaling molecules (Adipokines). Independent lines of investigation have implicated the novel Adipokine chemerin as a regulator of adipogenesis, inflammation, and glucose metabolism through interactions with the cognate cell surface receptor chemokine-like receptor 1. Increased levels of chemerin that occur with obesity are hypothesized to be a causal factor in the development of type 2 diabetes as a consequence of dysregulation of the key physiological processes regulated by this Adipokine. This review summarizes current research on the biological roles of chemerin and chemokine-like receptor 1, and highlights key questions to guide future research on the role of this Adipokine in mediating obesity and the development of type 2 diabetes.
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chemerin exacerbates glucose intolerance in mouse models of obesity and diabetes
Endocrinology, 2010Co-Authors: Matthew C Ernst, Mark E Issa, Kerry B Goralski, Christopher J SinalAbstract:Obesity, characterized by an excess of adipose tissue, is an established risk factor for cardiovascular disease and type 2 diabetes. Different mechanisms linking obesity with these comorbidities have been postulated but remain poorly understood. Adipose tissue secretes a number of hormone-like compounds, termed Adipokines, that are important for the maintenance of normal glucose metabolism. Alterations in the secretion of Adipokines with obesity are believed to contribute to the undesirable changes in glucose metabolism that ultimately result in the development of type 2 diabetes. In the present study, we have shown that serum levels of the novel Adipokine chemerin are significantly elevated in mouse models of obesity/diabetes. The expression of chemerin and its receptors, chemokine-like receptor 1, chemokine (C-C motif) receptor-like 2, and G protein-coupled receptor 1 are altered in white adipose, skeletal muscle, and liver tissue of obese/diabetic mice. Administration of exogenous chemerin exacerbates glucose intolerance, lowers serum insulin levels, and decreases tissue glucose uptake in obese/diabetic but not normoglycemic mice. Collectively, these data indicate that chemerin influences glucose homeostasis and may contribute to the metabolic derangements characteristic of obesity and type 2 diabetes.
Philippe Grandjean - One of the best experts on this subject based on the ideXlab platform.
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possible impact of early life exposure to perfluoroalkyl substances on later childhood Adipokine concentrations in serum
Social Science Research Network, 2021Co-Authors: Philippe Grandjean, Yuhsuan Shih, Louise Helskov Jorgensen, Flemming Nielsen, Pal Weihe, Esben BudtzjorgensenAbstract:Background: Early-life exposure to perfluoroalkyl substances (PFASs) has been linked to metabolic health changes during later childhood, and a role of Adipokines is suspected. Aims: We examined the relative impact of PFAS exposure prenatally and during infancy on childhood Adipokine concentrations in serum. Subjects: All children belonged to a prospective birth cohort born in the Faroe Islands in 2007-2009 and followed up through to age 9 years. Study design: Adipokine concentrations in serum were measured at birth and age 9 years. Developmental PFAS exposure was determined from serum concentrations of the five major PFASs at birth and 18 months. Infancy PFAS exposures were estimated by structural equations. Outcome measures: Adipokines measured in serum included adiponectin, leptin, leptin receptor, and resistin. The adjusted regression coefficients for the estimated infancy-age PFAS exposures were compared with those obtained for measured PFAS concentrations at birth and age 18 months, with consideration of potential effect modification by sex. Results: Negative associations were found for resistin at age 9 years in regard to infancy PFAS exposures, and weak, positive associations for infancy exposures were observed for adiponectin. These associations tended to be stronger than prenatal exposures. Sex-dependence of the associations were not observed. Conclusions: Lowered serum-resistin concentrations at age 9 years were most strongly associated with early postnatal PFAS exposures. These findings suggest that infancy may represent a vulnerable time window for PFAS-associated metabolic programming.
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early life exposures to perfluoroalkyl substances in relation to Adipokine hormone levels at birth and during childhood
The Journal of Clinical Endocrinology and Metabolism, 2019Co-Authors: Philippe Grandjean, Colleen Shelly, Youssef Oulhote, Peter Plomgaard, Ruth FrikkeschmidtAbstract:BACKGROUND Birth cohort studies have linked exposure to perfluoroalkyl substances (PFASs) with child anthropometry. Metabolic hormone dysregulation needs to be considered as a potential adverse outcome pathway. We examined the associations between PFAS exposures and concentrations of Adipokine hormones from birth to adolescence. METHODS We studied 80 mother-child pairs from a Faroese cohort born in 1997 to 2000. Five PFASs were measured in maternal pregnancy serum and in child serum at ages 5, 7, and 13 years. Leptin, adiponectin, and resistin were analyzed in cord serum and child serum at the same ages. We fitted multivariable-adjusted generalized estimating equations to assess the associations of PFASs at each age with repeated Adipokine concentrations at concurrent and subsequent ages. RESULTS We observed tendencies of inverse associations between PFASs and Adipokine hormones specific to particular ages and sex. Significant associations with all Adipokines were observed for maternal and child 5-year serum PFAS concentrations, whereas associations for PFASs measured at ages 7 to 13 years were mostly null. The inverse associations with leptin and adiponectin were seen mainly in females, whereas the inverse PFAS associations with resistin levels were seen mainly in males. Estimates for significant associations (P value <0.05) suggested mean decreases in hormone levels (range) by 38% to 89% for leptin, 16% to 70% for adiponectin, and 33% to 62% for resistin for each twofold increase in serum PFAS concentration. CONCLUSIONS These findings suggest Adipokine hormone dysregulation in early life as a potential pathway underlying PFAS-related health outcomes and underscore the need to further account for susceptibility windows and sex-dimorphic effects in future investigations.
Concepción Peiró - One of the best experts on this subject based on the ideXlab platform.
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Visfatin/ Nampt: an Adipokine with cardiovascular impact,”Mediators
2020Co-Authors: Tania Romacho, Carlos F Sánchez-ferrer, Concepción PeiróAbstract:Adipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed Adipokines. Visfatin was initially identified as a novel Adipokine with insulin-mimetic properties in mice. This Adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhancing factor (PBEF) and the enzyme nicotinamide phosphoribosyltransferase (Nampt). Enhanced circulating visfatin/Nampt levels have been reported in metabolic diseases, such as obesity and type 2 diabetes. Moreover, visfatin/Nampt circulating levels correlate with markers of systemic inflammation. In cardiovascular diseases, visfatin/Nampt was initially proposed as a clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage, with a potential prognostic value. Nevertheless, beyond being a surrogate clinical marker, visfatin/Nampt is an active player promoting vascular inflammation, and atherosclerosis. Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this Adipokine an active factor in the development and progression of atherosclerosis. Further research is required to fully understand the mechanisms mediating the cellular actions of this Adipokine and to better characterize the factors regulating visfatin/Nampt expression and release in all these pathologic scenarios. Only then, we will be able to conclude whether visfatin/Nampt is a therapeutical target in cardiometabolic diseases
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visfatin nampt an Adipokine with cardiovascular impact
Mediators of Inflammation, 2013Co-Authors: Tania Romacho, Carlos F Sanchezferrer, Concepción PeiróAbstract:Adipose tissue is acknowledged as an endocrine organ that releases bioactive factors termed Adipokines. Visfatin was initially identified as a novel Adipokine with insulin-mimetic properties in mice. This Adipokine was identical to two previously described molecules, namely, pre-B cell colony-enhancing factor (PBEF) and the enzyme nicotinamide phosphoribosyltransferase (Nampt). Enhanced circulating visfatin/Nampt levels have been reported in metabolic diseases, such as obesity and type 2 diabetes. Moreover, visfatin/Nampt circulating levels correlate with markers of systemic inflammation. In cardiovascular diseases, visfatin/Nampt was initially proposed as a clinical marker of atherosclerosis, endothelial dysfunction, and vascular damage, with a potential prognostic value. Nevertheless, beyond being a surrogate clinical marker, visfatin/Nampt is an active player promoting vascular inflammation, and atherosclerosis. Visfatin/Nampt effects on cytokine and chemokine secretion, macrophage survival, leukocyte recruitment by endothelial cells, vascular smooth muscle inflammation and plaque destabilization make of this Adipokine an active factor in the development and progression of atherosclerosis. Further research is required to fully understand the mechanisms mediating the cellular actions of this Adipokine and to better characterize the factors regulating visfatin/Nampt expression and release in all these pathologic scenarios. Only then, we will be able to conclude whether visfatin/Nampt is a therapeutical target in cardiometabolic diseases.
Farshid Guilak - One of the best experts on this subject based on the ideXlab platform.
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serum and synovial fluid lipidomic profiles predict obesity associated osteoarthritis synovitis and wound repair
Scientific Reports, 2017Co-Authors: Kelly A Kimmerling, Dianne Little, Farshid GuilakAbstract:High-fat diet-induced obesity is a major risk factor for osteoarthritis (OA) and diminished wound healing. The objective of this study was to determine the associations among serum and synovial fluid lipid levels with OA, synovitis, Adipokine levels, and wound healing in a pre-clinical obese mouse model of OA. Male C57BL/6 J mice were fed either a low-fat (10% kcal) or one of three high-fat (HF, 60% kcal) diets rich in saturated fatty acids (SFAs), ω-6 or ω-3 polyunsaturated FAs (PUFAs). OA was induced by destabilization of the medial meniscus. Mice also received an ear punch for evaluating wound healing. Serum and synovial fluid were collected for lipidomic and Adipokine analyses. We demonstrated that the serum levels of ω-3 PUFAs were negatively correlated with OA and wound size, but positively correlated with adiponectin levels. In contrast, most ω-6 PUFAs exhibited positive correlations with OA, impaired healing, and inflammatory Adipokines. Interestingly, levels of pentadecylic acid (C15:0, an odd-chain SFA) and palmitoleic acid were inversely correlated with joint degradation. This study extends our understanding of the links of FAs with OA, synovitis and wound healing, and reports newly identified serum and synovial fluid FAs as predictive biomarkers of OA in obesity.