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The role of gut microbiota in childhood obesity. A review of evidence and perspectives
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Abstracts/Appetite 89 (2015) 301–330
C1QTNF5 expression is increased in adipose tissue from obese children and is regulated by TNFα in adipocytes J.T. SCHWARTZE, K. LANDGRAF, D. ROCKSTROH, D. LÖFFLER, K. SCHEUERMANN, J. KRATZSCH, W. KIESS, A. KÖRNER. Center for Pediatric Research Leipzig (CPL), Liebigstr. 21, 04103-Leipzig, Germany. [email protected] C1q tumor necrosis factor-related protein 5 (C1QTNF5, encodes CTRP5) has recently been identified as a novel adipocytokine. We aimed to assess the potential role of CTRP5 in early metabolic and cardiovascular dysfunction in obese children. To evaluate the relationship with adipose tissue (AT) composition, we assessed relative C1QTNF5 mRNA expression in subcutaneous (sc) AT samples obtained from 132 lean (N = 83) and obese children (N = 49) aged 9.17y ± 5.62 (0.14–18.5). Adipocyte size was determined in a Coulter counter after fixation in osmium. CTRP5 serum levels from 178 lean (N = 71) and obese (N = 107) children aged 12.95y ± 2.96 (7.53– 18.84) were assessed by ELISA to evaluate the association with glucose metabolism. To assess potential regulation by inflammatory cytokines we stimulated human adipocytes with TNFα (10 ng/ml) for 24 hours and assessed C1QTNF5 levels. Relative C1QTNF5 mRNA levels were 3.4-fold (P = 0.01) increased in sc AT samples from obese children and positively correlated with BMI SDS (r = 0.19, P = 0.02) and mean adipocyte size (r = 0.46, P = 0.005). TNFα stimulated C1QTNF5 expression 2-fold (P < 0.001) in human adipocytes. Circulating CTRP5 serum levels were not significantly altered in overweight and obese children compared to lean controls and did not correlate with any markers of metabolic and cardiovascular dysfunction, such as HOMA, the reactive hyperemia index, or intima media thickness. C1QTNF5 mRNA expression increases with the degree of obesity and particularly with adipocyte hypertrophy. In mature adipocytes, this increase can be stimulated by TNFα. However, serum levels of CTRP5 were not associated with the degree of obesity or associated comorbidities in children. http://dx.doi.org/10.1016/j.appet.2014.12.095
The role of gut microbiota in childhood obesity. A review of evidence and perspectives C.E. FONVIG a,b, A.F. PIHL a, T. HANSEN b, O. PEDERSEN b, J.-C. HOLM a. a Department of Pediatrics, The Children’s Obesity Clinic, Holbæk, Denmark, b The Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, University of Copenhagen, Denmark. [email protected] Recent evidence suggests that obesity is associated with phylogenetic changes in the gut microbiota, which could potentially reveal new avenues for obesity prevention and treatment. This review is focusing on recent advances addressing the potential role of the human gut microbiota in childhood and adolescent onset obesity. A systematic search for papers between 1995 and 2014 addressing childhood obesity and the gut microbiota was conducted. Recently, a growing number of associations between the gut microbiota and childhood obesity and its related disorders have emerged. The gut microbial ecology is affected by numerous factors including diet, mode of delivery, host genome, and intake of pre-, pro-, and antibiotics. The gut microbiota is responsible for many actions in the human body, such as providing energy for the intestinal mucosa, improving de novo synthesis of glucose or lipids, and regulating the secretion of a wide range of hormones involved in appetite, glucose-, and lipid homeostasis. A vast number of variables are influencing the gut microbial ecology. New advances in metagenomic sequencingbased techniques and advanced bioinformatic analyses are able to provide high-resolution mapping of the human gut microbiome. When such cohort and interventional analyses are combined with mechanistic studies of the pathogenic potential of altered human gut microbiota in germ-free mice it opens for a series of avenues for elucidating the more specific roles – if any – of gut microbiota in the pathogenesis of childhood-onset obesity. http://dx.doi.org/10.1016/j.appet.2014.12.096
Abstracts/Appetite 89 (2015) 301–330
C1QTNF5 expression is increased in adipose tissue from obese children and is regulated by TNFα in adipocytes J.T. SCHWARTZE, K. LANDGRAF, D. ROCKSTROH, D. LÖFFLER, K. SCHEUERMANN, J. KRATZSCH, W. KIESS, A. KÖRNER. Center for Pediatric Research Leipzig (CPL), Liebigstr. 21, 04103-Leipzig, Germany. [email protected] C1q tumor necrosis factor-related protein 5 (C1QTNF5, encodes CTRP5) has recently been identified as a novel adipocytokine. We aimed to assess the potential role of CTRP5 in early metabolic and cardiovascular dysfunction in obese children. To evaluate the relationship with adipose tissue (AT) composition, we assessed relative C1QTNF5 mRNA expression in subcutaneous (sc) AT samples obtained from 132 lean (N = 83) and obese children (N = 49) aged 9.17y ± 5.62 (0.14–18.5). Adipocyte size was determined in a Coulter counter after fixation in osmium. CTRP5 serum levels from 178 lean (N = 71) and obese (N = 107) children aged 12.95y ± 2.96 (7.53– 18.84) were assessed by ELISA to evaluate the association with glucose metabolism. To assess potential regulation by inflammatory cytokines we stimulated human adipocytes with TNFα (10 ng/ml) for 24 hours and assessed C1QTNF5 levels. Relative C1QTNF5 mRNA levels were 3.4-fold (P = 0.01) increased in sc AT samples from obese children and positively correlated with BMI SDS (r = 0.19, P = 0.02) and mean adipocyte size (r = 0.46, P = 0.005). TNFα stimulated C1QTNF5 expression 2-fold (P < 0.001) in human adipocytes. Circulating CTRP5 serum levels were not significantly altered in overweight and obese children compared to lean controls and did not correlate with any markers of metabolic and cardiovascular dysfunction, such as HOMA, the reactive hyperemia index, or intima media thickness. C1QTNF5 mRNA expression increases with the degree of obesity and particularly with adipocyte hypertrophy. In mature adipocytes, this increase can be stimulated by TNFα. However, serum levels of CTRP5 were not associated with the degree of obesity or associated comorbidities in children. http://dx.doi.org/10.1016/j.appet.2014.12.095
The role of gut microbiota in childhood obesity. A review of evidence and perspectives C.E. FONVIG a,b, A.F. PIHL a, T. HANSEN b, O. PEDERSEN b, J.-C. HOLM a. a Department of Pediatrics, The Children’s Obesity Clinic, Holbæk, Denmark, b The Novo Nordisk Foundation Center for Basic Metabolic Research, Section of Metabolic Genetics, University of Copenhagen, Denmark. [email protected] Recent evidence suggests that obesity is associated with phylogenetic changes in the gut microbiota, which could potentially reveal new avenues for obesity prevention and treatment. This review is focusing on recent advances addressing the potential role of the human gut microbiota in childhood and adolescent onset obesity. A systematic search for papers between 1995 and 2014 addressing childhood obesity and the gut microbiota was conducted. Recently, a growing number of associations between the gut microbiota and childhood obesity and its related disorders have emerged. The gut microbial ecology is affected by numerous factors including diet, mode of delivery, host genome, and intake of pre-, pro-, and antibiotics. The gut microbiota is responsible for many actions in the human body, such as providing energy for the intestinal mucosa, improving de novo synthesis of glucose or lipids, and regulating the secretion of a wide range of hormones involved in appetite, glucose-, and lipid homeostasis. A vast number of variables are influencing the gut microbial ecology. New advances in metagenomic sequencingbased techniques and advanced bioinformatic analyses are able to provide high-resolution mapping of the human gut microbiome. When such cohort and interventional analyses are combined with mechanistic studies of the pathogenic potential of altered human gut microbiota in germ-free mice it opens for a series of avenues for elucidating the more specific roles – if any – of gut microbiota in the pathogenesis of childhood-onset obesity. http://dx.doi.org/10.1016/j.appet.2014.12.096