Artykuły w czasopismach: „Adiposity”

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Kotchen, T. A. "Adiposity-Sensitive and Adiposity-Resistant Hypertension?" American Journal of Hypertension 21, nr 10 (1.10.2008): 1074. http://dx.doi.org/10.1038/ajh.2008.257.

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Dong, Hongbo, Xiaoyuan Zhao, Hong Cheng i Jie Mi. "Childhood adiposity, adult adiposity, and bone health". Pediatric Investigation 5, nr 1 (marzec 2021): 6–11. http://dx.doi.org/10.1002/ped4.12244.

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Cornier, Marc-Andre, Jean-Pierre Després, Nichola Davis, Daurice A. Grossniklaus, Samuel Klein, Benoit Lamarche, Francisco Lopez-Jimenez i in. "Assessing Adiposity". Circulation 124, nr 18 (listopad 2011): 1996–2019. http://dx.doi.org/10.1161/cir.0b013e318233bc6a.

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Ludwig, David S., i Mark I. Friedman. "Increasing Adiposity". JAMA 311, nr 21 (4.06.2014): 2167. http://dx.doi.org/10.1001/jama.2014.4133.

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Campbell, Michele Wen-Chien, Joanne Williams, John B. Carlin i Melissa Wake. "Is the adiposity rebound a rebound in adiposity?" International Journal of Pediatric Obesity 6, nr 2-2 (czerwiec 2011): e207-e215. http://dx.doi.org/10.3109/17477166.2010.526613.

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Juonala, Markus, Costan G. Magnussen, Gerald S. Berenson, Alison Venn, Trudy L. Burns, Matthew A. Sabin, Sathanur R. Srinivasan i in. "Childhood Adiposity, Adult Adiposity, and Cardiovascular Risk Factors". Obstetrical & Gynecological Survey 67, nr 3 (marzec 2012): 156–58. http://dx.doi.org/10.1097/ogx.0b013e3182483780.

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Juonala, Markus, Costan G. Magnussen, Gerald S. Berenson, Alison Venn, Trudy L. Burns, Matthew A. Sabin, Sathanur R. Srinivasan i in. "Childhood Adiposity, Adult Adiposity, and Cardiovascular Risk Factors". New England Journal of Medicine 365, nr 20 (17.11.2011): 1876–85. http://dx.doi.org/10.1056/nejmoa1010112.

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Stockman, J. A. "Childhood Adiposity, Adult Adiposity, and Cardiovascular Risk Factors". Yearbook of Pediatrics 2013 (styczeń 2013): 223–25. http://dx.doi.org/10.1016/j.yped.2012.03.093.

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Hughes, A. R., A. Sherriff, A. R. Ness i J. J. Reilly. "Timing of Adiposity Rebound and Adiposity in Adolescence". PEDIATRICS 134, nr 5 (13.10.2014): e1354-e1361. http://dx.doi.org/10.1542/peds.2014-1908.

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Landsberg, Beate, i Regina Ensenauer. "Fetale Prägung von ernährungsmitbedingten Krankheiten und frühe Prävention – die Mutter-Kind-Kohorte PEACHES". Public Health Forum 27, nr 4 (18.12.2019): 279–82. http://dx.doi.org/10.1515/pubhef-2019-0065.

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Zusammenfassung Mit dem globalen Anstieg von Adipositas und Komorbiditäten im Kindes- und Jugendalter gewinnen Primärpräventionskonzepte zunehmend an Bedeutung. Mithilfe der prospektiven Kohorte PEACHES (Programming of Enhanced Adiposity Risk in CHildhood – Early Screening), die Mütter mit bereits vor der Schwangerschaft bestehender Adipositas und deren Kinder einschließt, werden frühe Einflussfaktoren und Risikomarker für kindliches Übergewicht und assoziierte metabolische Erkrankungen erforscht, um gezielte Präventionsstrategien zu entwickeln.

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de Lima, Josivan G., Lúcia H. C. Nóbrega i Alexandre B. C. de Souza. "Body Adiposity Index Indicates Only Total Adiposity, Not Risk". Obesity 20, nr 6 (czerwiec 2012): 1140. http://dx.doi.org/10.1038/oby.2012.3.

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Damay, Vito, i Alberta Claudia Undarsa. "Correlation of Waist to Height Ratio with Leptin Serum Level in Coronary Artery Disease". Indonesian Journal of Cardiology 38, nr 4 (19.08.2018): 195–201. http://dx.doi.org/10.30701/ijc.v38i4.784.

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Background: Adiposity assessment plays an important role in coronary artery disease (CAD) prevention. One of the adiposity parameter in major CAD management guideline is waist to height ratio (WHtR). Adiposity promotes the pathogenesis of coronary atherosclerosis by involving adipokines released by adipose tissue. Leptin is obesity identic adipokine which is used as prognostic predictor of cardiovascular event. This study aims to analyze correlation between WHtR and leptin serum level. Method: A cross sectional study was performed to 37 stable CAD patients undergone elective coronary angiography in Heart Catheterization Laboratory Dr Hasan Sadikin Hospital, Bandung, West java in July 2014 Results: Mean age of the subjects was 56.7± 9.12 years old with mean age of men (n=32) and women (n=5) were 55.9±9.47 years old and 62±3.54 years old consecutively. There were 30 (81%) subjects classified as obese (WHtR≥0.5) with mean WHtR 0.54±0,06. Median value of leptin serum was 8599.90 pg/ml (780-36929.3 pg/ml). Based on rank-spearman correlation test, a positive moderate correlation was significantly found between WHtR and Leptin serum level (Spearman’s rho = 0.5, p= 0.001). Conclusion: Positive correlation was found between WHtR and leptin serum level. Hence, WHtR might be useful as indicator of leptin serum level which has been used as a prognostic biomarker in CAD patients Abstrak Latar belakang: Penilaian adipositas merupakan bagian dari upaya preventif penyakit jantung koroner (PJK). Salah satu parameter antropometri adipositas yang digunakan pada panduan tatalaksana PJK adalah pengukuran rasio lingkar pinggang/tinggi badan (LP/TB). Adipositas diketahui berperan dalam patomekanisme terbentuknya aterosklerosis koroner melalui pelepasan adipositokin oleh jaringan adiposa. Leptin merupakan adipositokin identik adiposit yang digunakan sebagai biomarka indikator prognostik kejadian kardiovaskular. Penelitian ini bertujuan untuk menganalisa korelasi LP/TB dengan kadar leptin serum. Metode: Studi potong lintang dengan menganalisis antropometri LP/TB dan kadar leptin serum pada 37 pasien PJK yang menjalani angiografi elektif di Laboratorium Kateterisasi Jantung RSUP Dr.Hasan Sadikin, Bandung, Jawa Barat pada bulan Juli 2014. Hasil: Rerata usia subjek adalah 56.7± 9.12 tahun dengan rerata usia pria (n=32) dan wanita (n=5) secara berurutan adalah 55.9±9.47 tahun dan 62±3.54 tahun. Terdapat 30 (81%) subjek tergolong obesitas (nilai LP/TB ≥0,5) dengan rata-rata LP/TB 0.54±0,06. Nilai median leptin serum 8599.90 pg/ml (780-36929.3 pg/ml). Berdasarkan uji korelasi rank-spearman, terdapat korelasi positif bermakna antara LP/TB dengan kadar leptin serum (Spearman rho = 0.5, p= 0.001). Kesimpulan: Terdapat korelasi positif bermakna antara pemeriksaan antropometri LP/TB dengan kadar leptin serum. Rasio lingkar pinggang/tinggi badan dapat digunakan sebagai salah satu indikator kadar leptin serum yang merupakan biomarka prognostik kardiovaskular.

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Bloomgarden, Z. T. "Adiposity and Diabetes". Diabetes Care 25, nr 12 (1.12.2002): 2342–49. http://dx.doi.org/10.2337/diacare.25.12.2342.

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Purcell, Henry, i Caroline Day. "Achieving acceptable adiposity". British Journal of Diabetes & Vascular Disease 8, nr 4 (lipiec 2008): 159–61. http://dx.doi.org/10.1177/1474651408096947.

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Jørgensen, Jens O. L., Nina Vahl, Sannen Fisker, Helene Nørrelund, Sten Nielsen, Rolf Dall i Jens S. Christiansen. "Somatopause and Adiposity". Hormone Research 48, nr 5 (1997): 101–4. http://dx.doi.org/10.1159/000191337.

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Flint, Harry J. "Antibiotics and adiposity". Nature 488, nr 7413 (sierpień 2012): 601–2. http://dx.doi.org/10.1038/488601a.

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Vernon, R. G., R. G. P. Denis i A. Sørensen. "Signals of adiposity". Domestic Animal Endocrinology 21, nr 4 (listopad 2001): 197–214. http://dx.doi.org/10.1016/s0739-7240(01)00121-7.

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Gaida, J. E., J. L. Cook i S. L. Bass. "Adiposity and tendinopathy". Disability and Rehabilitation 30, nr 20-22 (styczeń 2008): 1555–62. http://dx.doi.org/10.1080/09638280701786864.

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Alimujiang, Aliya, Catherine Appleton, Graham A. Colditz i Adetunji T. Toriola. "Adiposity during early adulthood, changes in adiposity during adulthood, attained adiposity, and mammographic density among premenopausal women". Breast Cancer Research and Treatment 166, nr 1 (12.07.2017): 197–206. http://dx.doi.org/10.1007/s10549-017-4384-4.

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Lee, Jane J., S. Natasha Beretvas i Jeanne H. Freeland-Graves. "Abdominal Adiposity Distribution in Diabetic/Prediabetic and Nondiabetic Populations: A Meta-Analysis". Journal of Obesity 2014 (2014): 1–20. http://dx.doi.org/10.1155/2014/697264.

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Excess fat in the abdomen can be classified generally as visceral and subcutaneous adiposity. Evidence suggests that visceral adiposity has greater implications for diabetes than other fat depots. The purpose of this study is to explore the disparities in the distribution of abdominal adiposity in diabetic/prediabetic and nondiabetic populations and to identify moderators that influence the pattern of central obesity via a meta-analysis technique. The Hedges’gwas used as a measure of effect size and 95% confidence interval was computed. A total of 41 relevant studies with 101 effect sizes were retrieved. Pooled effect sizes for visceral and subcutaneous adiposity were 0.69 and 0.42, respectively. Diabetic/prediabetic populations exhibited greater visceral and subcutaneous adiposity compared to nondiabetic populations (Z=10.35,P<0.05). Significant moderator effects of gender (Z=-2.90) and assessment method of abdominal adiposity (Z=-2.17) were found for visceral fat (P<0.05), but not for subcutaneous fat. Type of health condition influenced both visceral (Z=-5.10) and subcutaneous (Z=-7.09) abdominal adiposity volumes (P<0.05). Abdominal adiposity distributions were significantly altered in the diabetic/prediabetic population compared to the nondiabetic population. Gender, assessment method of abdominal adiposity, and type of health conditions (diabetic/prediabetics) were identified as crucial moderators that influence the degree of abdominal adiposity.

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Ebadi-Vanestanagh, Marziyeh, Roghayeh Molani-Gol, Leili Faraji-Gavgani i Mohammad Alizadeh. "Neck circumference, visceral adiposity, and hypertension: does upper body adiposity outperforms visceral adiposity in terms of hypertension predictions?" Arterial Hypertension 25, nr 1 (31.03.2021): 22–28. http://dx.doi.org/10.5603/ah.a2021.0005.

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Yajnik, C. S. "Obesity epidemic in India: intrauterine origins?" Proceedings of the Nutrition Society 63, nr 3 (sierpień 2004): 387–96. http://dx.doi.org/10.1079/pns2004365.

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The epidemic of ‘obesity’ in India is not appreciated because BMI underestimates the adiposity of Indians. Specific adiposity measurements are necessary for recognition of the adiposity of ‘thin’ Indians. The origin of this adiposity is only beginning to be understood. In addition to a possible genetic predisposition, intrauterine ‘programming’ might be responsible, although in the ‘thrifty phenotype’ hypothesis the adiposity of the ‘thin’ fetus has not been appreciated. Dutch men who faced ‘winter hunger’ during the first trimester of their in utero life have become more obese as adults. Low birth weight predicts central obesity in some studies, including studies in urban children. It has also been shown that small and thin Indian newborns (weight 2·7?kg and ponderal index 2·4?kg\m3) have poor muscle and visceral mass but higher adiposity for a given weight compared with white Caucasian babies. This body composition is influenced by maternal adiposity before pregnancy and by aspects of maternal nutritional intake and circulating nutrient concentrations during pregnancy. There are no strong paternal determinants of adiposity at birth. Adiposity may be an integral part of the orchestrated adjustments made to support ‘brain preservation’ during intrauterine growth, because brain tissue is predominantly fat. Increased nutrition in the face of a genetic predisposition or multigenerational undernutrition increases maternal insulin resistance in late pregnancy and promotes fetal adiposity even in absence of marked hyperglycaemia. Further research is necessary to define the role of specific nutrients and metabolites in the intrauterine processes promoting adiposity before maternal interventions to curtail the epidemic of obesity and diabetes are planned.

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Wang, K. W., E. Kearsley, N. Falzone, A. Fleming, S. Burrow, R. J. de Souza, L. Thabane i M. C. Samaan. "PS1 - 176 Where Have All the Fat Cells Gone? A Comparative Analysis of Adiposity Patterns in Childhood Brain Tumor Survivors and Non-Cancer Controls". Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, S4 (październik 2016): S11. http://dx.doi.org/10.1017/cjn.2016.359.

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Brain tumors are the most common solid tumors in children in Canada. While technological advances have increased their survival rates, survivors of childhood brain tumors (SCBT) often develop obesity, which can reduce lifespan and quality of life. While adiposity is a known factor for cardiometabolic disorders in the general population, adiposity patterns in SCBT have not been determined. This study aims to investigate how adiposity patterns differ between SCBT and non-cancer controls, and how lifestyle and treatment factors may contribute to these patterns. Methods: Fifty-nine SCBT and 108 non-cancer controls were recruited from the clinics at McMaster Children’s Hospital. Sociodemographic and lifestyle details were collected using standardized tools to assess diet, physical activity, and sleep. Brain tumor type, location and treatment details were obtained from medical records. Total and visceral adiposity were determined by total fat mass (FM) as well as waist-to-hip (WHR) and waist-to-height ratio (WHTR). Results: SCBT have higher total and visceral adiposity, while BMI is similar to controls. Female SCBT who received radiotherapy and/or chemotherapy have higher adiposity. A dietary pattern of white bread and fried foods with low dark bread was positively associated with adiposity. Lower physical activity levels, but not sleep durations, were associated with higher adiposity. Conclusion: SCBT have higher visceral and total adiposity than non-cancer controls. Sex, chemoradiotherapy, high fat diet, and physical inactivity, can contribute to these adiposity patterns. These results provide multiple points of entry to design interventions that reduce adiposity, and may improve long-term outcomes in SCBT.

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Sun, Cong, Anne-Louise Ponsonby, John B. Carlin, Minh Bui, Costan G. Magnussen, Trudy L. Burns, Terho Lehtimaki i in. "Childhood adiposity, adult adiposity, and the ACE gene insertion/deletion polymorphism". Journal of Hypertension 36, nr 11 (listopad 2018): 2168–76. http://dx.doi.org/10.1097/hjh.0000000000001816.

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Kryst, Łukasz, Magdalena Żegleń, Iwona Wronka, Agnieszka Woronkowicz, Inez Bilińska-Pawlak, Rituparna Das, Rana Saha, Sukanta Das i Parasmani Dasgupta. "Anthropometric variations in different BMI and adiposity levels among children, adolescents and young adults in Kolkata, India". Journal of Biosocial Science 51, nr 4 (4.12.2018): 603–18. http://dx.doi.org/10.1017/s0021932018000354.

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AbstractThe objective of the study was to analyse selected anthropometric features of children, adolescents and young adults from middle-class families in Kolkata, India, by BMI and adiposity categories. Standardized anthropometric measurements of 4194 individuals (1999 male and 2195 female) aged 7–21 were carried out between the years 2005 and 2011. The results were compared by BMI and adiposity categories. Statistical significance was assessed using two-way-ANOVA and linear regression analysis was performed. The study population could be differentiated in terms of BMI and adiposity categories for all examined anthropometric characteristics (p≤ 0.001). After taking age into consideration, differences were observed for males in the case of body height and humerus breadth in BMI and adiposity categories, and for femur breadth in the case of adiposity categories. For females, differences were noted in body height measurements in BMI and adiposity categories, a sum of skinfold thicknesses in BMI categories, and upper-arm and calf circumferences in adiposity categories. The patterns of differences in the BMI categories were found to be similar to those in adiposity categories. The linear regression analysis results showed that there was a significant relationship between BMI and body fat ratio in the examined population. Underweight individuals, and those with low adiposity, were characterized by lower extremity circumferences and skeletal breadths. These features reached highest values in overweight/obese persons, characterized by high body fat. However, the differences observed between each BMI and adiposity category, in most cases, were only present in early childhood.

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Narciso Santiago, Leandro, Priscila Custódio Martins i Diego Augusto Santos Silva. "Association between excess peripheral, central and general adiposity with high blood pressure in adolescents in southern Brazil." Journal of Human Growth and Development 32, nr 1 (31.01.2022): 120–28. http://dx.doi.org/10.36311/jhgd.v32.12969.

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Introduction: excess adiposity is one of the main risk factors for cardiovascular diseases, including high blood pressure. Children and adolescents with obesity and hypertension are at greater risk of morbidity and mortality in adulthood. Objective: to analyze the association between excess peripheral, central and general adiposity with high blood pressure in adolescents in southern Brazil. Methods: this is a cross-sectional study with 1,132 adolescents (16.50 ± 1.14 years) of both sexes. Measurements were performed with the oscillometric method using digital sphygmomanometer, considering high systolic and diastolic blood pressure, values above the 95th percentile for sex and age. Peripheral adiposity (triceps skinfold) and central adiposity (subscapular skinfold) were classified as high from the 90th percentile of the Centers for Disease Control and Prevention reference distribution. For excess general adiposity, triceps and subscapular skinfold above the 90th percentile were simultaneously considered. Logistic regression was used with 5% significance level. Results: male adolescents with high peripheral, central and general adiposity were, respectively, 2.43 (95% CI: 1.14; 5.19), 3.50 (95% CI: 1.66; 7.41) and 2.47 (95% CI: 1.01; 6.18) times more likely of having high SBP. Male adolescents with excess general adiposity were more likely of developing high diastolic blood pressure (OR: 3.31; 95% CI: 1.41; 7.70). Female adolescents with excess central and general adiposity were 4.15 (95% CI: 1.97; 8.77) and 3.30 (95% CI: 1.41; 7.77) times more likely of developing high diastolic blood pressure, respectively. Conclusion: male adolescents with excess peripheral, central and general adiposity were more likely of having high systolic blood pressure and high diastolic blood pressure when presenting high general adiposity. In addition, female adolescents with high excess central and general adiposity were more likely of having high diastolic blood pressure.

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Lian, Rong, Zheng-He Wang, Zhi-Yong Zou, Yan-Hui Dong, Yi-De Yang i Jun Ma. "Does a Healthy Lifestyle Lower the Elevated Risk of Obesity Caused by Caesarian Section Delivery in Children and Adolescents?" Nutrients 14, nr 17 (26.08.2022): 3528. http://dx.doi.org/10.3390/nu14173528.

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Background: Both caesarean section (CS) and lifestyle were linked with child adiposity. This study aimed to investigate whether CS delivery is linked with elevated risk of child adiposity regardless of a healthy lifestyle. Methods: All the subjects in this study came from a baseline survey of a national school-based program on healthy lifestyle interventions against adiposity among Chinese children and adolescents. A questionnaire was used to collect the information on delivery mode and lifestyle. According to the weighted lifestyle score, subjects were categorized into healthy, intermediate, and unhealthy lifestyle. Results: A total of 44,961 children aged 6–18 years were enrolled in the current study. Overall, 41.9% (18,855/44,961) of children were delivered by CS. Compared with children delivered by vaginal delivery, children delivered by CS had a higher adiposity risk (OR = 1.56; 95%CI: 1.46–1.66; p < 0.001) after adjustment for age, sex, region, mother adiposity, ethnicity, and weighted lifestyle factors. Compared with children with a healthy lifestyle, children with an unhealthy lifestyle had a higher risk of child adiposity (OR = 1.31; 95%CI: 1.19–1.44). Children delivered by CS who had an unhealthy lifestyle had a 106% higher (OR = 2.06; 95%CI: 1.79–2.37) risk of child adiposity compared with children delivered by vaginal delivery who had a healthy lifestyle. However, keeping a healthy lifestyle in later life seems not to offset the increased risk of child adiposity caused by CS (OR = 1.59; 95%CI: 1.39–1.82). Conclusions: Both CS and unhealthy lifestyle were linked with child adiposity risk. Keeping a healthy lifestyle did not counteract the elevated risk of child adiposity caused by CS.

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Anwar, Mohammad Y., Laura M. Raffield, Leslie A. Lange, Adolfo Correa i Kira C. Taylor. "Genetic underpinnings of regional adiposity distribution in African Americans: Assessments from the Jackson Heart Study". PLOS ONE 16, nr 8 (4.08.2021): e0255609. http://dx.doi.org/10.1371/journal.pone.0255609.

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Background African ancestry individuals with comparable overall anthropometric measures to Europeans have lower abdominal adiposity. To explore the genetic underpinning of different adiposity patterns, we investigated whether genetic risk scores for well-studied adiposity phenotypes like body mass index (BMI) and waist circumference (WC) also predict other, less commonly measured adiposity measures in 2420 African American individuals from the Jackson Heart Study. Methods Polygenic risk scores (PRS) were calculated using GWAS-significant variants extracted from published studies mostly representing European ancestry populations for BMI, waist-hip ratio (WHR) adjusted for BMI (WHRBMIadj), waist circumference adjusted for BMI (WCBMIadj), and body fat percentage (BF%). Associations between each PRS and adiposity measures including BF%, subcutaneous adiposity tissue (SAT), visceral adiposity tissue (VAT) and VAT:SAT ratio (VSR) were examined using multivariable linear regression, with or without BMI adjustment. Results In non-BMI adjusted models, all phenotype-PRS were found to be positive predictors of BF%, SAT and VAT. WHR-PRS was a positive predictor of VSR, but BF% and BMI-PRS were negative predictors of VSR. After adjusting for BMI, WHR-PRS remained a positive predictor of BF%, VAT and VSR but not SAT. WC-PRS was a positive predictor of SAT and VAT; BF%-PRS was a positive predictor of BF% and SAT only. Conclusion These analyses suggest that genetically driven increases in BF% strongly associate with subcutaneous rather than visceral adiposity and BF% is strongly associated with BMI but not central adiposity-associated genetic variants. How common genetic variants may contribute to observed differences in adiposity patterns between African and European ancestry individuals requires further study.

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Christou, Demetra D., Gary L. Pierce, Ashley E. Walker, Moon-Hyon Hwang, Jeung-Ki Yoo, Meredith Luttrell, Thomas H. Meade, Mark English i Douglas R. Seals. "Vascular smooth muscle responsiveness to nitric oxide is reduced in healthy adults with increased adiposity". American Journal of Physiology-Heart and Circulatory Physiology 303, nr 6 (15.09.2012): H743—H750. http://dx.doi.org/10.1152/ajpheart.00394.2012.

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Vascular smooth muscle responsiveness to nitric oxide, as assessed by nitroglycerin-induced dilation (NID), is impaired in clinical cardiovascular disease, but its relation to adiposity is unknown. We determined the relation of NID to total and abdominal adiposity in healthy adults varying widely in adiposity. In 224 men and women [age, 18–79 years; body mass index (BMI), 16.4–42.2 kg/m2], we measured NID (brachial artery dilation to 0.4 mg sublingual nitroglycerin), total body adiposity [BMI and percent body fat (percent BF via dual-energy X-ray absorptiometry)], and indexes of abdominal adiposity [waist circumference (WC) and waist-to-hip ratio (WHR)]. In a subgroup ( n = 74), we also measured total abdominal fat (TAF), abdominal visceral fat (AVF), and subcutaneous fat (ASF) using computed tomography. Based on multiple linear regression, NID was negatively related to BMI [part correlation coefficient ( rpart) = −0.19, P = 0.004] and abdominal adiposity (WC, rpart = −0.22; WHR, rpart = −0.19; TAF, rpart = −0.36; AVF, rpart = −0.36; and ASF, rpart = −0.30; all P ≤ 0.009) independent of sex, but only tended to be related to total percent BF ( rpart = −0.12, P = 0.07). In a subgroup of subjects with the highest compared with the lowest amount of AVF, NID was 35% lower ( P = 0.003). Accounting for systolic blood pressure, HDL cholesterol, glucose, insulin resistance, adiponectin, and brachial artery diameter reduced or abolished some of the relations between NID and adiposity. In conclusion, NID is or tends to be negatively associated with measures of total adiposity (BMI and percent BF, respectively) but is consistently and more strongly negatively associated with abdominal adiposity. Adiposity may influence NID in part via other cardiovascular risk factors.

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Ali, Hira, Joseph M. Zmuda, Ryan K. Cvejkus, Erin E. Kershaw, Allison L. Kuipers, Elizabeth A. Oczypok, Victor Wheeler, Clareann H. Bunker i Iva Miljkovic. "Wnt Pathway Inhibitor DKK1: A Potential Novel Biomarker for Adiposity". Journal of the Endocrine Society 3, nr 2 (3.01.2019): 488–95. http://dx.doi.org/10.1210/js.2018-00325.

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Abstract Emerging evidence indicates that ectopic skeletal muscle adiposity may be a risk factor for type 2 diabetes (T2D), especially in persons of African ancestry. In vitro studies suggest that a Wnt pathway inhibitor, Dickkopf-related protein 1 (DKK1), plays a role in adiposity regulation and could be a biomarker for adiposity in humans. The objective of this study was to test whether serum DKK1 levels relate to adiposity measures in a cohort from an African ancestry population at high risk for T2D. Fasting serum DKK1 was measured in a sample of 159 men of African ancestry aged ≥40 years (mean age ± SD, 63.5 ± 8.2 years; mean body mass index, 27.8 ± 4.5 kg/m2). Anthropometrics included total-body and trunk adiposity measured by dual-energy x-ray absorptiometry and lower-leg skeletal muscle density measured by CT [which reflects the intramuscular adiposity content (mg/cm3)]. Serum DKK1 was positively correlated with BMI (r = 0.20; P = 0.01), waist circumference (r = 0.15; P = 0.046), DXA total-body adiposity (r = 0.24; P = 0.003), and DXA trunk adiposity (r = 0.21; P = 0.009), independent of age and height. In addition, serum DKK1 was inversely correlated with skeletal muscle density (r = −0.25; P = 0.002), independent of age, BMI, and calf muscle area. No significant correlation was found between serum DKK1 and fasting serum glucose or insulin levels or insulin resistance estimated by homeostasis model assessment. These findings suggest that higher levels of serum DKK1 may be associated with greater overall, central, and ectopic skeletal muscle adiposity. Further studies are needed to unravel the potential role of DKK1 in the regulation of adiposity in humans.

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Ekelund, Ulf, Maria Hildebrand i Paul J. Collings. "Physical activity, sedentary time and adiposity during the first two decades of life". Proceedings of the Nutrition Society 73, nr 2 (19.02.2014): 319–29. http://dx.doi.org/10.1017/s0029665114000019.

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High amounts of time spent sedentary and low levels of physical activity have been implicated in the process of excessive adiposity gains in youth. The aim of this review is to discuss the role of physical activity, sedentary time and behaviour (i.e. television (TV)-viewing) in relation to adiposity during the first two decades of life with a specific focus on whether the association between sedentary time, and behaviour and adiposity is independent of physical activity. We identified nine cohort studies (three prospective) whether sedentary time was associated with adiposity independent of physical activity. Eight of these studies suggested that sedentary time was unrelated to adiposity when physical activity was taken into account. Results from studies (n 8) examining the independent association between TV-viewing and adiposity independent of physical activity were mixed. Those that observed a positive association between TV-viewing and adiposity independent of physical activity discussed that the association may be due to residual confounding. A few additional studies have also challenged the general notion that low levels of physical activity leads to fatness and suggested that higher baseline fatness may be predictive of a decline in physical activity. It appears unlikely that higher levels of sedentary time are associated with or predictive of, higher levels of adiposity when physical activity is controlled for in youth. Specific sedentary behaviours such as TV-viewing may be associated with adiposity independent of physical activity but the results may be explained by residual confounding.

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Parkinson, Kathryn N., Ashley J. Adamson, Laura Basterfield, Jessica K. Reilly, Ann Le Couteur i John J. Reilly. "Influence of adiposity on health-related quality of life in the Gateshead Millennium Study cohort: longitudinal study at 12 years". Archives of Disease in Childhood 100, nr 8 (2.06.2015): 779–83. http://dx.doi.org/10.1136/archdischild-2014-307498.

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ObjectiveTo examine whether adiposity is associated with an impaired quality of life (an individual's perception of their life) in general population samples in early adolescence.Design and methodsRelationships between a direct measure of adiposity (fat mass index from bioimpedance) and a proxy measure (waist circumference), and a generic (KIDSCREEN-27) and a weight-specific measure of health-related quality of life (HRQoL, Impact of Weight on Quality of Life-Kids (IWQOL-Kids)) were examined in a longitudinal population-based cohort of young adolescents aged 12 years (n=519). The effects of change in adiposity over time (from 7 years and 9 years) were also examined (n=331–445 in longitudinal analyses).ResultsImpairment in HRQoL was associated with current adiposity but it was not predicted by earlier adiposity. At 12 years, higher adiposity was associated with lower Physical Well-Being on KIDSCREEN-27, and with lower Total Scores on the weight-specific IWQOL-Kids instrument, the latter particularly in girls.ConclusionsHealth and education professionals need to be aware in their clinical practice that higher adiposity impairs HRQoL in general populations of young adolescents. Further research would be useful to determine whether or not children of primary school age self-reporting lower HRQoL are more likely to develop higher adiposity later in adolescence or early adulthood.

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Liu, Weiming, Jiawen Ling, Yiyi Chen, Yan Wu i Peirong Lu. "The Association between Adiposity and the Risk of Glaucoma: A Meta-Analysis". Journal of Ophthalmology 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/9787450.

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Purpose. This meta-analysis was conducted to determine the potential association between adiposity and glaucoma incidence.Materials and Methods. A comprehensive literature search was performed in PubMed and ISI Web of Science. A meta-analysis was conducted using STATA software.Results. Fifteen eligible studies involving 2,445,980 individuals were included to investigate the association between adiposity and glaucoma incidence. The relative risks (RRs) were pooled with 95% confidence intervals (CI) by using a random-effects model. The pooled RR between adiposity and elevated intraocular pressure (IOP) was 1.73 (95% CI, 1.18–2.54), whereas that between adiposity and open-angle glaucoma (OAG) was 0.97 (95% CI, 0.83–1.13). The pooled RR between abdominal adiposity and glaucoma was 1.28 (95% CI, 1.15–1.41), whereas that between general adiposity and glaucoma was 1.09 (95% CI, 0.87–1.37). Results of subgroup analysis by sex indicated the association between adiposity and glaucoma in the female group (RR, 1.31; 95% CI, 1.05–1.64), but not in the male group (RR, 1.11; 95% CI, 0.77–1.60). The pooled RR of cohort studies and cross-sectional studies were 1.00 (95% CI, 0.84–1.20) and 1.22 (95% CI, 0.89–1.66), respectively.Conclusions.Adiposity has a higher risk of elevated IOP, and abdominal adiposity has a positive association with glaucoma, especially in female patients.

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Marshall, Nicole, Kent Thornburg i Jonathan Purnell. "Sex Related Impact of Maternal Adiposity on Neonatal Adiposity and Metabolic Status". Current Developments in Nutrition 4, Supplement_2 (29.05.2020): 1033. http://dx.doi.org/10.1093/cdn/nzaa054_105.

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Abstract Objectives Women with obesity are at increased risk to have large for gestational age neonates. Our study aimed to understand the association between maternal adiposity and neonatal adiposity and metabolic markers. Methods This was a prospective cohort study of healthy women with singleton pregnancies enrolled at 12–16 or 37–38 weeks gestation. Maternal fat mass was determined by air displacement plethysmography. Infant fat mass was determined by skin fold thickness. Cord blood was collected at delivery. Linear regression was used to determine the association of maternal adiposity with infant birth weight, fat mass, and glucose, insulin, lipid, and adipokine levels. Results One hundred eighty five women were enrolled. Demographics (mean, min-max): maternal age 32.9 years (18.8–43.8), maternal pre-pregnancy BMI 27.2 kg/m,2 (17.5–54.0), gestational age at delivery 39.5 weeks (34–42), birthweight 3.46 kg (2.1–5.0). Newborn leptin levels were associated with maternal pre-pregnancy BMI (p-value 0.0070, r2 0.0468), maternal fat mass at 12 and 37 weeks, and maternal %body fat at 12 and 37 weeks. There were no others associations among maternal adiposity and infant adiposity or metabolic markers. When analyzed by fetal sex, female infant birthweight was associated with maternal pre-pregnancy BMI (p-value 0.025, r2 0.055), female fat mass was associated with pre-pregnancy BMI and maternal fat mass at 37 weeks (p-value 0.024, r2 0.069), and female %body fat was associated with maternal fat mass at 37 weeks (p-value 0.0239, r2 0.069). Female infant HDL was lower at birth with increasing maternal fat mass at 12 weeks gestation (p-value 0.0405, r2 0.121). Female infant leptin levels were increased with maternal adiposity including pre-pregnancy BMI, maternal fat mass at 37 weeks, maternal %body fat, and gestational weight gain. Female infant adiponectin levels were lower with increasing maternal pre-pregnancy BMI (p-value 0.0468, r2 0.0538). There were no associations between maternal adiposity and male infant adiposity or metabolic markers. Conclusions Maternal adiposity was associated with increased neonatal leptin levels, but not neonatal adiposity or metabolic markers. Female, but not male, infants had higher birthweight, fat mass, %body fat, and leptin levels and lower HDL and adiponectin levels with increasing maternal adiposity. Funding Sources NICHD.

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Kanna, Balavenkatesh. "Adiposity of the Heart". Annals of Internal Medicine 145, nr 7 (3.10.2006): 553. http://dx.doi.org/10.7326/0003-4819-145-7-200610030-00018.

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Leslie, Bruce R. "Adiposity of the Heart". Annals of Internal Medicine 145, nr 7 (3.10.2006): 554. http://dx.doi.org/10.7326/0003-4819-145-7-200610030-00019.

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Zema, Michael J. "Adiposity of the Heart". Annals of Internal Medicine 145, nr 7 (3.10.2006): 554. http://dx.doi.org/10.7326/0003-4819-145-7-200610030-00020.

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Iacobellis, Gianluca, i Arya M. Sharma. "Adiposity of the Heart". Annals of Internal Medicine 145, nr 7 (3.10.2006): 554. http://dx.doi.org/10.7326/0003-4819-145-7-200610030-00021.

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Szczepaniak, Lidia S., Jonathan M. McGavock, Ronald G. Victor i Roger H. Unger. "Adiposity of the Heart". Annals of Internal Medicine 145, nr 7 (3.10.2006): 555. http://dx.doi.org/10.7326/0003-4819-145-7-200610030-00022.

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Luchsinger, Jose, i Richard Mayeux. "Adiposity and Alzheimers Disease". Current Alzheimer Research 4, nr 2 (1.04.2007): 127–34. http://dx.doi.org/10.2174/156720507780362100.

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Luchsinger, José A., i Deborah R. Gustafson. "Adiposity and Alzheimerʼs disease". Current Opinion in Clinical Nutrition and Metabolic Care 12, nr 1 (styczeń 2009): 15–21. http://dx.doi.org/10.1097/mco.0b013e32831c8c71.

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Wilson, Carol. "Risedronate and marrow adiposity". Nature Reviews Endocrinology 6, nr 11 (21.10.2010): 597. http://dx.doi.org/10.1038/nrendo.2010.163.

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Warming-Larsen, Aage. "Ketone metabolism in adiposity". Acta Medica Scandinavica 130, S206 (24.04.2009): 424–33. http://dx.doi.org/10.1111/j.0954-6820.1948.tb12075.x.

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Katagiri, Hideki, Tetsuya Yamada i Yoshitomo Oka. "Adiposity and Cardiovascular Disorders". Circulation Research 101, nr 1 (6.07.2007): 27–39. http://dx.doi.org/10.1161/circresaha.107.151621.

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Addison, Odessa, Paul C. LaStayo, Leland E. Dibble i Robin L. Marcus. "Inflammation, Aging, and Adiposity". Journal of Geriatric Physical Therapy 35, nr 2 (2012): 86–94. http://dx.doi.org/10.1519/jpt.0b013e3182312b14.

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Flint, D. J. "Immunological manipulation of adiposity". Biochemical Society Transactions 24, nr 2 (1.05.1996): 418–22. http://dx.doi.org/10.1042/bst0240418.

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Nilsson, Peter M. "Adiposity and Vascular Aging". Hypertension 66, nr 2 (sierpień 2015): 270–72. http://dx.doi.org/10.1161/hypertensionaha.115.05621.

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Gustafson, Deborah. "Adiposity indices and dementia". Lancet Neurology 5, nr 8 (sierpień 2006): 713–20. http://dx.doi.org/10.1016/s1474-4422(06)70526-9.

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Flint, David J. "Immunological manipulation of adiposity". Proceedings of the Nutrition Society 51, nr 3 (grudzień 1992): 433–39. http://dx.doi.org/10.1079/pns19920056.

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Bradley, Conor A. "PPARγ controls marrow adiposity". Nature Reviews Endocrinology 14, nr 1 (10.11.2017): 3. http://dx.doi.org/10.1038/nrendo.2017.152.

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