BACKGROUND: Subjects with Prader-Willi syndrome (PWS) have a reduced life expectancy due to cardiovascular disease. Increased systemic low-grade inflammation is postulated as a contributor, despite reported lower visceral fat mass and increased insulin sensitivity. OBJECTIVES: Our aim was to compare inflammatory markers and arterial stiffness in PWS and adiposity-matched obese control subjects. DESIGN: We conducted a cross-sectional cohort study comparing 12 PWS subjects, 12 obese subjects matched for percentage body fat and central abdominal fat mass, and 10 healthy normal-weight subjects. MAIN OUTCOME MEASURES: Dual-energy x-ray absorptiometry was used to assess body composition, flow cytometry to quantify activation markers on immun e cells, and ELISA for measurement of C-reactive protein, adiponectin, and IL-6. Insulin resistance was estimated by homeostasis model assessment and arterial stiffness by applanation tonometry. RESULTS: PWS and obese subjects had similarly increased homeostasis model assessment and arterial stiffness. Nevertheless, PWS subjects showed significantly higher IL-6 (4.9 + or - 1.0 vs. 2.5 + or - 0.4 pg/ml; P = 0.02) and nonsignificantly higher C-reactive protein (10.5 + or - 3.2 vs. 4.0 + or - 1.0 ng/ml; P = 0.08). Neutrophil activation markers CD66b and CD11b were higher in PWS compared to obese subjects (P < 0.01), reflecting an activated innate immune system. These markers were positively related to central adiposity in lean and obese subjects (r = 0.49; P < 0.05), but not in PWS subjects. CONCLUSIONS: PWS subjects compared to adiposity-matched obese subjects demonstrate similar insulin resistance but increased low-grade inflammation. The dissociation of inflammation and central adiposity suggests that activation of innate immunity may be either a specific genetic feature of PWS or linked to the commonly associated obstructive sleep apnea syndrome, and might offer a treatment target to reduce cardiovascular disease.
BACKGROUND: Subjects with Prader-Willi syndrome (PWS) have a reduced life expectancy due to cardiovascular disease. Increased systemic low-grade inflammation is postulated as a contributor, despite reported lower visceral fat mass and increased insulin sensitivity. OBJECTIVES: Our aim was to compare inflammatory markers and arterial stiffness in PWS and adiposity-matched obese control subjects. DESIGN: We conducted a cross-sectional cohort study comparing 12 PWS subjects, 12 obese subjects matched for percentage body fat and central abdominal fat mass, and 10 healthy normal-weight subjects. MAIN OUTCOME MEASURES: Dual-energy x-ray absorptiometry was used to assess body composition, flow cytometry to quantify activation markers on immun e cells, and ELISA for measurement of C-reactive protein, adiponectin, and IL-6. Insulin resistance was estimated by homeostasis model assessment and arterial stiffness by applanation tonometry. RESULTS:PWS and obese subjects had similarly increased homeostasis model assessment and arterial stiffness. Nevertheless, PWS subjects showed significantly higher IL-6 (4.9 + or - 1.0 vs. 2.5 + or - 0.4 pg/ml; P = 0.02) and nonsignificantly higher C-reactive protein (10.5 + or - 3.2 vs. 4.0 + or - 1.0 ng/ml; P = 0.08). Neutrophil activation markers CD66b and CD11b were higher in PWS compared to obese subjects (P < 0.01), reflecting an activated innate immune system. These markers were positively related to central adiposity in lean and obese subjects (r = 0.49; P < 0.05), but not in PWS subjects. CONCLUSIONS:PWS subjects compared to adiposity-matched obese subjects demonstrate similar insulin resistance but increased low-grade inflammation. The dissociation of inflammation and central adiposity suggests that activation of innate immunity may be either a specific genetic feature of PWS or linked to the commonly associated obstructive sleep apnea syndrome, and might offer a treatment target to reduce cardiovascular disease.
Authors: T Cadoudal; M Buléon; C Sengenès; G Diene; F Desneulin; C Molinas; S Eddiry; F Conte-Auriol; D Daviaud; P G P Martin; A Bouloumié; J-P Salles; M Tauber; P Valet Journal: Int J Obes (Lond) Date: 2014-01-10 Impact factor: 5.095
Authors: Andrea M Haqq; Michael J Muehlbauer; Christopher B Newgard; Steven Grambow; Michael Freemark Journal: J Clin Endocrinol Metab Date: 2010-10-20 Impact factor: 5.958
Authors: J E Whittington; A J Holland; D J Driscoll; N Hodebeck-Stuntebeck; A Hoctor Journal: Orphanet J Rare Dis Date: 2022-02-21 Impact factor: 4.123