Abstract
Aim: To study serum progranulin (PGRN) level in children with obesity and its relationship to inflamamatory markers and visceral fat. Methods: Fifty obese children and 50 controls aged 10-18 years were recruited. Demographic, anthropometric and biochemical features were collected according to a standard protocol. Serum progranulin levels, serum IL-6 and hsCRP were measured using ELISA. Insulin resistance was calculated by the homeostasis model (HOMA-IR) using the following formula: HOMA-IR = fasting insulin (mU/L) × fasting glucose (mmoL/L)/ 22.5. The maximum visceral fat thickness (VFT) and the minimum subcutaneous fat thickness (SFT) were measured by ultrasonography. Results: In the obese group, a significant increase was found in serum PGRN (48.87 ± 42.33 ng/mL) compared to control group (30.18 ± 23.82 ng/mL). Progranulin correlated significantly with VFT (r = 0.475), IL6 (r = 0.368), Insulin(r = 0.440) and HOMA-IR (r = 0.379). The mean serum progranulin in the high tertile VFT group was significantly higher than those in the low tertile and middle tertile groups (P = 0.030 and P = 0.039 respectively). VFT was highly positively correlated to progranulin, SFT, IL6, insulin, HOMA-IR and hsCRP (P = 0.001, 0.000, 0.001, 0.001, 0.003 and 0.003). However, the correlation coefficient between SFT and progranulin was insignificant. Summary: we demonstrated for the first time that serum PGRN concentrations increased in Egyptian obese children. The concentrations of serum PGRN correlated closely with visceral fat and IL6. Conclusion: PGRN may contribute to the pathogenesis of chronic inflammation in obesity. It could be a novel marker of visceral fat in obesity. Thus PGRN could be a potential therapeutic target for management of chronic inflammation in obesity.
Highlights
Childhood obesity has more than doubled in children and tripled in adolescents in the past 30 years [1]
visceral fat thickness (VFT) was highly positively correlated to progranulin, subcutaneous fat thickness (SFT), IL6, insulin, HOMA-IR and hsCRP (P = 0.001, 0.000, 0.001, 0.001, 0.003 and 0.003)
2006 cited that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes [5]
Summary
Childhood obesity has more than doubled in children and tripled in adolescents in the past 30 years [1]. 2006 cited that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes [5]. Several factors including adipocyte hypertrophy, hypoxia and stresses in adipose tissue could either directly or as a sequence of patho-mechanisms induce an inflammatory process in adipose tissue. Recent studies consistently support a hypoxia response in the adipose tissue in obese animals. The observations have led to formation of an exciting concept, adipose tissue hypoxia (ATH), in the understanding of major disorders associated with obesity. ATH may provide cellular mechanisms for chronic inflammation, macrophage infiltration, adiponectin reduction, leptin elevation, adipocyte death [7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
