ABSTRACT
Background: The present study was aimed to determine the prevalence of obesity among adolescent students (11-17 years) and to study the correlation between the behaviors related eating, sedentary activities, dietary pattern and physical activities and obesity.Methods: The study was conducted among1007 students as a case control study. Prevalence of obesity was calculated using centres for disease control and prevention (CDC) growth chart. Risk factors for obesity were assessed by using questionnaires which include 18 questions in four broad categories. And association of risk factors and obesity has been analysed by using multivariate logistic regression model.Results: A total of 1007 school going adolescents were included in present study, out of this 50.94% were boys and 49.06% were girls. The prevalence of obesity in present study population was 4.27%. Prevalence of obesity was more among boys than girls. (53.49% vs 46.51%). On multivariate logistic regression factors V5, V6, V8, V10, V12, V13, and V14 are associated with obesity and risk factors V3, V4, V7, V11 are not associated with obesity, factors V15, V16, V17, V18 are associated with onset of adolescent obesity.Conclusions: Adolescent obesity is a major health problem in Udaipur, Rajasthan and it requires timely intervention to prevent the complication and co morbidities.
ABSTRACT
Following the discovery of interleukin (IL)-17 producing T helper (Th17) cells as a distinct lineage of CD4+ T helper cells it became clear that these cells play an important role in the host defense against extracellular fungal and bacterial pathogens and participate in the pathogenesis of multiple inflammatory and autoimmune disorders. Depending on the microenvironment, Th17 cells can alter their differentiation programme ultimately giving rise to either protective or pro-inflammatory pathogenic cells. We found that besides the conventional in vitro protocol for Th17 differentiation by transforming growth factor-beta (TGF-β) plus IL-6 cytokines, a combination of IL-23 plus IL-6 can also induce Th17 cells. The Th17 cells induced by IL-23 plus IL-6 (termed as effector Th17, Teff17 cells) are pathogenic upon adoptive transfer into non-obese diabetic (NOD) mice contributing to the development of type 1 diabetes (T1D) while cells induced by TGF-β plus IL-6 (termed as regulatory T cells, Treg17 cells) are non pathogenic and regulatory, and suppressed the pathogenic T cells in T1D. These cells differentially expressed a number of cytokines where Teff17 cells exhibited an increase in granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-22 whereas Treg17 cells demonstrated increased expression of IL-21 and immunosuppressive cytokine IL-10. Differentiation of Th17 cells is controlled by a transcription factor, RORγT although these cells also express variable levels of T-bet and FoxP3 transcription factors. This points to a dual functional role of Th17 subsets in autoimmune diseases particularly T1D. We suggest that similar to conventional regulatory T cells (Treg), induction of regulatory Treg17 cells could play an important role in modulating and preventing certain autoimmune diseases.