Abstract
Background:Obesity is one of the most common yet neglected public health problems in both the developed and developing countries. Metabolic syndrome (MS) is a multiplex of risk factor for the development of type 2 diabetes (T2D) and cardiovascular disease (CVD) and it reflects the clustering of multiple risk factors resulting from obesity and insulin resistance. Despite its predominance in obese individuals, MS does occur in non-obese individuals. Many individuals characterised as normal weight as per their body mass index (BMI), have increased visceral adiposity thereby leading to an unfavourable inflammatory cytokine profile. There are limited studies from India with respect to inflammatory cytokines in obesity and MS in general and non-obese patients with MS in particular.Materials and Methods:An observational cross-sectional study was carried out in patients with MS with or without obesity. Anthropometric parameters such as height, weight and waist girth were measured and BMI was calculated. Serum levels of TNF-α, IL-6 and adiponectin were measured by using the enzyme-linked immunosorbent assay.Results:A significant proportion of individuals categorised as normal weight had an increased waist circumference which correlated with BMI, acanthosis nigricans (AN) and fatty liver. There was no statistically significant difference in the cytokine levels in obese and non-obese patients with MS; similarly among non-obese patients with MS, cytokine levels were comparable in patients with or without abdominal obesity. However, triglycerides inversely correlated with adiponectin levels and there was no significant correlation between the cytokines and other parameters of MS.Conclusion:There was no significant difference in various metabolic and inflammatory parameters between obese and non-obese patients with MS. Even in non-obese group, there were no differences in metabolic and inflammatory markers between individuals with or without abdominal obesity. This finding indicates that apart from adipose tissue, other factors are also responsible for the development of MS and its associated proinflammatory profile. There could be a significant contribution of genetic and epigenetic factors which needs to be further explored.
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