Adipose tissue not only acts as an energy reservoir but also acts like a remote endocrine organ and has an important role in regulating energy homeostasis and metabolism by communicating with liver, skeletal muscle, and the brain 
. Recently, the new adipokine chemerin has been characterized to be associated with increased white cell mass, and obesity induced inflammation in adipose tissue 
. Conde and his group 
have identified a novel role of chemerin stating that chemerin along with other adipokines such as leptin, adiponectin, lipocalin and serum amyloid A3 are also expressed in non-adipose tissues especially the chondrocytes. This is plausible that these adipokines may then regulate chondrocyte biology and bone development, apart from their role in metabolic diseases. This may be reflected as altered adipokine secretion which in turn promotes chronic inflammatory state in rheumatic disease, including cartilage, synovium, bone and various immune cells 
. Chemerin, is a 16 kDa protein secreted in an inactive form as prochemerin and is activated through the cleavage of the C-terminus by inflammatory and coagulation serine proteases 
. In mice, chemerin mRNA is highly expressed in white adipose tissue, liver and lung, and chemerin knockdown impairs differentiation of adipocytes, reduces the expression of GLUT4 while increasing expression of IL-6 and insulin receptor and reduces lipolysis 
. Furthermore, in humans, plasma chemerin levels were significantly associated with obesity parameters in several different populations 
. Collectively, this suggests that chemerin may play a role in the metabolic function of mature adipocytes.
Our results identified a significant increase in serum chemerin levels in obese subjects, related to the amount of total percentage of body fat. Chemerin prominently revealed a strong positive correlation with increasing weight, BMI, waist and hip circumference and body fat percentage, in a healthy population. This data is consistent with previously published reports whereby gene expressions as well as protein levels of chemerin and chemerin’s receptor, CMKLR1 were significantly increased in mice fed a high fat diet 
. A marked increase in chemerin concentration was also observed in obese individuals, linking with subcutaneous and omental adipose tissue, BMI, WHR, and skinfold thickness 
. These studies are in agreement with the findings of our study.
We also established that the fasting glucose and insulin levels were raised in obese subjects despite having no complaints or symptoms of diabetes, these levels along with HOMA-IR showed a strong positive correlation with chemerin, while QUICKI had a negative correlation. Previous studies have shown significant positive correlations between chemerin levels and fasting blood glucose, fasting insulin, HOMA-IR, HbA1c, independent of age and BMI were observed in subjects with type II diabetes compared to normal glycemic subjects 
. These studies are consistent with our data, however it is important to note that our data only incorporated and reported findings in healthy subjects whereas other studies performed these associations in diabetic humans and mice. Taken together, this may deduce a role for chemerin as a screening tool in individuals who have higher visceral fat accumulation contrasting to being in the range of normal weight category, which is seen commonly in Asian population. This is important, since BMI has some limitations as a measure of adiposity across populations 
Fasting glucose levels and HOMA-IR remained independently associated with chemerin levels even after adjustment for age and BMI. Thus we can confidently conclude that chemerin levels may affect glucose homeostasis and therefore may lead to the development of insulin resistance 
. These elevated serum chemerin levels observed in human and mice suggest that chemerin might also influence the dysregulation of glucose metabolism that often occurs with obesity, via the induction of insulin resistance especially in skeletal muscle. Recent studies demonstrated that chemerin induces insulin resistance in skeletal muscle by inhibiting insulin-stimulated Akt1 phosphorylation and activating the 5 AMP-activated protein kinase (AMPK) 
, glycogen synthase kinase 3 phosphorylation, and glucose uptake 
.This decreased uptake could either be a result of down regulation of glucose transporters or competitive inhibition of chemerin to these receptors. Further studies are required to evaluate these mechanisms.
Here, we demonstrated that in a healthy group of subjects, serum cholesterol, triglyceride and LDL-C were significantly higher in obese versus lean and overweight subjects, and that a strong positive correlation of cholesterol, triglycerides and LDL-C exists with chemerin, while serum levels of HDL-C showed non-significant negative correlation with chemerin concentration. These findings are comparable to various studies 
with a slight variation in our results being reported in healthy subjects as opposed to diabetic subjects. Positive correlations between triglycerides, HDL-C and systemic chemerin was also identified in normal glycemic patients by Bozaoglu et al.
but no correlations were observed by Becker et al.
, Weigert et al
& Landgraf et al.
. These associations were lost after adjusting data for age and BMI, but cholesterol levels showed a positive correlation with chemerin even after that. These observations suggest that chemerin could also be a regulator of fat metabolism.
A strong positive correlation with diastolic blood pressure was observed in this study. Comparable results were observed suggesting that serum chemerin levels were significantly associated with systolic hypertension even after adjusting for anthropometric variables 
however no correlation of blood pressure with chemerin was identified by and Hah et al
. We clearly demonstrated that serum chemerin levels are associated with parameters of metabolic syndrome including hypertension regardless of presence of other metabolic syndrome components, signifying that chemerin may also be a distinctive regulator of blood pressure because of its significant correlation with diastolic pressure. Moreover, it has been shown that chemerin is structurally similar to Bradykinin which is also involved in blood pressure regulation 
.This effect of chemerin on blood pressure may also relate to its high expression by kidneys, which is the primary regulator of blood pressure 
Studies have reported that chemerin demonstrated no gender dimorphism in a cohort of type II diabetic patients 
in 55 healthy volunteers 
& in non-obese chronic hepatitis patients 
. In contrast Tan et al
and Bozaoglu et al
found that chemerin levels increased with age and that there appears to be no diurnal variation in chemerin levels. However we found no significant association between chemerin levels and age, similar to a study in a group of pregnant females 
. While Landgraf et al
reported no correlation between sex and chemerin levels but a negative relation with age and circulating levels especially in boys. These differences may be due to the variations in culture and environmental settings.
Chemerin may provide an exciting connection between obesity, inflammation and obesity related pathophysiological changes in humans. Even though a relationship of elevated serum levels in obesity and metabolic syndrome has been suggested, further studies are required that will provide valuable insight to verifying the function of chemerin and determine whether excess chemerin increases adiposity and deranges metabolic function or whether elevated chemerin levels are a consequence or compensatory response during and following the development of obesity and its co morbidities which may lead to the potential therapeutic role of chemerin to these prevalent disorders.
Obesity and physical inactivity are two primary risk factors for the development of hypertension, insulin resistance and dyslipidemia. Significant associations between chemerin levels and various phenotypes of the metabolic syndrome were observed in our population. These findings suggest that chemerin may provide an interesting screening or diagnostic tool for obesity and its complications in humans and may represent a widespread phenotypic relationship that is not population-specific. Whether chemerin is a cause or consequence of these disorders remains to be elucidated and requires further investigation.