Abstract:

Background: Obesity is a well recognised as a state of chronic low grade inflammation and the main source of complement factors is the adipose tissue which is associated with Insulin Resistance, altered glucose and lipid metabolism, all of which promote the development of metabolic & cardiovascular disorders. Objective: Till date no study has been conducted in Indian ethnic population exploring the relationship of serum complement C3 with obesity and disorders like diabetes, dylipidemia and hypertension so our objective was to study the effect obesity & associated disorders on serum C3 levels. Material & Methods: The present study included 290 subjects (121 men & 169 women) out of which 203 (70 %) were overweight 61 (21 %) were obese class I and 26 (9 %) were Class II obese according to International Diabetes Federation (IDF) - Modified ATP III criteria. Biochemical parameters like Serum C3, Fasting sugar levels, serum Insulin levels and lipid profile were measured. Homeostasis model of assessment for insulin resistance (HOMA-IR) was calculated. Statistical analysis was done by Medcalc.v11.5.0.0.software. Results: Mean C3 levels in total no. patients were 148.61± 38.82 mg/dl. As BMI increased, there was significant increase in serum levels of C3. When the distribution of variables were studied in both sexes, no statistically significant differences were found for all variables except Age, BMI, blood pressure & C3 levels. Serum C3 also correlated significantly with BMI (r = 0.812, P< 0.0001), insulin resistance (r= 0.262, P <0.001), Triglyceride (r = 0.338, P < 0.001) & LDL (r= 0.431, P < 0.001). As associated disorders with obesity increased, there was significant increase in levels of C3 than only obese patients with no other associated disorders. (ANOVA, P< 0.001). Conclusion: In this study, association of serum C3 with increase in BMI was established & also relationship of C3 with Insulin levels, Insulin resistance and cardiovascular risk factors was found. Our study concluded that obesity associated with dyslipidemia, diabetes & hypertension have a significant effect in increasing the levels of serum C3 concentration. 

References:

[1]. Odum E.P., Asekomeh E.G., Ntuen N.A., Young E.E. Cardio metabolic Risk Factors in Obese Subjects. Journal of Dental and Medical Sciences. 2014; 13 (4): 63-67.

[2]. PW Peake, AD Kriketos, LV Campbell and JA Charlesworth. Response of the alternative complement pathway to an oral fat load in first-degree relatives of subjects with Type II diabetes. International Journal of Obesity 2005; 29: 429–435.

[3]. Setareh Dehdashtihaghighat, Abolfazl Mehdizadehkashi, Amirmohsen Arbabi, Mohadeseh Pishgahroudsari, Shahla Chaichian. Assessment of C-reactive Protein and C3 as Inflammatory Markers of Insulin Resistance in Women with Polycystic Ovary Syndrome: A Case-Control Study. J Reprod Infertil. 2013; 14(4):197-201.

[4]. M.M.J. van Greevenbroek, C.G. Schalkwijk, C.D.A. Stehouwer. Obesity-associated low-grade inflammation in type 2 diabetes mellitus: causes and consequences. The journal of medicine 2 0 13; 71(4): 174-187.

[5]. Riyaz somani, victoria r. Richardson, kristina f. Standeven, PETER J et al. Elevated Properdin and Enhanced Complement Activation in First-Degree Relatives of South Asian Subjects With Type 2 Diabetes. Diabetes care 2102; 35: 894-899.

[6]. Muscari A, Sbano D, Bastagli L, Poggiopollini G, Tomassetti V, Forti P et al. Effects of weight loss and risk factor treatment in subjects with elevated serum C3, an inflammatory predictor of myocardial infarction. Int J Cardiol 2005;100: 217–223.

[7]. Engstrom G, Hedblad B, Janzon L, Lindgarde F. Weight gain in relation to plasma levels of complement factor 3: results from a population-based cohort study. Diabetologia 2005; 48: 2525–2531.

[8]. Halkes CJ, Van Dijk H, de Jaegere PP, Plokker HW, van Der Helm Y, Erkelens DW et al. Postprandial increase of complement component 3 in normolipidemic patients with coronary artery disease: effects of expanded-dose simvastatin. Arterioscler Thromb Vasc Biol 2001; 21: 1526–1530.

[9]. Onat A, Uzunlar B, Hergenc G, Yazici M, Sari I, Uyarel H et al. Cross-sectional study of complement C3 as a coronary risk factor among men and women. Clin Sci (London) 2005; 108, 129–135.

[10]. Van Oostrom AJ, Alipour A, Plokker TW, Sniderman AD, Cabezas MC. The metabolic syndrome in relation to complement component 3 and postprandial lipemia in patients from an outpatient lipid clinic and healthy volunteers. Atherosclerosis 2007; 190: 167–173.

[11]. Standards of Medical Care in Diabetes. American Diabetes Association. Diabetes Care 2005; 28 (Suppl 1): S4–S36.

[12]. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance ad b-cell function from fasting plasma glucose ad insulin concentration in man. Diabetologia 1985; 28: 412–419.

[13]. Friedewald WT, Levy RI, Fredricson DS. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of preparative ultracentrifuge. Clin Chem 1972; 18: 499–502.

[14]. Mohammed-Ali V, Pinkey JH, Coppack SW. Adipose tissue as an endocrine and paracrine organ. Int J Obes 1998; 22: 1145–1158.

[15]. A Hernandez-Mijares, MM Jarabo-Bueno, A Lopez-Ruiz, E Sola-Izquierdo, C Morillas-Arin, ML Martínez-Triguero. Levels of C3 in patients with severe, morbid and extreme obesity: its relationship to insulin resistance and different cardiovascular risk factors. International Journal of Obesity 2007; 31: 927–932.

[16]. Cianflone K. Acylation stimulating protein and the adipocyte. J Endocrinol 1997; 155: 203–206.

[17]. Weyer C, Tataranni PA, Pratley RE. Insulin action and insulinemia are closely related to the fasting complement C3, but not acylation stimulating protein concentration. Diabetes Care 2000; 23: 779–785.

[18]. Ylitalo K, Porkka KV, Meri S, Nuotio I, Suurinkeroinen L, Vakkilainen J et al. Serum complement and familial combined hyperlipidemia. Atherosclerosis 1997; 129: 271–277.

[19]. Hansson GK, Jonasson L, Seifert PS, Stemme S. Immune mechanisms in atherosclerosis. Arteriosclerosis 1989; 9: 567–578.

[20]. Koistinen HA, Vidal H, Karonen SL, Dusserre E, Vallier P, Koivisto VA et al. Plasma acylation stimulating protein concentration and subcutaneous adipose tissue C3 mRNA expression in nondiabetic and type 2 diabetic men. Arterioscler Thromb Vasc Biol 2001; 21: 1034–1039.

[21]. Mohamed-Ali V, Goodrick S, Rawesh A, Katz DR, Miles JM, Yudkin JS et al. Subcutaneous adipose tissue release IL6 but no TNF-a in vivo. J Clin Endo Metab 1997; 82: 4196–4200.

[22]. Yudkin JS, Stehouwer CD, Emeis JJ, Coppack SW. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role for

cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol 1999; 19: 972–978.

[23]. Sniderman AD, Maslowska M, Cianflone K. of mice and men (and women) and the acylation-stimulating protein pathway. Curr Opin Lipidol 2000; 11: 291–296.

[24]. Bhavita Patel, Dilip Taviad, Brahmareddy Malapati, Rita Shah. Complement Component C3: Relationship with Obesity, Insulin resistance and Cardiovascular Risk markers. International Journal of Medical and Health Sciences 2015; 4(3): 351-356.