The global incidence of obesity is escalating at epidemic proportions. The obesity related co-morbidities include increased incidence of the metabolic syndrome, type-2 diabetes (T2DM), hypertension, dyslipidaemia and chronic low-grade inflammation [1, 2].
Interestingly, Hotamisligil et al  in 1993 suggested that chronic low-grade inflammation plays a role in the pathophysiology of obesity in general and of insulin resistance in particular. This has subsequently been supported by the demonstration of a correlation between circulating levels of inflammatory markers and both T2DM  and atherosclerosis in humans [[5–8]].
White adipose tissue (WAT) is an important endocrine organ that secretes molecules, referred to as adipokines . The chronic low-grade inflammation of obesity is characterized by increased concentrations of circulating inflammatory adipokines and cytokines [[10–13]]. Importantly, the inflammatory and metabolic pathways are linked. WAT is infiltrated with macrophages in response to adipocyte hypertrophy and the associated increase in monocyte chemotactic protein-1 (MCP-1) expression [14, 15]. Increased circulating concentrations of MCP-1 are in humans predictive of both diabetes risk independently of other traditional risk factors  and atherosclerosis [17, 18]. Furthermore, differentiation of monocytes into macrophages starts in plasma, when monocytes are activated in response to postprandial triglyceride rich lipoproteins [19, 20] and free fatty acids . While MCP-1 is now regarded as a key inflammatory marker, CC chemokine ligand-5 (CCL5/RANTES) has in recent years emerged as a potentially therapeutic target in the prevention of atherosclerosis [22, 23]. The interaction between CCL5/RANTES and monocytes facilitates the adherence and transmigration of monocytes through the arterial wall  initiating the atherosclerotic process. CCL5/RANTES antagonisms have been demonstrated to reduce atherosclerotic lesions in mice . Furthermore, CCL5/RANTES is up-regulated in WAT of obese compared to lean subjects  facilitating macrophage infiltration of adipose tissue.
Though, the impact of dietary protein on postprandial inflammation has not been thoroughly elucidated, the impact of diet in general on low-grade inflammation has been demonstrated (reviewed in ). Thus, a positive correlation to postprandial inflammation has been demonstrated for total energy intake in healthy men [27, 28] and a diet rich in saturated fat in overweight subjects . Moreover dyslipidaemia characteristically for obesity, i.e. hypertriglyceridaemia, elevated apolipoprotein (Apo) B and small, dense low-density lipoproteins (LDL) has been positively correlated to low-grade inflammation in abdominally obese subjects with and without the metabolic syndrome . The composition of meal fatty acids play an important role for low-grade inflammation in humans i.e. n-3 polyunsaturated fatty acids (PUFA) being anti-inflammatory while n-6 PUFA and saturated fatty acids appear to be pro-inflammatory [[31–33]]. The impact of dietary carbohydrate on postprandial inflammation is controversial [26, 34].
Less is known about the influence of dietary protein on postprandial inflammation. Arya et al  demonstrated that meat with high fat content is more pro-inflammatory compared to lean meat in healthy subjects. Moreover, an inverse relationship has been demonstrated between dairy product consumption and low-grade inflammation in healthy subjects  and obese subjects .
We hypothesize that dietary protein sources may exert a differential impact on acute postprandial low-grade inflammation. In the present study we focused on the two inflammatory markers MCP-1 and CCL5/RANTES. As cod protein, gluten, casein and whey protein have been demonstrated to elicit differential postprandial lipid, glucose and hormone responses in healthy , overweight  and type-2 diabetic subjects  these four protein sources originating from fish, crops and milk may be suitable for assessing the impact of dietary protein on postprandial low-grade inflammation. The differential impact of the four protein sources on postprandial triglycerides and insulin may particularly reveal correlated differential responses on postprandial low-grade inflammation.