**3.2 Linking metabolic syndrome, obesity and type 2 diabetes**

Obesity, in excess of visceral adiposity, is closely related to insulin resistance, hyperglycemia, dyslipidemia and hypertension; taken together, these group of metabolic disorders are termed "metabolic syndrome [22]. Abdominal obesity is the key component of the metabolic syndrome, with a predominance of intraabdominal visceral fat accumulation, indirectly measured by waist circumference in clinical practice. Research has shown that a chronic low-grade inflammation and an activation of the immune system are involved in the pathogenesis of obesity-related insulin resistance and type 2 diabetes [23]. The investigators noted that the systemic inflammatory markers are risk factors for the development of type 2 diabetes and its macrovascular complications. Besides, adipose tissue, liver, muscle and pancreas are themselves sites of inflammation when there is obesity. An infiltration of macrophages and other immune cells is observed in these tissues associated with a cell population shift from anti-inflammatory to a pro-inflammatory profile. It is noteworthy that these cells are crucial for the production of pro-inflammatory cytokines, which act in an autocrine and paracrine manner to interfere with insulin signaling in peripheral tissues or induce β-cell dysfunction and subsequent insulin deficiency. Most especially, the pro-inflammatory interleukin-1β is implicated in the pathogenesis of type 2 diabetes through the activation of the NLRP3 inflammasome.
