| Chapter 2: | Background |
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It is characterized by several metabolic risk factors clustering in one individual (21, 22), which has been established as a powerful risk factor for type 2 diabetes (23) and cardiovascular disease (24) and is associated with increased mortality from cardiovascular disease and all causes (25).
2.1.2.1 Complex Interrelationship Among Components of the Metabolic Syndrome
It remains unclear whether the “metabolic syndrome” represents a unified construct, which reflects one underlying pathogenic pathway. Initial studies showed that fasting and post-glucose hyperinsulinemia were associated with obesity, hyperglycemia, hypertension, hypertriglyceridemia, and low HDL-cholesterol concentrations in cross-sectional studies. In addition, prospective studies suggested that fasting insulin concentrations increased the risk of hypertension, decreased HDL cholesterol, high triglyceride, and type 2 diabetes (23, 26). Based on these findings, the authors suggested that hyperinsulinemia / insulin resistance might be the link underlying these co-occurring multiple metabolic abnormalities (23, 26).
Recent investigations have pointed out that visceral obesity had a central role in developing the metabolic syndrome. Some cross-sectional studies have reported that visceral adiposity is a significant independent predictor/marker of insulin resistance (27–29). A prospective study in Japanese Americans showed that greater visceral adiposity increases the risk of IGT independent of insulin action (30). A short-term weight-loss trial reported that decrease in intra-abdominal visceral fat lowered blood pressure in obese hypertensive women (31).
The precise link between the triad of adiposity, insulin sensitivity, and triglycerides is still obscure. There are three possible mechanisms between triglycerides and insulin resistance.