Chapter 2: | Background |
First, insulin resistance causes high triglycerides; second, high triglycerides cause peripheral insulin resistance; and finally, the association between triglycerides and peripheral insulin resistance is caused by factors influencing both triglycerides and peripheral insulin resistance, for example, adiposity (32). Some investigators suggested that insulin resistance might be an effect rather than a cause and proposed an alternative concept. This hypothesis emphasized the limited capacity of the human body in buffering and disposing lipid fuels (33). When lipid availability exceeded this capacity, adipocytes, especially the intra-abdominal fat would expand, which provided fatty acids for excessive synthesis of very low density lipoprotein-triglyceride (VLDL-TG) (34,35). Excessive fluxes of lipid fuels would lead to deposition of triglyceride in liver and skeletal muscle. Long-term ectopic over-accumulation of lipids in these non-adipose tissues would impair insulin sensitivity and insulin secretion (36) and cause additional metabolic dysfunction such as hyperuricemia and hypertension (37).
The complex interrelationship between the constituents of the metabolic syndrome challenges careful assessment of associations by using traditional statistical techniques. Factor analysis reconstructs the original variables and reduces a large number of interrelated original variables to a small number of latent factors, which still retain the majority of information from the original variables (38). Therefore, factor analysis is well suited for developing a simpler set of factors of the metabolic syndrome. This technique has been applied in dozens of studies in different populations (39–48).
The majority of exploratory factor analysis reported that the metabolic syndrome comprised of three or four uncorrelated common factors, representing obesity, insulin-glucose metabolism, lipid profile, and blood pressures. Usually, the factor representing obesity combined with lipid and/or insulin variables.