BACKGROUND: Metabolic syndrome includes abdominal obesity, diabetes type 2, hypertension, dyslipidemia, derangements of fibrinolysis, and atherosclerosis. Since abdominal obesity is one of the major components of the insulin resistance syndrome (IRS), an attempt was made to evaluate the interrelationships between the magnitude of obesity and the components of the syndrome. METHODS: A cross-sectional study of 123 subjects with type 2 diabetes, of whom 31 were normal body weight and 92 had varying degrees of obesity was conducted. The participants were investigated in terms of clinical and laboratory findings of IRS. Fasting and 30-min (early) plasma glucose and serum insulin excursions in response to oral glucose challenge (75 g) were determined. The peripheral and hepatic insulin resistance (insensitivity) was calculated by homeostasis model assessment (HOMA). RESULTS: Clinical and biochemical findings were compared with the components of the IRS, and demonstrated that a rise in fasting as well as 30-min insulin secretion increases as abdominal body fat (obesity) increases. There was also a significant and proportional correlation between the magnitude of abdominal obesity and the components of metabolic syndrome. CONCLUSION: Abdominal adiposity appears to have a pivotal role in the development of IRS.
BACKGROUND:Metabolic syndrome includes abdominal obesity, diabetes type 2, hypertension, dyslipidemia, derangements of fibrinolysis, and atherosclerosis. Since abdominal obesity is one of the major components of the insulin resistance syndrome (IRS), an attempt was made to evaluate the interrelationships between the magnitude of obesity and the components of the syndrome. METHODS: A cross-sectional study of 123 subjects with type 2 diabetes, of whom 31 were normal body weight and 92 had varying degrees of obesity was conducted. The participants were investigated in terms of clinical and laboratory findings of IRS. Fasting and 30-min (early) plasma glucose and serum insulin excursions in response to oral glucose challenge (75 g) were determined. The peripheral and hepatic insulin resistance (insensitivity) was calculated by homeostasis model assessment (HOMA). RESULTS: Clinical and biochemical findings were compared with the components of the IRS, and demonstrated that a rise in fasting as well as 30-min insulin secretion increases as abdominal body fat (obesity) increases. There was also a significant and proportional correlation between the magnitude of abdominal obesity and the components of metabolic syndrome. CONCLUSION: Abdominal adiposity appears to have a pivotal role in the development of IRS.