Abstract. Obesity is associated with dyslipidaemia and increased morbidity and mortality from premature atherosclerosis and diabetes mellitus. Particularly, hypertriglyceridaemia is a characteristic finding in patients with obesity. In addition, the elevated levels of triglycerides may be an important risk factor for development of the obesity‐related complications. Lipoprotein lipase activity in skeletal muscle tissue (mLPL) has previously been found to be an important factor regulating the concentration of serum triglycerides. To describe the relationship between mLPL, triglycerides and fatness/fat distribution in more detail we have investigated these parameters under basal conditions and during insulin stimulation in 20 obese females. During hyperinsulinaemia (204 μU ml‐1) for 4 h the mLPL activity decreased from 528 ± 52 nmol FFA g‐1 to 412 ± 44 (P< 0.001). Basal mLPL was negatively correlated with serum triglycerides (r= ‐0.48, P<0.05) and positively correlated with HDL‐cholesterol (r = 0–58, P<0.01). Employing multiple variance analysis it was found that both BMI and WHR were negatively correlated to mLPL, however, the impaired lipid profile (high triglyceride, low HDL‐cholesterol, high FFA) could only be related to BMI and not to WHR in these obese females. However, reduced insulin‐action (insulin resistance) was closely related to abdominal fatness determined by WHR both in relation to the insulin‐effect on mLPL as well as for the insulin‐effect on whole‐body glucose metabolism (clamp‐study). A tendency to a positive correlation was observed between the impaired insulin‐stimulated glucose disposal and the reduced insulin‐effect on mLPL (r = 0.41, P = 0.08) indicating that mLPL might be an indicator of muscle insulin sensitivity. In conclusion, reduced mLPL activity seems to play a role for the increased triglyceride levels associated with obesity and the mLPL activity seems to be negatively influenced by both total fatness and abdominal fatness. Finally, mLPL is an insulin sensitive enzyme where short‐term insulin infusion inhibits the enzyme activity.
|Tidsskrift||European Journal of Clinical Investigation|
|Status||Udgivet - apr. 1993|