Skeletal muscle lipoprotein lipase activity was positively correlated with glucose infusion rate (r = 0.58, p < 0.0001), supporting insulin resistance as a factor behind lipoprotein abnormalities.
Observational (n=28)
How do obesity, insulin resistance, and hyperinsulinemia affect skeletal muscle lipoprotein lipase activity and cardiovascular risk factors?
Insulin resistance is significantly correlated with reduced skeletal muscle lipoprotein lipase activity, supporting its role in the dyslipidemia and hypertension characteristic of the metabolic syndrome.
Effect estimate: r = 0.58
p-value: p=<0.0001
The relative effects of obesity, alone or in combination with insulin resistance and hyperinsulinemia (with or without diabetes), on lipoprotein concentrations, blood pressure, and other risk factors for cardiovascular disease were investigated in 28 men (mean age, 63 years). Special attention was given to lipoprotein lipase (LPL) activity in tissues and to postheparin plasma LPL activity and hepatic lipase activity and their relation to insulin resistance. The 28 men fulfilled the entrance criteria of the study so that they could be allocated to one of the four groups (seven in each group): 1) normal body weight, normal fasting insulin level, and normal glucose tolerance (controls); 2) the same as in group 1 but with moderate obesity; 3) the same as in group 2 but with fasting hyperinsulinemia; 4) the same as in group 3 but with non-insulin-dependent diabetes mellitus. Glucose infusion rate for the control group was 8.1 +/- 2.1 mg/kg body wt/min (mean +/- SD) at an insulin infusion rate of 56 milliunits/m2/min. The average values in groups 2, 3, and 4 were 6.0 +/- 0.7, 3.2 +/- 0.5, and 1.9 +/- 1.0 mg/kg body wt/min, respectively. Concentrations of very low density lipoproteins as well as blood pressure and urate concentrations were highest and those of high density lipoproteins were lowest in the two hyperinsulinemic groups (groups 3 and 4). Skeletal muscle LPL activity was 46 +/- 23, 41 +/- 25, 23 +/- 6, and 31 +/- 13 milliunits/g wet wt (mean +/- SD) in the four groups, respectively. There was a positive correlation between glucose infusion rate and muscle LPL activity (r = 0.58, p less than 0.0001). The hepatic lipase activity was positively correlated with the insulin area under the curve of the intravenous glucose tolerance test (r = 0.35, p = 0.02). Furthermore, blood pressure, free fatty acid concentration, liver enzymes, and urate concentrations were significantly correlated with glucose infusion rate at the clamp test. These data give further support for insulin resistance as an important factor behind the observed lipoprotein abnormalities and blood pressure elevations as part of the insulin resistance syndrome characteristic for obese and diabetic patients.
Pollare et al. (1991) conducted an observational in Obesity and insulin resistance (n=28). Skeletal muscle lipoprotein lipase activity was positively correlated with glucose infusion rate (r = 0.58, p < 0.0001), supporting insulin resistance as a factor behind lipoprotein abnormalities.