Summary
Insulin has an exacerbating effect on endogenous hypertriglyceridemia. Experiments
were carried out in order to study the acute effects of insulin in 6 patients with
endogenous hypertriglyceridemia and 6 controls. 0.1 Unit insulin/kg body weight was
injected into the portal vein. Blood samples were taken from the portal and hepatic
veins and analysed for FFA, glycerol, VLDL-triglycerides (VLDL-TG) and insulin. Liver
blood flow was measured with cardiogreen. This technique allowed a study of the acute
effect of insulin on the hepatic extraction of substrates and on the hepatic production
of VLDL-TG.
Under basal conditions the production of VLDL-TG in patients with endogenous hypertriglyceridemia
was not statistically different from the production in controls. The results did not
provide statistical proof of a correlation between the production and the hepatic
uptake of VLDL-TG precursors; however, the production was negatively correlated to
the hepatic clearance rate of insulin.
During a one-hour observation period after the application of insulin, the production
of VLDL-TG was decreased in controls and increased in patients with endogenous hypertriglyceridemia.
The application of insulin was also followed by a decreased uptake of free fatty acids
and glycerol, this change being similar in controls and in patients with endogenous
hypertriglyceridemia. There was no correlation between the effect of insulin on the
production of VLDL-TG and on the uptake of substrates by the liver. It is concluded
that insulin has a direct effect on the production of VLDL-TG which is independent
of substrate supply. The adverse effect of insulin in endogenous hypertriglyceridemia
may reflect some type of impaired hepatic responsiveness to insulin.
Key-Words
Hypertriglyceridemia
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Hyperinsulinism
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VLDL
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Insulin Resistance
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Obesity
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Liver
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Free Fatty Acids
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Indocyanin
-
Glycerol
-
Blood Flow
