Key result
Glucagon decreased serum triglyceride concentration and circulating VLDL apoprotein in eulipemic and hyperlipemic rats by inhibiting amino acid incorporation into hepatic lipoprotein apoprotein.
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Glucagon's inhibition of VLDL synthesis in vitro remains unproven in humans; leaves open any clinical role in lipid disorders.
The effect of glucagon on serum lipids and very low density lipoproteins (VLDL) has been examined in the eulipemic and the hyperlipemic rat. An inhibition of amino acid incorporation into hepatic lipoprotein apoprotein was observed, with an associated decrease in circulating VLDL apoprotein, decreased serum triglyceride concentration, and a loss of the pre-beta band as judged by serum lipoprotein electrophoresis. The data suggest that an important action of this hormone is to decrease the synthesis of the protein moiety of the VLDL; this may contribute to the hypolipemic action of glucagon by introducing a limitation in hepatic lipoprotein production.
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R. Philip Eaton (1973) studied Eulipemic and hyperlipemic state. Glucagon was evaluated on Serum lipids and very low density lipoproteins (VLDL). Glucagon decreased serum triglyceride concentration and circulating VLDL apoprotein in eulipemic and hyperlipemic rats by inhibiting amino acid incorporation into hepatic lipoprotein apoprotein.
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