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Hormonal regulation of lipoprotein lipase activity from 5-day-old rat hepatocytes
J Julve1, M Q Robert, M Llobera
1Departament de Bioquimica i Biologia Molecular, Universitat de Barcelona, Spain.
Insights
Lipoprotein lipase (LPL) activity in rat liver is high at birth and decreases during suckling. Hormones like glucagon and dexamethasone increase LPL activity, while others like estradiol decrease it, influencing its extinction.
Area of Science:
- Biochemistry
- Endocrinology
- Molecular Biology
Background:
- Lipoprotein lipase (LPL) activity in rat liver is high at birth and during early suckling, then declines to adult levels by weaning.
- The precise mechanisms regulating the gradual decrease and eventual extinction of LPL expression during this period remain unclear.
Purpose of the Study:
- To investigate the effects of various hormones on LPL activity released from hepatocytes of 5-day-old rats.
- To elucidate the hormonal regulation contributing to the decline of liver LPL activity during postnatal development.
Main Methods:
- Incubation of hepatocytes isolated from 5-day-old rats.
- Measurement of LPL activity released into the medium over 3 hours in the presence of heparin.
- Administration of different doses of various hormones, including dexamethasone, glucagon, ethinylestradiol, testosterone, progesterone, prolactin, insulin, adrenaline, and noradrenaline.
Main Results:
- Dexamethasone and glucagon dose-dependently increased LPL activity release (30-60% and 20-60%, respectively).
- Ethinylestradiol, testosterone, progesterone, and prolactin significantly decreased LPL activity (50-60%) independent of dose.
- Adrenaline increased LPL activity (20-40%), while noradrenaline decreased it (40-50%). Insulin had no effect.
Conclusions:
- Hormonal factors play a significant role in regulating LPL activity in the neonatal rat liver.
- Glucagon and adrenaline effects align with adenylate cyclase/protein kinase A pathway activation, suggesting a role in increased LPL expression.
- High estradiol levels during suckling may contribute to the extinction of liver LPL activity.
Abstract:
Lipoprotein lipase (LPL) activity is known to be synthesized, active and functional in the 1-day-old rat liver: it peaks just at birth triggered by parturition. During suckling LPL mRNA, LPL synthesis and LPL activity are still high at 5 days and then fade reaching adult values at weaning. How LPL expression is gradually extinguished is not known. Therefore we studied the effect of different doses of several hormones on LPL activity released by incubated hepatocytes from 5-day-old rats. In the presence of heparin the release of LPL activity in the medium was linear until 3 h and was always significantly increased vs. without heparin. At 3 h in the presence of heparin the main hormonal effects were: dose-dependent increase (30-60%) with dexamethasone; dose-dependent increase (20-60%) with glucagon; dose-independent decrease (50-60%) with ethinylestradiol, testosterone, progesterone and prolactin; no effect with insulin; 20-40% increase with adrenaline < 1 mM but 40-50% decrease with noradrenaline < 10 microM. Increase of LPL release by glucagon and adrenaline agrees with the increased LPL expression we previously found in an undifferentiated hepatoma cell line when the adenylate cyclase/protein kinase A pathway was activated. The effect of glucagon is concordant with our previous observations that fasting increases liver LPL activity in neonatal rats. The high estradiol levels known to be present in male and female 9-19-day-old rats might contribute to liver LPL extinction during suckling.