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Decrease in alkaline triglyceride lipase in primary cultured hepatocytes from mice with sarcoma 180.

H Masuno, H Okuda

    Lipids
    |July 1, 1985
    PubMed
    Summary
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    Hepatocytes from tumor-bearing mice showed reduced alkaline triglyceride lipase activity compared to normal mice. This enzyme activity decreased further during cell culture in tumor-bearing mice.

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Oncology

    Background:

    • Hepatocytes play a crucial role in metabolic functions.
    • Cancer can significantly alter cellular functions and enzyme activities.
    • Understanding these alterations is key to comprehending cancer's systemic effects.

    Purpose of the Study:

    • To characterize primary cultured hepatocytes from normal and tumor-bearing mice.
    • To investigate the impact of Sarcoma 180 tumor on hepatocyte function, specifically alkaline triglyceride lipase activity.

    Main Methods:

    • Isolation and culture of primary hepatocytes from normal and Sarcoma 180-bearing mice.
    • Assessment of cell viability and DNA stability.
    • Measurement of protein synthesis and secretion using (3H)leucine.

    Related Experiment Videos

  • Quantification of alkaline triglyceride lipase activity in cell homogenates.

    • Main Results:

    • Hepatocytes from both groups exhibited high initial viability (>90%) and DNA stability for 3 days.
    • Protein synthesis and secretion rates were similar in hepatocytes from normal and tumor-bearing mice.
    • Alkaline triglyceride lipase activity was significantly lower (one-third) in hepatocytes from tumor-bearing mice compared to normal mice.
    • Hepatocytes from tumor-bearing mice showed a diminished increase in enzyme activity during culture.

    Conclusions:

    • Sarcoma 180 tumor significantly impairs alkaline triglyceride lipase activity in mouse hepatocytes.
    • Hepatocytes from tumor-bearing mice exhibit reduced capacity for enzyme activity increase during culture.
    • These findings suggest a metabolic dysfunction in hepatocytes associated with tumor burden.