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Experimental hyperlipidemia in rats.

C Gianoulakis, A C Nestruck, M Lis

    Annales De La Nutrition Et De L'Alimentation
    |January 1, 1979
    PubMed
    Summary
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    A mammotropic tumor in rats caused hyperlipidemia, increasing lipids and lipoproteins. Clofibrate treatment reversed some effects and altered cellular responses, suggesting a potential therapeutic avenue for tumor-induced metabolic disorders.

    Area of Science:

    • Endocrinology
    • Metabolic Research
    • Oncology

    Background:

    • Mammotropic tumors can secrete hormones like ACTH, GH, and prolactin.
    • Tumor-induced hormonal imbalances can lead to metabolic dysregulation, including hyperlipidemia.
    • Understanding these mechanisms is crucial for managing associated health risks.

    Purpose of the Study:

    • To investigate the metabolic effects of a mammotropic tumor (MtT-F4) in male Fisher rats.
    • To examine the impact of ACTH on adipose tissue lipolysis and cyclic nucleotide accumulation in tumor-bearing rats.
    • To evaluate the efficacy of clofibrate in mitigating tumor-induced hyperlipidemia.

    Main Methods:

    • Implantation of MtT-F4 tumor into male Fisher rats.
    • Measurement of plasma lipid profiles (free fatty acid, triglyceride, cholesterol, lipoproteins), glucose, glycerol, and uric acid.

    Related Experiment Videos

  • Stimulation of isolated adipose tissue cells with ACTH and dibutyryl cyclic AMP.
  • Administration of clofibrate in the diet to assess its therapeutic effects.

    • Main Results:

    • Tumor implantation led to significant hyperlipidemia, increased plasma lipids and lipoproteins, and decreased uric acid.
    • Adipose cells from tumor-bearing rats showed enhanced lipolytic response and cyclic AMP accumulation upon ACTH stimulation.
    • Clofibrate treatment normalized serum triglycerides, partially reversed cholesterol elevation, and modulated cyclic GMP accumulation in fat cells.

    Conclusions:

    • MtT-F4 tumor induces significant hyperlipidemia and alters adipose tissue responsiveness to ACTH.
    • Clofibrate demonstrates potential in managing tumor-associated hyperlipidemia by affecting lipid metabolism and cellular signaling.
    • Further research is warranted to elucidate the precise molecular pathways involved.