1955EndocrinologyRequires access

THE EFFECT OF TESTOSTERONE PROPIONATE ON MUSCLE GLYCOGEN IN ALLOXAN DIABETIC RATS1

Harry L. Saunders, SAMUEL L. LEONARD

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Abstract

GROWTH hormone stimulates glycogen deposition in skeletal muscles of normal and hypophysectomized rats, but not in alloxan diabetic rats (Illingworth and Russell, 1951). Since testosterone acts similarly to growth hormone in increasing glycogen stores in skeletal muscles (Leonard, 1952 a,b), an investigation was made to determine if a normal insulin supply is required for glycogen deposition by testosterone. In view of the differences in behavior of different skeletal muscles to glycopexic hormones (Leonard, 1952b, 1953), three representative muscles were studied, namely the rectus femoris, diaphragm and levator ani. methods Adult normal and castrated male rats of the Long-Evans, strain weighing between 200–300 gm., were used. Diabetes was produced by the administration of alloxan monohydrate (175 mg./kg. body weight) intraperitoneally, after a 72 hour fast. In the castrated rats, alloxan was administered 23 days after castration. Four days later, blood samples from the tail vein were drawn and blood sugar levels determined by the Somogyi (1945) modification of the Nelson method (1944).

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GROWTH hormone stimulates glycogen deposition in skeletal muscles of normal and hypophysectomized rats, but not in alloxan diabetic rats (Illingworth and Russell, 1951). Since testosterone acts similarly to growth hormone in increasing glycogen stores in skeletal muscles (Leonard, 1952 a,b), an investigation was made to determine if a normal insulin supply is required for glycogen deposition by testosterone. In view of the differences in behavior of different skeletal muscles to glycopexic hormones (Leonard, 1952b, 1953), three representative muscles were studied, namely the rectus femoris, diaphragm and levator ani. methods Adult normal and castrated male rats of the Long-Evans, strain weighing between 200–300 gm., were used. Diabetes was produced by the administration of alloxan monohydrate (175 mg./kg. body weight) intraperitoneally, after a 72 hour fast. In the castrated rats, alloxan was administered 23 days after castration. Four days later, blood samples from the tail vein were drawn and blood sugar levels determined by the Somogyi (1945) modification of the Nelson method (1944).

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Available abstract

GROWTH hormone stimulates glycogen deposition in skeletal muscles of normal and hypophysectomized rats, but not in alloxan diabetic rats (Illingworth and Russell, 1951). Since testosterone acts similarly to growth hormone in increasing glycogen stores in skeletal muscles (Leonard, 1952 a,b), an investigation was made to determine if a normal insulin supply is required for glycogen deposition by testosterone. In view of the differences in behavior of different skeletal muscles to glycopexic hormones (Leonard, 1952b, 1953), three representative muscles were studied, namely the rectus femoris, diaphragm and levator ani. methods Adult normal and castrated male rats of the Long-Evans, strain weighing between 200–300 gm., were used. Diabetes was produced by the administration of alloxan monohydrate (175 mg./kg. body weight) intraperitoneally, after a 72 hour fast. In the castrated rats, alloxan was administered 23 days after castration. Four days later, blood samples from the tail vein were drawn and blood sugar levels determined by the Somogyi (1945) modification of the Nelson method (1944).

Key concepts: Internal medicine, Endocrinology, Glycogen, Testosterone propionate, Alloxan, Testosterone (patch), Castration, Skeletal muscle

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