In a previous paper, the author reported that the amount of urinary estrogen was found to be related to the serum lipid levels. The present paper deals with the effects of estradiol on the metabolism of carboxyl labeled fatty acid, comparing these effects with those of other anticholesterol drugs.
1) In the estradiol-administered rats, the radioactivity of cholesterol ester in the serum was significantly decreased 2 hours after the injection and returned to normal 24 hours after the injection, while the radioactivity of cholesterol ester in the liver was increased 2 hours after the injection and a more significant increase was seen 24 hours later. Two hours after the injection, the serum phospholipid had showed a significantly increased radioactivity, which returned to normal 24 hours after the injection. The radioactivity of triglyceride in the serum was decreased 2 hours after the injection and returned to normal 24 hours after the injection.
2) In the animals treated with triiodothyropropionic acid, the radioactivity of cholesterol ester in the serum and kidney was significantly decreased, while that of the liver remained within the normal range. The radioactivity of phospholipid and triglyceride in the serum and tissues seemed to be decreased.
3) In the heparin or MER-29 administered rats, the radioactivity of lipids in the serum and tissues did not show any signficant changes.

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The effect of adrenocortical hormones on carbohydrate metabolism was investigated in white male rabbits.
1) In the fasting group, it suppressed the increase of liver glycogen but it activated, against the decrease of muscle glycogen, and caused the liver lactate to increase instead of decreasing. It had no effect on the increase of muscle lactate, but increased blood sugar slightly.
2) In the nonfasting group, it suppressed the increase of liver glycogen but promoted a decrease of muscle glycogen and had no effect on decreasing the lactate in the liver and muscle. It did not only prevent a decrease of blood sugar, but also increased it slightly.
3) In the amino acid-administered, it accelerated a decrease but recovered the liver glycogen, and inhibited the increase of liver glycogen. But it prevented the remarkable decrease of liver lactate, was an influence on the decreasing muscle lactate and contributed to the increase of blood sugar.
4) In the glucose-and fat-injected, it shortened the increase of liver glycogen, turned the muscle glycogen from an increase to a decrease, entended the decrease of liver lactate and promoted the lowering of muscle lactate. On the other hand, it prolonged the peak of the increase of blood sugar from 3 hours to 8 hours.
5) In the glucose-administered, it mitigated the remarkably increasing liver glycogen, turned the muscle glycogen from an increase to a decrease, reduced the liver lactate and caused the increase of blood sugar to become higher.
6) In the adrenotectmized, it progressive reduced the liver glycogen and the muscle glycogen. But it decreased remarkably the liver lactate, turned the muscle lactate from a decrease to an increase. On the other hand, it prevented not only the reduction of blood sugar, but also caused it to increase.
7) In the glucose-administered, it increased the liver glycogen 3 hours after administration and then decreased ; it decreased the muscle glycogen 8 hours after administration. It increased remarkably the liver lactate progressively, and reduced the muscle lactate. It increased the blood sugar 3 hours after administration.
8) In the aminoacid-administered, it decreased the liver glycogen and the lactate. It increased the muscle glycogen a little, 3 and 8 hours after. It increased the muscle lactate and decreased remarkably 12 hours after. It decreased the blood sugar 3 hours after and more remarkably 12 hours after.
9) By the pretreatment of cortical hormone injection, the liver glycogen increased remarkably. The liver glycogen decreased progressively. The muscle glycogen decreased but the liver lactate increased. The blood sugar tended to increase.
10) In the glucose-administered, it decreased the liver glycogen progressively, promoted the increase of liver lactate, decreased the muscle glycogen progressively and had no effect on the muscle lactate. But it decreased the blood sugar relatively.
11) In the aminoacid-administered, it decreased the liver glycogen progressively, suppressed the 8 hour-after decrease of liver lactate, decreased the muscle glycogen and suppressed the decrease of the muscle lactate.
12) In the glucose-and fat-injected, it decreased the liver glycogen progressively suppressed the decrease of liver lactate and decreased the muscle glycogen, but it did influence the muscle lactate. In addition, it accelerated the increase of blood sugar for a long time.

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