The Drosophila malate dehydrogenase, or malic enzyme (ME) encoded by the Men gene, is a non-mitochondrial enzyme recovered in the cytosolic fraction. By using mutation in the Men gene and deficiencies uncovering this locus, we could show that the ME activity recovered in cytosolic fractions originates exclusively from the Men gene located at map position 87D-1 on the right arm of the 3rd chromosome. We found that juvenile hormone (JH) can induce ME activity by two mechanisms. One mechanism corresponds to a direct effect of JH on the enzyme, whose activity was enhanced by a twofold factor in the absence of transcription and translation. This enhancement can be noticed 1 h after JH treatment and lasts for approx 3-4 h. The other mechanism involves the transcription of the MEN gene. In the absence of inhibitors the induction of ME activity by JH is increased by a three to fourfold factor and extends over a period of 10-16 h. Since induction of ME activity by JH and JH analogs displayed a dose-response curve, specific for each tested component, we concluded that the hormonal action could be mediated through a receptor. The use of two temperature sensitive mutations deficient in the production of ecdysteroid, ecd1 and su(f)ts67g revealed that ME response to JH requires the presence of a minimal level of the steroid hormone ecdysone, showing a complex hormonal regulatory circuit in the execution of the JH response.
The thyroid monoamine oxidase (MAO) activity was measured in rats after hypophysectomy and TSH treatment to find out whether the thyroid MAO activity can be modified with TSH. Hypophysectomy decreased MAO activity in the thyroid gland of rats. The administration of TSH (2.5 U kg-1 daily for 5 days) to hypophysectomized rats increased MAO activity and fully compensated the absence of the pituitary. These data suggest that the thyroid gland MAO activity is under the regulatory influence of TSH.
Insulin and catecholamines are known to exert effects on hepatocyte growth and metabolism. The binding of insulin, the plasma levels of insulin (INS), and the plasma catecholamine levels of epinephrine (EPI) and norepinephrine (NE) were measured during liver regeneration after partial hepatectomy (PH). A significant decrease (p < 0.05) of INS receptor binding capacity was found at 1, 2, and 3 days after operation. A single insulin injection (2.5 IU/kg body weight) at 24 h after sham operation or partial hepatectomy did not affect these changes of INS binding to hepatocytes. The plasma insulin and glucose levels were similar in both hepatectomized and sham-operated rats. Within 20 min after liver resection or sham operation, plasma NE and EPI concentrations increased rapidly. Then, a significant decrease was observed in plasma catecholamine levels at 1 h after laparotomy and PH. In both groups, laparotomized and partially hepatectomized plasma levels of NE at 4 h reached control values and remained unchanged at the 4- and 24-h periods. After PH, the levels of EPI remained elevated at 4 h in comparison with laparotomy. Adrenal tyrosine hydroxylase mRNA levels were significantly elevated at 4 h in both PH and sham-operated groups. These results suggest that signals that are initiated by catecholamines and transduced through second messengers presumably participate in the trigger mechanism of liver regeneration, while insulin (considered as a secondary mitogen) enhances a stimulus for liver regeneration.
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