Influence of ACTH secreting tumor (MtTF4) on fetal rat adrenal gland steroidogenesis in vitro in prolonged pregnancy

Pregnant female rats with ACTH secreting tumor (MtTF4) have prolonged pregnancy and cannot deliver. The fetuses of tumor bearing females have in prolonged pregnancy on days 24 and 25 of pregnancy greater body weight and smaller adrenal weight as compared to intact fetuses of the 22nd day of pregnancy. The fetal adrenal glands converted to vitro 4-14C progesterone to radioactive 11-deoxycorticosterone (DOC), corticosterone (B), 18-hydroxy-11-deoxycorticosterone (18-OH-DOC), 18-hydroxy-corticosterone (18-OH-B) and aldosterone. Fetal adrenal glands in prolonged pregnancy synthetized in vitro less amount of radioactive DOC, B and 18-OH-DOC. A negative relationship exists between the maternal corticosterone which passes the placenta to fetuses and corticosteroidogenesis of fetal adrenal glands. These results indicate the possibility that fetal rat adrenal glands with their corticosteroids participate in pregnancy and influence normal delivery.     

The mechanism of liver splanchnomegaly produced by a transplantable pituitary mammotropic tumor in rats.

The mechanism of liver splanchnomegaly developed in rats bearing a transplantable pituitary mammotropic tumor which secretes large amounts of ACTH and prolactin has been studied. The results indicate that in the first phase of tumor growth liver enlargement could be due to hypertrophy, and later mainly to hyperplasia which overcomes hypertrophy. The adrenal glands were found to play an essential role in the process of liver splanchnomegaly because adrenalectomy prevented the disproportional growth of the liver. Evidence is presented showing that glucocorticoids are the dominant hormones responsible for the development of liver splanchnomegaly.     

Oxidation of hepatic carnitine palmitoyl transferase-I (CPT-I) impairs fatty acid beta-oxidation in rats fed a methionine-choline deficient diet

There is growing evidence that mitochondrial dysfunction, and more specifically fatty acid β-oxidation impairment, is involved in the pathophysiology of non-alcoholic steatohepatitis (NASH). The goal of the present study was to achieve more understanding on the modification/s of carnitinepalmitoyltransferase-I (CPT-I), the rate-limiting enzyme of the mitochondrial fatty acid β-oxidation, during steatohepatitis. A high fat/methionine-choline deficient (MCD) diet, administered for 4 weeks, was used to induce NASH in rats.We demonstrated that CPT-I activity decreased, to the same extent, both in isolated liver mitochondria and in digitonin-permeabilized hepatocytes from MCD-diet fed rats.At the same time, the rate of total fatty acid oxidation to CO(2) and ketone bodies, measured in isolated hepatocytes, was significantly lowered in treated animals when compared to controls. Finally, an increase in CPT-I mRNA abundance and protein content, together with a high level of CPT-I protein oxidation was observed in treated rats. A posttranslational modification of rat CPT-I during steatohepatitis has been here discussed.     

SDS-PAGE analysis of caput epididymis proteins in rats receiving a zinc deficient diet

Caput epididymis proteins from control, pairfed and zinc deficient (ZD) wistar weanling albino rats after 2-, 4-, 6- and 8-weeks were examined using SDS-PAGE followed by densitometric scanning of the gels. In comparison to the control and pairfed rats, ZD rats displayed new proteins. These included a Mr 42 kDa from 2ZD, Mr 47.5, 27.5, 23.2 and 16.0 kDa from 4ZD and Mr 87 and 14.2 kDa from 6ZD group. The 8ZD group, however, revealed no additional protein bands over controls. Further, several other proteins were missing from ZD rats. These included Mr 93 and 71 kDa from 2ZD; 93, 90, 79, 67, 62, 55 and 15.3 kDa from 4ZD; 60, 45.5, 34, 30 and 24 kDa from 6ZD and 41.5, 33 and 27.5 kDa bands from 8ZD group. The results indicate that the induced Zn-deficient state may be responsible for the altered protein patterns in the caput epididymis. The duration of low Zn uptake period also appears to influence the protein pattern in caput epididymis.