PubMed Health⌕ Search

Biomedical subjects

M B Lipsett

Publications and source records attributed to M B Lipsett.

At least 55 records · Page 3Linked to original sources
PubMed1979

Interaction of drugs, hormones, and nutrition in the causes of cancer.

Hormones may act as promoters in the carcinogenic process, and occasionally their metabolites may act as antihormones or have new physiologic effects. Drugs can interact with the endocrine system in many ways. They can promote secretion of a hormone, alter its rate of removal from plasma, change plasma protein-binding characteristics, or modify routes of metabolism. Estrogens have a preparative effect on the uterine endometrium. There are biologic, clinical and epidemiologic reasons for believing that estrogen administration to postmenopausal women increases the risk for endometrial cancer. Although there are similar biologic reasons to associate prolonged estrogenic stimulation with breast cancerr, evidence for such an association is weak. Oral contraceptive use has been associated with a variety of hepatocellular tumors. Although estrogens, per se, can effect several hepatic functions, it seems likely that the 17 alpha-alkyl and 17 alpha-ethinyl functions of the progestins and estrogens are involved in this process. The role of estrogen use during pregnancy in the causation of vaginal cancer in female offspring and the role of androgens in prostate cancer have been discussed.

Anovulation↗
PubMed1979

Evidence that testosterone can suppress pituitary gonadotropin secretion independently of peripheral aromatization.

Testosterone (T) was given to normal men with and without the concomitant administration of the aromatase inhibitor, delta 1-testolactone (Teslac), to examine the role of peripheral aromatization of T in gonadotropin regulation. When T was administered alone by continuous iv infusion (15 mg/day for 4 days), serum T increased 3-fold (P less than 0.01) and estradiol (E) increased by 50% (P less than 0.01). These changes were associated with a 50% decrease in serum LH and FSH concentrations (P less than 0.01). When T was infused into men taking Teslac (2000 mg/day), serum T levels doubled (P less than 0.01), but E levels did not change (13.4 +/- 1.5 vs. 13.5 +/- 1.0 pg/ml; P = NS). This pattern of plasma steroids, increased T and unchanged E, was also associated with significantly decreased serum LH and FSH concentrations (14.5 +/- 0.4 vs. 8.0 + 0.4 mIU/ml and 9.9 +/- 2.5 vs. 5.8 +/- 0.1 mIU/ml, respectively; P less than 0.01). These data support the hypothesis that T or one of its metabolites can modulate LH and FSH secretion independently of peripheral aromatization to E.

Adult↗
PubMed1979

Relative binding of testosterone and estradiol to testosterone-estradiol-binding globulin.

The binding of estradiol (E2) and testosterone (T) to testosterone-estradiol-binding globulin (TeBG) was studied in vivo at 37 C by three independent methods: equilibrium dialysis, steady state polyacrylamide gel electrophoresis, and TeBG-ligand dissociation kinetics. Equilibrium dialysis was performed at 37 C with the dialysate containing human serum albumin in amounts equivalent to that of the plasma dialysand. Scatchard analysis indicated that under these conditions E2 does not measurably bind to TeBG, while T has a Kd of 3.7 X 10(-10) M. Similarly, Scatchard-type analysis of E2 binding to TeBG in steady state polyacryalmide gel electrophoresis at 37 C revealed no high affinity saturable binding, while dihydrotestosterone was bound with a Kd of 2.7 X 10(-10) M. Examination of the dissociation kinetics of T and E2 ffrom TeBG revealed that the mean (+/-SD) T1/2 of dissociation of T from plasma at 37 C (10.8 +/- 2.4 min) was significantly shortened to 3.5 +/- 0.4 min by saturation of plasma with dihydrotestosterone (P less than 0.01), whereas that of E2 (8.9 +/- 1.4 min) was not changed (9.6 +/- 3.0 min). These data suggest that TeBG is not an important binder of plasma E2 at physiological temperatures and explain the observation that in diseases characterized by high TeBG levels, such as hyperthyroidism and liver disease, the MCR and free E2 levels have generally been normal.

Adult↗
PubMed1978

Hormonal correlates of normal and abnormal follicle growth after puberty in humans and other primates.

After the menarche, changing levels of gonadotrophins, prolactin and sex steroid hormones in peripheral blood are accompanied by ovulation and corpus luteum formation in one follicle, and atresia in the remaining follicles maturing during each menstrual cycle. Available evidence suggests that blood levels of steroid hormones reflect in large part the secretory activity of the ovary containing a pre-ovulatory follicle and most probably of that follicle itself (see Chapter 6). These steroid secretions and those of the corpus luteum coordinate hypothalamic-pituitary-ovarian function. Within the ovary, sex steroid hormones mediate effects of gonadotrophins and prolactin on follicle maturation and participate in determining the fate of individual follicles.

Animals↗
PubMed1976

Androgen binding proteins of testis, epididymis, and plasma in man and monkey.

Androgen-binding protein (ABP) has been found in the cytosol of testicular and epididymal homogenates of several sub-primate species. In those species which had the plasma androgen binding protein, testosterone-estradiol-binding globulin (TeBG), ABP and TeBG were found to be physically similar. We investigated the possibility that ABP might exist in monkey and man using the cytosol of testicular and epididymal homogenates and aspirates obtained by direct micropuncture of the rete testis. In polyacrylamide gel electrophoresis, pH 7.8, testicular and epididymal cytosols of monkey and man were found to contain several binding proteins of different size and net charge that bind dihydrotestosterone. These binding proteins were either indistinguishable from TeBG or could be related to TeBG as size and/or charge isomers. No ABP was detectable in up to 200 mul of monkey rete testis fluid obtained by direct micropuncture, though ABP is detectable in as little as 5 mul of rat rete testis fluid. The data suggest that the ABP's detected in the testicular and epididymal cytosols in monkey and man represent isomeric forms of plasma TeBG, and their presence in testicular cytosol most likely derives from blood contamination.

Androgens↗
PubMed1975

Regulation of FSH secretion: use of hydroxyurea to deplete germinal epithelium.

Hydroxyurea, a chemotherapeutic agent that prevents mitosis by inhibiting DNA synthesis, was administered to adult male rats for 70 days. Plasma FSH and LH showed no systematic trend although severe germinal cell depletion was produced. These data suggest that the cell(s) of the seminiferous tubule involved in FSH regulation must be either the type A spermatogonium or the Sertoli cell.

Animals↗
PubMed1975

Hormones, nutrition, and cancer.

The effects of obesity on steroid metabolism in women with breast and uterine cancer have been considered. Obesity may increase plasma estrone by two mechanisms, a higher rate of secretion of the estrone precursor, androstenedione, and a higher rate of conversion of androstenedione to estrone. Obesity may alter routes of metabolism of androgens and estrogens. The excretion of specific urinary metabolites can therefore be altered by obesity alone. Thus, steroid indices of relative cancer risk or responsiveness must be constructed with due attention to obesity, one of many important variables.

Androstenedione↗