PubMed Health⌕ Search

Biomedical subjects

K Reddi

Publications and source records attributed to K Reddi.

At least 37 records · Page 2Linked to original sources
PubMed1991

The source of inhibin secretion during the human menstrual cycle.

The source of inhibin secretion during the human menstrual cycle was investigated in two ways. The concentration of inhibin was compared in samples obtained from the ovarian and peripheral veins of 41 women undergoing hysterectomy. In 13 of the women, the corpus luteum was enucleated at operation and the peripheral concentration of inhibin measured at intervals for 24 h. Inhibin was assayed by a heterologous RIA using an antiserum raised against 31 kilodalton bovine inhibin. The concentrations of estradiol and progesterone in the peripheral and ovarian veins were similar to those previously reported. During the early follicular phase, the geometric mean inhibin concentrations were found to be significantly higher in both the right and left ovarian veins than the peripheral vein (180.4 and 157.7 vs. 78.7 U/L: P less than 0.02) but no difference was found in the late follicular phase between the vein draining the dominant ovary and the contralateral ovarian vein (231.1 vs. 193.4 U/L: NS). The inhibin concentrations in the veins draining the ovary bearing a corpus luteum were, however, significantly higher than those in the contralateral ovarian veins during the mid (409.1 vs. 203.6 U/L: P less than 0.02) and late (287.1 vs. 153.2 U/L: P less than 0.01) luteal phases. After enucleation of the corpus luteum, the inhibin concentration fell from the level seen before lutectomy (134.4 U/L) to 80.0 U/L at 24 h (P less than 0.01). This study demonstrates conclusively that the human corpus luteum secretes inhibin. No increase in inhibin secretion was seen from the dominant follicle in the late follicular phase. This casts doubt on the hypothesis that the selective suppression of FSH during the follicular phase is due to inhibin from the dominant follicle.

Adult↗
PubMed1990

Increased and intermittent prostaglandin release from amnion detected by a new superfusion technique for full thickness fetal membrane.

Prostaglandin E2 (PGE) and F2 alpha (PGF) release by the intact fetal membranes is described using a novel superfusion technique allowing for the independent assessment of prostaglandin release from the amnion and chorio-decidua whilst maintaining the anatomical integrity of the fetal membranes. The effect of labour on prostaglandin release is described. Using this system it was confirmed that the amnion is a major site of prostaglandin release and possibly production. Labour resulted in a significant increase of both PGE and PGF release from the amnion side only (Pre-labour: PGE 918 pg/cm2/3h, PGF 370 pg/cm2/3h; Labour: PGE 2993 pg/cm2/3h, PGF 662 pg/cm2/3h). No change in either PGE or PGF release from the chorio-decidual side was observed in relation to labour. In addition a change in the pattern of prostaglandin release from the amnion was observed in tissues obtained after the onset of labour. In 6 of 8 samples obtained after spontaneous labour an intermittent or pulsatile release of both PGE and PGF was observed from the amnion side as compared to the steady state of prostaglandin release from all 10 samples obtained before labour.

Amnion↗
PubMed1990

Metabolic profiles and lipoprotein lipid concentrations in non-obese and obese patients with polycystic ovarian disease.

Clinical parameters, androgen status and lipoprotein lipid profiles were assessed in 10 non-obese and 10 obese patients with polycystic ovarian disease (PCOD) and reference subjects matched for age, height and weight. Both obese and non-obese women with PCOD had significantly higher androgen levels when compared to the reference groups. When comparison of lipoprotein lipid profiles were made between groups, non-obese women with PCOD had significantly higher total cholesterol, triglycerides and LDL-cholesterol levels than non-obese reference subjects. Obese PCOD women manifested significantly higher total cholesterol, LDL-cholesterol, cholesterol/HDL, and LDL/HDL values than did obese reference subjects. Correlations between serum androgens and lipoprotein lipid concentrations in PCOD and normal women were unhelpful. Both non-obese and obese patients with PCOD had significantly higher systolic and diastolic blood pressures (BPs) than the reference groups. Thus, both non-obese and obese women with PCOD manifest hyperandrogenaemia which may result in a male pattern of lipoprotein lipid concentrations.

Adolescent↗
PubMed1990

Prostaglandins in dysfunctional labour; evidence for altered production of prostaglandin F2 alpha.

Dysfunctional labour was studied in relation to prostaglandin concentrations in amniotic fluid and production by fetal membranes. Initial clinical validation of the model established the presence of hypokinetic labour with no evidence of obstruction to the fetal progress. Prostaglandin F2 alpha (PGF2 alpha) and 13, 14 dihydro-15-keto-prostaglandin-F2 alpha concentrations in the amniotic fluid were low despite relatively normal concentrations of prostaglandin E2. Membranes removed from patients with the condition released very low concentrations of PGF2 alpha from the amniotic side with no alteration on the choriodecidual side of the membrane. Studies of free and phospholipid-associated arachidonic acid indicated normal release of arachidonic acid in dysfunctional labour. No changes in amniotic fluid-related inhibitors and stimulators of prostaglandin synthetase were detected. It is suggested that PGF2 alpha production is impaired in dysfunctional labour and that this prostaglandin is primarily involved in the progress of labour.

Amniotic Fluid↗
PubMed1990

Pharmacological 'rescue' of the corpus luteum results in increased inhibin production.

Inhibin production by the corpus luteum was investigated by undertaking pharmacological rescue of the corpus luteum with hCG in four healthy women. Blood samples were collected daily for two menstrual cycles. Starting 7 days after the LH surge in the second cycle, incremental doses of hCG (125-8000 IU) were administered daily for 7 days resulting in hCG levels comparable to those seen in normal pregnancy. Following hCG, the luteal phase was prolonged and there were significant increases in the plasma concentrations of inhibin (P less than 0.05), and oestradiol (P less than 0.05). The progesterone concentration was maintained at the mid-luteal phase peak and as a result was significantly higher than those on the equivalent days of the control cycle (P less than 0.05). It was concluded that rescue of the corpus luteum with physiological levels of hCG resulted in a significant output of inhibin, thus suggesting that the corpus luteum is a significant source of inhibin in early pregnancy.

Adult↗
PubMed1990

Circulating bioactive follicle stimulating hormone and immunoreactive inhibin levels during the normal human menstrual cycle.

To examine the relationship between circulating levels of bioactive FSH (B-FSH) and immunoactive inhibin and oestradiol we studied five women during ovulatory cycles. Daily blood samples were collected from each subject during one menstrual cycle. B-FSH was measured using a modified, highly sensitive in-vitro rat granulosa cell bioassay. The inclusion of IGF-1 (10 micrograms/l) and transferrin (50 mg/l) in the assay system enhanced granulosa cell responsiveness to FSH and resulted in increased assay sensitivity. Inhibin was measured by a heterologous radioimmunoassay (RIA) using an antibody raised against 31 kDa bovine inhibin. Bioactive FSH (B-FSH) levels were closely correlated to those of immunoactive FSH (I-FSH, r = 0.79, P less than 0.001) throughout the cycle. Peak levels of B-FSH were observed during the early follicular phase (day -13, 44.7 +/- 9.6 IU/l, mean +/- SEM) and during the midcycle surge (35.2 +/- 6.2 IU/l); lowest levels occurring during the luteal phase (nadir 3.9 +/- 0.27 IU/l). Plasma oestradiol levels increased significantly during the follicular phase (P less than 0.001) to a peak on day -1 and were negatively correlated with B-FSH during the late follicular phase (day -8 to -1; r = -0.45, P less than 0.02). There was no change in the concentration of inhibin (range 55.3-72.3 U/l) during the follicular phase until day -2 after which an increase to a midcycle peak of 139 +/- 10.6 U/l was observed. No correlation was observed between inhibin and B-FSH during the follicular phase. A second increase in the concentration of inhibin was seen during the luteal phase; peak levels occurred by day 6 (311 +/- 25.8 U/l), remained elevated until day 12, and were negatively correlated with B-FSH (r = -0.53, P less than 0.001). No correlation was observed between oestradiol and inhibin or B-FSH during the luteal phase. We conclude that (1) oestradiol secretion from the growing follicle is primarily responsible for the negative feedback regulation of B-FSH resulting in a change from peak levels in the early follicular phase to basal levels in the late follicular phase; (2) significant and sustained increase in peripheral inhibin concentrations occur mostly during the luteal phase; and (3) regulation of FSH secretion by inhibin occurs primarily in the luteal phase. These results suggest a temporal relationship between oestradiol and inhibin in the negative feedback regulation of FSH in vivo.

Adult↗
PubMed1990

Inhibin secretion after treatment with an LHRH agonist and subsequent ovarian hyperstimulation induced by FSH in the macaque (Macaca arctoides).

The effect of ovarian hyperstimulation with 'pure' FSH on serum concentrations of immunoreactive inhibin in macaques in which endogenous gonadotrophin secretion and ovarian activity had been suppressed by an LHRH agonist implant was studied. Four stump-tailed macaques were treated with an LHRH agonist implant in the early follicular phase of the cycle. After a transient stimulatory phase oestradiol secretion was markedly suppressed, and the rises in progesterone and inhibin observed after ovulation were absent. At 8 weeks after implant administration, when serum LH was only just detectable, FSH (Metrodin) was administered to the LHRH agonist-treated macaques once daily for 9 days (75 i.u. on Day 0, 35 i.u. Days 1-8). FSH treatment stimulated a marked increase in oestradiol and immunoreactive inhibin secretion in the absence of a rise in serum progesterone concentrations. Comparison of the FSH-induced pattern of inhibin secretion with the profile during the normal menstrual cycle showed that during the normal cycle inhibin is secreted into the peripheral blood almost exclusively during the luteal phase in the macaque, but stimulation of follicular development by exogenous FSH was associated with a rise in inhibin concentrations in the absence of ovulation. These results suggest that this non-physiological rise in inhibin may be one of the factors involved in the changes in endogenous gonadotrophin secretion which can occur during ovarian hyperstimulation.

Animals↗
PubMed1989

Insulin and C-peptide secretion in non-obese patients with polycystic ovarian disease.

Plasma glucose, immunoreactive insulin (IRI) and C-peptide responses during an oral glucose tolerance test (oGTT) were assessed in 11 non-obese patients with polycystic ovarian disease (PCOD) and 11 reference subjects matched for age, height and weight. Also, 6 patients with PCOD and 6 normal women were subjected to intravenous glucose tolerance testing (ivGTT) On oGTT, all subjects exhibited normal glucose tolerance; however, PCOD patients had significantly higher mean plasma glucose levels at 30, 60, 90 and 120 min and higher mean incremental glucose areas. In addition the patients with polycystic ovaries showed higher mean basal IRI and C-peptide levels, higher mean glucose stimulated IRI and C-peptide levels and higher mean incremental IRI and C-peptide values. The molar ratios of C-peptide/IRI were significantly lower in the PCOD group at all time intervals after glucose stimulation when compared to the normal women. During ivGTT, there were significantly higher mean glucose levels at 5, 40, 50 and 60 min in the PCOD group when compared to the reference group. The IRI response to intravenous glucose in the PCOD women was similar to the reference group. The findings on oGTT suggest that non-obese patients with PCOD have increased pancreatic IRI secretion as well as impaired hepatic extraction of the hormone.

Administration, Oral↗
PubMed1988

Intrauterine pressure studies in multigravid patients in spontaneous labour: effect of oxytocin augmentation in delayed first stage.

Uterine activity was assessed by measuring the uterine activity integral (UAI) in 116 black multigravid patients in spontaneous active labour at term. Although individual patients showed a wide range of mean UAI levels, normal labour (group I, n = 54) was associated with a mean UAI level of 1640 kPas/15 min which was higher than the mean level observed in patients in whom delay in cervical dilatation occurred in active labour. The patients who failed to progress in labour were treated with oxytocin infusion and 32 of them made good progress in labour and achieved vaginal delivery (group IIa: mean UAI pre-oxytocin treatment 1040 (SD 424) kPas/15 min, post-oxytocin 1890 (SD 559) kPas/15 min). The other 23 patients required operative delivery (group IIb) despite correction of uterine activity after oxytocin treatment (pre-oxytocin mean UAI 1230 (SD 570) kPas/15 min, post-oxytocin 1815 (SD 650) kPas/15 min). The rate of oxytocin infusion varied between patients from 2 to 16 mU/min but in 75% uterine activity was corrected to normal levels by a dose of less than or equal to 8 mU/min. It is concluded that delay in progress in labour is associated with lower intrauterine pressures than are present in normal labour, and that management of patients presenting with inefficient uterine action may benefit from the use of uterine activity integral measurements.

Female↗
PubMed1987

Differential regulation of prostaglandin production by inhibitors and stimulators in amniotic fluids during normal and dysfunctional labor.

The regulatory effect of amniotic fluid factors on prostaglandin production by sheep seminal vesicle prostaglandin synthetase was determined using samples obtained before and after the onset of labor. Variations in the enzyme incubation conditions permitted the effects on both prostaglandin E (PGE) and prostaglandin F (PGF) production to be assessed. Amniotic fluid obtained before the onset of labor and during early labor resulted in a net stimulation of PGE production and no difference was observed between these two groups. Samples obtained before and during early labor had no net effect on PGF production. However, when samples obtained late in labor were tested, there was a greater stimulation of PGF and less of PGE compared to early labor suggesting a preference for PGF production rather than PGE in late labor. When samples obtained from patients in dysfunctional labor were compared to normal labor, no difference on the effect of either PGE or PGF production was observed. This implies that the decreased PGF previously described in dysfunctional labor is due to an intrinsic abnormality of the fetal membranes rather than inhibition of prostaglandin production by factors mediated via the amniotic fluid.

Amniotic Fluid↗
PubMed1987

Evidence for insulin resistance in nonobese patients with polycystic ovarian disease.

In this study seven normal weight Indian patients with polycystic ovarian disease (PCOD) with no evidence of acanthosis nigricans and 7 age- and weight-matched normal Indian women were studied to determine whether PCOD patients were insulin-resistant. While all 14 women had normal glucose tolerance, the PCOD women had significantly higher mean plasma glucose levels at 30 and 60 min and higher mean incremental glucose areas [incremental areas: PCOD, 9.0 +/- 2.2 (+/- SEM); normal women, 4.0 +/- 0.8 mmol/L; P less than 0.05]. Insulin responses were significantly higher in the PCOD compared to normal women (incremental areas: PCOD, 623.8 +/- 78.3; normal women, 226.2 +/- 30.3 microU/mL; P less than 0.001). Both serum testosterone and androstenedione levels correlated with the insulin areas (r = 0.82; P less than 0.001 and r = 0.86; P less than 0.001, respectively). [125I] Insulin binding to erythrocytes revealed decreased maximum specific binding in the PCOD women (6.9 +/- 0.6%) compared to that in normal women (9.2 +/- 0.7%; P less than 0.02). While Scatchard analysis revealed similar receptor numbers, ID50 values demonstrated decreased receptor affinity in the women with PCOD. In conclusion, in the absence of acanthosis nigricans, nonobese patients with PCOD are insulin resistant, and this insulin resistance correlates with the hyperandrogenism.

Adult↗
PubMed1987

Amniotic membrane production of prostaglandin F2 alpha is reduced in dysfunctional human labor: results of in vivo and in vitro studies.

Mobilization of arachidonic acid from glycerophospholipids and prostaglandin (PG) release from fetal membranes were studied in women with dysfunctional labor in the absence of cephalopelvic disproportion or fetal malposition. Using superfusion of intact amnion and chorion, we found a slight decrease in PGE and a more significant decrease in PGF release by the amniotic side of the fetal membrane obtained from women with dysfunctional labor compared to that in women with normal labor (PGE: normal labor, 2992 pg/cm2.h; dysfunctional labor, 1846 pg/cm2.h; P less than 0.05; PGF: normal labor, 662 pg/cm2.h; dysfunctional labor, 204 pg/cm2.h; P less than 0.02). Release of both prostanoids was significantly greater from the amniotic side in tissues obtained after labor compared to that in prelabor tissue. Analysis of arachidonic acid (by gas liquid chromatography) and phospholipid content (by two-dimensional thin layer chromatography) confirmed metabolic disposal of arachidonic acid from the amnion after the onset of labor. However, no difference in either phospholipid or phospholipase A2-releasable arachidonic acid of individual phospholipid classes was found in amnion tissue from women with normal and dysfunctional labor, suggesting similar activities of phospholipase A2 in these two groups. The finding of decreased free and phospholipase A2-releasable arachidonic acid of the total lipid extract of the amnion of women with dysfunctional labor could suggest further metabolic exhaustion of the substrate or failure of liberation of this fatty acid from glycerophospholipids by enzymes other than phospholipase A2, such as phospholipase C or diacyl and monoacylglycerolipases.

Adult↗
PubMed1986

Insulin secretion in Indian patients with impaired glucose tolerance.

The insulin response to a 75 g oral glucose load was studied in 26 indian patients with impaired glucose tolerance (IGT) and 26 controls matched for age, sex and weight. There were no significant differences between the mean insulin responses and incremental insulin areas between the patients with IGT and controls. However, when the patients were divided into obese and non-obese subgroups and their mean insulin levels compared, the obese patients with IGT had significantly higher insulin levels at 120 minutes than the obese controls.

Adult↗
PubMed1986

Endocrine studies in patients with isolated gonadotrophin-releasing hormone deficiency.

Twelve black women with isolated gonadotrophin deficiency were studied. After administration of intravenous gonadotrophin-releasing hormone (GnRH), all patients had subnormal gonadotrophin responses. However, after priming with subcutaneous GnRH (in 9 patients) follicle-stimulating hormone responses improved in 4 patients and luteinizing hormone responses in 7 patients. Prolactin responses to intravenous thyrotrophin-releasing hormone were significantly decreased at 20 and 60 minutes, when compared with reference subjects (P less than 0.01). In response to insulin-induced hypoglycaemia, prolactin responses were heterogeneous in 11 patients, while those of growth hormone were suboptimal in 8 of the 11 patients tested.

Black or African American↗
PubMed1986

Clinical studies in black women with isolated gonadotrophin-releasing hormone deficiency.

Twelve black patients with primary amenorrhoea as a result of hypogonadotrophic hypogonadism were studied to establish the diagnosis of isolated gonadotrophin-releasing hormone (GnRH) deficiency. All were eunuchoid with poor development of breasts and pubic hair. Chromosomal complement was female and none had midline facial defects or anosmia. Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels were low or undetectable, while the levels of other pituitary hormones were normal. Patients did not respond to clomiphene citrate administration, but did bleed in response to an oestrogen/progestagen combination and responded to human menopausal gonadotrophin. This study clearly establishes that isolated GnRH deficiency occurs in black women and suggests that the male:female ratio is different from that in white populations.

Adult↗