The homeodomain protein, Pit-1/GHF-1, is capable of binding to and activating cell-specific elements of both the growth hormone and prolactin gene promoters.

Studies were conducted to determine whether the trans-acting protein Pit-1/GHF-1 can bind to and activate promoter elements in both the GH and PRL genes that are necessary for cell-specific expression. Four pituitary cell lines that differentially express the endogenous GH and PRL genes were examined for their ability to activate GH and PRL promoter constructs containing sequences necessary for cell-specific expression (CSEs). Plasmids containing one CSE, -96 PRL and -104 GH, were similarly expressed in each of the four cell lines. Of the plasmids containing two CSEs, -173 PRL was always activated to a greater extent than -145 GH, with this relative activation being stronger in GC and GH1 cells than in 235-1 and GH4C1 cells. Protein-DNA binding assays were used to show that the GH and PRL CSEs specifically bound two highly abundant nuclear proteins (31 and 33 kDa). The two proteins were present at similar levels in all four pituitary cell lines and were recognized by a Pit-1/GHF-1 antibody. In contrast, HeLa and Rat2 cells did not activate transfected GH or PRL plasmids and did not contain nuclear proteins that specifically bound to the GH and PRL CSEs. However, cotransfection of these cells with the expression vector RSV-Pit-1/GHF-1 resulted in the activation of -173 PRL and -145 GH (PRL greater than GH). HeLa cells transfected with RSV-Pit-1/GHF-1 also contained 31- and 33-kDa nuclear proteins that bound to the GH and PRL CSEs. These results show that Pit-1/GHF-1 is present at levels in pituitary cell lines that are sufficient to activate the minimal elements in both the GH and PRL promoters necessary for cell-specific expression of these genes.

Changes in the pulsatile pattern of luteinizing hormone secretion during the rat estrous cycle.

To ascertain whether changes in the pattern of GnRH release from the hypothalmus occur during the 4-day rat estrous cycle, the pattern of LH release was characterized on each day of the estrous cycle, and the results were interpreted in light of the changes in pituitary responsiveness to GnRH previously described by this laboratory to occur during this time. Blood samples were taken from intact, freely moving rats via venous catheters at 6- to 10-min intervals for 3-4 h. LH pulse height and LH interpulse interval were quantified on each day of the cycle, and the transition on the afternoon of proestrus from tonic LH release to the preovulatory LH surge was detailed. The effects on the pattern of LH release during estrus of small doses of GnRH (0.4 ng) and the continuous infusion of the opioid antagonist naloxone were also examined. Plasma LH concentrations (NIAMDD rat LH-RP-1) were determined with a highly sensitive LH RIA. LH pulses were identified using the PULSAR algorithim. The LH interpulse intervals of 46 +/- 2 min on diestrous-1 day, 49 +/- 4 min on diestrous day 2, and 60 +/- 8 min on proestrus immediately before the LH surge were not significantly different. There were no changes immediately preceding the preovulatory LH surge on the afternoon of proestrus in either the LH interpulse interval or the LH pulse height. Instead, the transition from tonic LH secretion to the preovulatory LH surge was found to occur abruptly. These data suggest that an abrupt increase in GnRH secretion during the afternoon of proestrus initiates the dramatic rise in LH concentrations. The pattern of LH secretion during the day of estrus differed significantly from that on the other days of the cycle in that no LH pulses were observed. However, the administration of small pulses of GnRH elicited physiological elevations in LH release. Furthermore, the continuous infusion of naloxone to estrous rats immediately stimulated a pulsatile pattern of LH secretion, with a LH interpulse of 56 +/- 4 min. These data indicate that the absence of LH pulses during estrus may result from a deficit in GnRH release. Similar modifications in GnRH release during the other days of the cycle were inferred from the observed changes in LH pulse heights. The LH pulse height of 21 +/- 3 ng/ml on diestrous day 2 was significantly less than the LH pulse height of 41 +/- 4 ng/ml on diestrous day 1 or 35 +/- 4 ng/ml on proestrus before the surge.(ABSTRACT TRUNCATED AT 400 WORDS)

The suppression of pulsatile luteinizing hormone secretion during lactation in the rat.

The inhibition of LH secretion during lactation may be the consequence of a pituitary insensitivity to GnRH stimulation and/or an inhibition of GnRH release from the hypothalamus. To assess the contribution that these mechanisms may make to the suppression of LH secretion during lactation, we described the pattern of LH secretion in lactating rats and the magnitude of LH secretion in response to a GnRH stimulus. We assessed the effect of the strength of the suckling stimulus (two and eight pups), the length of lactation (5 and 10 days), and the presence of the ovaries on the pattern of LH secretion. We also examined the pattern of LH secretion after removal of a large suckling stimulus. In the intact rat, the pattern of LH secretion during lactation was uniformly nonpulsatile, despite significant differences between animals suckling two and eight pups in pituitary responsiveness to GnRH. In intact rats suckling two pups during day 10 of lactation, significant LH secretion was stimulated by 0.4-ng pulses of GnRH every 50 min, while animals with eight pups secreted little LH in response to the same stimulus. It was concluded that a two-pup suckling stimulus was sufficient to completely suppress pulsatile GnRH release without affecting pituitary function, whereas an eight-pup suckling stimulus also depressed pituitary sensitivity to GnRH. In ovariectomized (ovx) rats suckling two pups, seven of nine animals showed no postcastration rise in LH secretion or evidence of pulsatile LH secretion during day 5 of lactation. In the remaining two animals, a castrate pattern of pulsatile LH secretion was observed, with a LH interpulse interval of 31 +/- 6 min. By day 10 of lactation, all animals suckling two pups had castration patterns of LH secretion, with a LH interpulse interval of 35 +/- 2 min, which was significantly different from the LH interpulse interval of 26 +/- 1 min observed in ovx animals without pups. Therefore, a two-pup suckling stimulus is capable of retarding the increase in LH pulse frequency characteristically seen in the rat after castration. In ovx rats suckling eight pups, the postcastration rise in LH secretion was completely inhibited in all animals examined on days 5 and 10 of lactation, and the pattern of LH secretion was uniformly nonpulsatile. A consistent pattern of pulsatile LH secretion was not reinitiated until 72 h after removal of the suckling stimulus (LH interpulse interval, 31 +/- 2 min).(ABSTRACT TRUNCATED AT 400 WORDS)

Reduction in psychopathology following bariatric surgery for morbid obesity.

BACKGROUND: Although there has been some disagreement, there is growing evidence now that psychopathology is a comorbidity of morbid obesity among patients seeking bariatric surgery. The aim of this study was to determine whether psychopathology decreases following this surgery. METHODS: Utilizing a national sample, this study focused on pre- and post-surgery scores on the Minnesota Multiphasic Personality Inventory, Second Edition (MMPI-2). The MMPI-2 was administered first during the pre-surgery medical examination, and again between 6 months and 1 year following surgery. RESULTS: Validity scale scores on the pre- and post-surgery MMPI-2s indicated that there was no impediment to interpreting the clinical scale scores of these tests. There was a pervasive pattern of statistically significant decreases in pre- to post-surgery clinical scale scores. Further, comparison of MMPI-2 clinical scale scores to available test norms showed that the number of participants showing signs of mental disorders was unusually high before surgery, and at or below the test norms following surgery. CONCLUSIONS: There is clear evidence in this study that psychopathology declines following bariatric surgery. The unusually high levels of psychopathology before surgery may be a joint function of the factors producing the morbid obesity, and a reaction to the obesity itself. That psychopathology declines following surgery to levels expected in the general population indicates that the patients were becoming more positive about their lives.

Evidence for the mitochondrial biosynthesis of 3R-hydroxy-5Z,8Z,11Z,1 4Z-eicosatetraenoic acid in the yeast Dipodascopsis uninucleata.

The biosynthesis of 3R-hydroxy-5Z, 8Z, 11Z,14Z-eicosatetraenoic acid (3R-HETE) from arachidonic acid (20:4n-6) by the hyphal-forming yeast, Dipodascopsis uninucleata, in cell-free enzyme extracts required CoASH, ATP, NAD+ and Mg2+; 3R-HETE was present as the CoA derivative in enzyme extracts and its biosynthesis was associated with mitochondria. Its synthesis was high from arachidonoyl-CoA (15% conversion of the substrate; 22 nmol mg protein(-1) x h), but significantly higher from trans-2-arachidonoyl-CoA (53 nmol mg protein(-1) x min). Aspirin, an inhibitor of prostaglandin endoperoxide synthase synthase (cyclooxygenase), did not significantly inhibit 3R-HETE biosynthesis in enzyme extracts, as opposed to antimycin A (46% inhibition). The chirality of 3-HETE was 95% R and 5% S. 3R-HETE has the same chirality as the products of peroxisomal enoyl-CoA hydratases of Neurospora crassa and Saccharomyces cerevisiae; the difference appears to be that in D. uninucleata the Renantiomers are synthesized in mitochondria. Exogenously supplied eicosapentaenoic acid was converted to 3-hydroxy 5Z,11Z,14Z,17Z-eicosapentaenoic acid by cell-free enzyme extracts though there was no requirement for a 5Z,8Z-diene structure for the biosynthesis of 3-hydroxylated fatty acids as 3-hydroxy-8Z,11Z,14Z, and 3-hydroxy-11Z,14Z,17Z-eicosatrienoic acids were synthesized from the corresponding fatty acids. We found no evidence for the synthesis of the prostaglandins F2alpha and E2.

The biosynthesis of oxylipins of linoleic and arachidonic acids by the sewage fungus Leptomitus lacteus, including the identification of 8R-Hydroxy-9Z,12Z-octadecadienoic acid.

When the sewage fungus Leptomitus lacteus was grown in liquid culture aerobically and then transferred to medium containing long-chain fatty acids, it produced a number of oxygenated fatty acids. From linoleic acid (18:2n-6), the major metabolite produced was R-8-hydroxy-9Z,12Z-octadecadienoic acid (8R-HODE), with additional quantities of 8,11-di-HODE, 11,16-di-HODE, and 11,17-di-HODE. Other fatty acid derivatives identified included 7-HODE, 10-HODE, and 13-hydroxy-octadecamonoenoic acid. Arachidonic acid (20:4n-6) was metabolized primarily to 18- and 19-hydroxy-eicosatetraenoic acids (18- and 19-HETE) also as R enantiomers, along with smaller quantities of 17-HETE, 9-HETE, 14,15-dihydroxy-eicosatrienoic acid and 11,12,19-trihydroxy-eicosatrienoic acid. The oxygenated products of long-chain fatty acids, in particular the biosynthesis of 8R-HODE, a compound classified as a precocious sporulation inducer, were similar to those produced by an unrelated fungal species in the Ascomycota, the take-all fungus Gaeumannomyces graminis. As in G. graminis, the biotransformation of linoleate to 8R-HODE was not significantly inhibited by exposure of the organism to CO. This indicated that the enzyme responsible for 8R-HODE biosynthesis in Leptomitus could be similar to that of G. graminis; yet we did not detect 7,8-di-HODE as a product of 18:2n-6 metabolism as in G. graminis. CO did inhibit the biosynthesis of 14,15-di-HETE, 18-HETE, and 19-HETE in L. lacteus, which suggested the involvement of a cytochrome P450-type monooxygenase. The biosynthesis of 8R-HODE from 18:2n-6 was found to occur in certain cell lysates, specifically in low speed (15,000 x g) supernatant, following cell disruption.

Developing and maintaining social interaction in profoundly retarded young males.

Social interaction was increased in five profoundly retarded males using formal training, stimulus control, and rewarded generalization procedures. Seven behaviors were monitored for each boy to determine whether correlated changes occurred in maladaptive behaviors as social interaction varied over the several phases of a withdrawal design that included multiple-baseline features. All five boys increased their social interaction and reduced unoccupied and self-stimulatory behavior. These changes were maintained as continuous reinforcement was reduced to a single response-contingent reinforcer per 15-minute session. Four follow-up probes showed the stability of the changes.

The surgical treatment of morbid obesity.

Obesity is the second leading cause of preventable death in the United States according to C. Everett Koop, M.D., former Surgeon General of the United States. The use of tobacco is the leading cause, but in the near future, obesity will become the first. Estimates of the percentage of adult Americans who are overweight range from 35% to 50%. Those who are morbidly obese (100 pounds or more overweight), number approximately 8 million. There is no doubt that obesity is a significant public health problem, particularly when its comorbidities are considered: diabetes, hyperlipidemia, hypertension, gastroesophageal reflux, cardiovascular disease, degenerative arthritis, cholelithiasis, respiratory insufficiency, cancer, sleep apnea, and many others. Serious medical problems are usually present in patients with morbid obesity. When significant long-term weight loss is accomplished for these patients, the comorbidities almost always improve or disappear entirely.

Regulation of gonadotropin secretion during lactation.

Lactation in the rat is characterized by an inhibition of ovarian cyclicity which correlates with a suppression of basal gonadotropin secretion, a decrease in the magnitude of estrogen-induced LH surges and a decrease in the postcastration rise en LH and FSH. Furthermore, pulsatile administration of GnRH (0.4 ng GnRH every 50 min) fails to elicit LH pulses in females nursing 8 pups but produces normal basal LH pulses in females nursing 2 pups. There is a good correlation during lactation among pituitary GnRH receptor content, pituitary responsiveness to GnRH and basal LH secretion. All of these parameters are greatly decreased in the presence of an 8-pup suckling stimulus but are generally normal in the presence of a 2-pup suckling stimulus. Taken together with data from other laboratories suggesting that GnRH positively regulates its own receptors, these data suggest that a large suckling stimulus decreases GnRH release from the hypothalamus. This hypothesis is supported by studies in which GnRH release in lactating rats was indirectly assessed by examining the pulsatile pattern of LH secretion. In intact rats suckling 2 or 8 pups on day 10 postpartum, the pattern of LH secretion was uniformly nonpulsatile. The suppression of pulsatile GnRH release in intact females suckling 2 pups does not appear to be due to the small suckling stimulus itself, because ovariectomized females suckling 2 pups exhibited pulsatile LH secretion on day 10 postpartum, but may be due to some ovarian factor acting within the CNS to inhibit GnRH release. In contrast, in ovariectomized females suckling 8 pups, pulsatile LH secretion was completely suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Postpartum preovulatory surge of gonadotropin secretion in the rat may be initiated by the labor process.

These studies attempted to identify the factors which stimulate the postpartum preovulatory surge of gonadotropin secretion in the rat. The time of parturition on Day 23 of pregnancy slightly affected the time of the postpartum gonadotropin surge which occurred that afternoon. Animals delivering early in the morning had postpartum gonadotropin surges earlier in the afternoon than animals delivering later in the day. To ascertain whether an afternoon time of day signal stimulates the postpartum gonadotropin surge, pentobarbital was administered immediately postpartum. Pentobarbital blocked the postpartum gonadotropin surge on the day of parturition in only 6 of 17 animals. Surprisingly, these animals all had gonadotropin surges the following day despite a large continuous suckling stimulus. To determine whether the process of parturition stimulates the postpartum gonadotropin surge, pups were delivered by cesarean section on Day 22 of pregnancy. Luteinizing hormone (LH) surges were not detected in cesarean-sectioned animals on the day of the operation, nor on the following day. However, cervical stimulation in the morning resulted in LH surges in 5 of 9 cesarean-sectioned rats later that day, at a time coincident with the afternoon time of day signal. These studies suggest that the postpartum gonadotropin surge results from an afternoon time of day signal which is activated by the cervical stimulation of the labor process.

Role of acyl-CoAs and acyl-CoA-binding protein in regulation of carbon supply for fatty acid biosynthesis.

Acyl-CoA esters inhibit the plastidial glucose 6-phosphate (Glc-6-P) transporter and the adenylate transporter; the IC(50) values for the inhibition by oleoyl-CoA (18:1-CoA) are 200-400 nM and 1-2 microM respectively. The inhibition of either of these processes significantly reduces the flux of carbon from Glc-6-P or from acetate into long-chain fatty acids. The effect is dependent on the acyl chain length, e.g. lauryl-CoA is less inhibitory than oleoyl-CoA, causing 34 and 68% inhibition respectively of Glc-6-P uptake after 30 s. The inhibition of Glc-6-P and ATP transport is alleviated by addition of an equivalent concentration of acyl-CoA-binding protein (ACBP) or BSA. Acyl-CoAs do not inhibit pyruvate or glucose transporters. The endogenous concentrations of acyl-CoAs and ACBP are similar during embryo maturation.

Role of proestrous progesterone secretion in suppressing basal pulsatile LH secretion during estrus of the estrous cycle.

These studies examined the mechanisms responsible for the paucity of basal LH pulses during estrus. We confirmed our earlier observations that constant infusion of naloxone during estrus results in the immediate appearance of pulsatile LH secretion during estrus, consisting of LH peak heights and LH interpulse intervals that are similar to those observed during other days of the estrous cycle. We then tested whether the proestrous surge of progesterone was responsible for the suppression of pulsatile LH secretion during estrus. Three treatment regimens were used on proestrus to either block progesterone secretion (pentobarbital) or block its action (progesterone antiserum or the progesterone antagonist, RU 486). After treatment at 12.00 h on proestrus, blood samples were collected during estrus every 10 min for 4 h, and the plasma samples were analyzed for the pattern of LH secretion. Treatment with pentobarbital (35 mg/kg at 12:00 h) blocked the proestrous surges of LH and progesterone and resulted in pulsatile LH secretion during estrus. The LH interpulse interval (72 +/- 7 min) was somewhat slower than that observed in the naloxone-infused animals (54 +/- 8 min). Simultaneous treatment with pentobarbital and progesterone at 12:00 h on proestrus completely prevented the appearance of LH pulses during estrus. Treatment with either progesterone antiserum (0.5 ml, i.v.) or RU 486 (1 mg s.c.) resulted in the initiation of pulsatile LH secretion during estrus. In the RU 486-treated animals, LH peak heights and LH interpulse intervals were similar to those observed in naloxone-infused animals and during other days of the estrous cycle.(ABSTRACT TRUNCATED AT 250 WORDS)

Fatty acid synthesis in pea root plastids is inhibited by the action of long-chain acyl- coenzyme as on metabolite transporters.

The uptake in vitro of glucose (Glc)-6-phosphate (Glc-6-P) into plastids from the roots of 10- to 14-d-old pea (Pisum sativum L. cv Puget) plants was inhibited by oleoyl-coenzyme A (CoA) concentrations in the low micromolar range (1--2 microM). The IC(50) (the concentration of inhibitor that reduces enzyme activity by 50%) for the inhibition of Glc-6-P uptake was approximately 750 nM; inhibition was reversed by recombinant rapeseed (Brassica napus) acyl-CoA binding protein. In the presence of ATP (3 mM) and CoASH (coenzyme A; 0.3 mM), Glc-6-P uptake was inhibited by 60%, due to long-chain acyl-CoA synthesis, presumably from endogenous sources of fatty acids present in the preparations. Addition of oleoyl-CoA (1 microM) decreased carbon flux from Glc-6-P into the synthesis of starch and through the oxidative pentose phosphate (OPP) pathway by up to 73% and 40%, respectively. The incorporation of carbon from Glc-6-P into fatty acids was not detected under any conditions. Oleoyl-CoA inhibited the incorporation of acetate into fatty acids by 67%, a decrease similar to that when ATP was excluded from incubations. The oleoyl-CoA-dependent inhibition of fatty acid synthesis was attributable to a direct inhibition of the adenine nucleotide translocator by oleoyl-CoA, which indirectly reduced fatty acid synthesis by ATP deprivation. The Glc-6-P-dependent stimulation of acetate incorporation into fatty acids was reversed by the addition of oleoyl-CoA.

Suppression of pulsatile LH secretion, pituitary GnRH receptor content and pituitary responsiveness to GnRH by hyperprolactinemia in the male rat.

To assess whether gonadotropin-releasing hormone (GnRH) release from the hypothalamus might be altered by hyperprolactinemia in the male rat, we measured in chronically hyperprolactinemic rats the pituitary GnRH receptor content and described the pattern of luteinizing hormone (LH) release during the postcastration rise in gonadotropin secretion 24 and 72 h after gonadectomy. In intact rats, the effect of hyperprolactinemia was determined by describing the pattern of LH secretion, pituitary GnRH receptor content and assessment of pituitary responsiveness to small doses of GnRH (1.0 ng). In addition, to determine the role endogenous opioids might play in inhibiting GnRH release in hyperprolactinemic rats, we examined the effect of both a continuous infusion and a bolus injection of the opioid antagonist naloxone on the pattern of LH release. Chronic hyperprolactinemia was achieved by implanting 4 pituitaries under the kidney capsules 3-4 weeks before study. Acute hyperprolactinemia was achieved by injecting rats with 1 mg ovine prolactin every 12 h for 3 days. Control animals were untreated or were chronically hyperprolactinemic rats in which the hyperprolactinemia was transiently reversed by treatment for 3 days with the dopamine agonist 2-alpha-bromoergocryptine. The mean LH concentration was greatly decreased at 24 postcastration in chronically hyperprolactinemic rats relative to controls. This decrease was associated with a decrease in LH pulse height and pulse amplitude and pituitary GnRH receptor content, but not with an increase in the LH interpulse interval. In contrast, the decrease in mean LH concentrations in hyperprolactinemic animals at 72 h postcastration was primarily associated with a significantly longer LH interpulse interval than that observed in control animals. Chronic hyperprolactinemia in intact rats decreased the pituitary GnRH receptor content, in addition to decreasing the mean LH concentrations during pulsatile GnRH administration. Chronic hyperprolactinemia also inhibited LH release relative to controls during the continuous 4-hour infusion of naloxone and in response to a bolus injection of naloxone. However, in acutely hyperprolactinemic intact male rats a bolus injection of naloxone increase LH secretion 20 min later to levels similar to those obtained in control rats. In summary, these results indicate that chronic hyperprolactinemia decreased LH secretion by primarily decreasing GnRH secretion as suggested by a decrease in pituitary GnRH receptor content and a decrease in LH pulse frequency and pulse amplitude.(ABSTRACT TRUNCATED AT 400 WORDS)

Inhibition by long-chain acyl-CoAs of glucose 6-phosphate metabolism in plastids isolated from developing embryos of oilseed rape (Brassica napus L.).

The effects of long-chain acyl-CoA (lcACoA) esters (both added exogenously and synthesized de novo) and acyl-CoA binding protein (ACBP) on plastidial glucose 6-phosphate (Glc6P) and pyruvate metabolism were examined using isolated plastids. The binding of lcACoA esters by ACBP stimulated the utilization of Glc6P for fatty acid synthesis, starch synthesis and reductant supply via the oxidative pentose phosphate (OPP) pathway. Stimulation occurred at low (1-10 microM) concentrations of ACBP. Pyruvate-dependent fatty acid synthesis was not directly affected by ACBP. However, addition of ACBP did increase the Glc6P-dependent stimulation of pyruvate utilization mediated through the OPP pathway. On the basis of these experiments, we conclude that lcACoA esters may inhibit Glc6P uptake into plastids, and that this inhibition is relieved by ACBP. We also suggest that utilization of other substrates for fatty acid synthesis may be affected by lcACoA/ACBP via their effects on the OPP pathway.

Inhibition of the glucose-6-phosphate transporter in oilseed rape (Brassica napus L.) plastids by acyl-CoA thioesters reduces fatty acid synthesis.

Addition of oleoyl-CoA (1 microM), or other acyl-CoA thioesters with a chain length of C(16) or greater, to oilseed rape plastids (Brassica napus L.) inhibited the rate of D-glucose 6-phosphate (Glc6P) uptake by 70% after 2 min. The IC(50) value for oleoyl-CoA inhibition of the transporter was approx. 0.2-0.3 microM. Inhibition was alleviated by the addition of acyl-CoA binding protein (ACBP) or BSA at slightly higher concentrations. Oleic acid (5-25 microM), Tween 40 (10 microM), Triton-X 100 (10 microM) and palmitoylcarnitine (5 microM) had no effect on Glc6P uptake. The uptake of [1-(14)C]Glc6P occurred in exchange for P(i), 3-phosphoglycerate or Glc6P at a typical rate of 30 nmol Glc6P/min per unit of glyceraldehyde-3-phosphate dehydrogenase (NADP(+)). The K(m(app)) of the Glc6P transporter for Glc6P was 100 microM. Neither CoA (0.3 mM) nor ATP (3 mM) inhibited Glc6P uptake, but the transporter was inhibited by 72% when ATP and CoA were added together. This inhibition was attributable to the synthesis of acyl-CoA thioesters, predominantly oleoyl-CoA and palmitoyl-CoA, by long-chain fatty acid-CoA ligase (EC 6.2.1.3) from endogenous fatty acids in the plastid preparations. Acyl-CoA thioesters did not inhibit the uptake of [2-(14)C]pyruvate or D-[1-(14)C]glucose into plastids. In vivo quantities of oleoyl-CoA and other long-chain acyl-CoA thioesters were lower than those for ACBP in early cotyledonary embryos, 0.7+/-0.2 pmol/embryo and 2.2+/-0.2 pmol/embryo respectively, but in late cotyledonary embryos quantities of long-chain acyl-CoA thioesters were greater than ACBP, 3+/-0.4 pmol/embryo and 1.9+/-0.2 pmol/embryo respectively.

Chemical characterization of neuroendocrine targets for progesterone in the female rat brain and pituitary.

The secretory products of some of the cell types which respond directly to actions of progesterone in the female rat brain and pituitary were determined by combining immunocytochemistry with autoradiography following systemic administration of the synthetic progestin ligand [3H]-R5020. Four major findings are reported: (1) Approximately 90% of the tyrosine hydroxylase (TH)-immunoreactive neurons in the hypothalamic arcuate nucleus have progesterone receptors, while TH-immunoreactive neurons in other portions of the hypothalamus (e.g. the periventricular region and the zona incerta) do not. (2) Approximately 30% of the beta-endorphin neurons in the hypothalamus have progesterone receptors. (3) None of the luteinizing hormone-releasing hormone neurons examined have progesterone receptors. (4) Approximately 98% of the cells in the anterior pituitary that have progesterone receptors contain luteinizing hormone. Lactotrophs do not contain progesterone receptors. Many progestin targets in the brain remain to be characterized chemically. The implications for progesterone-inducible genes and neuroendocrine control systems are discussed.