Endocrine (Endocrine)

Publications in this journal

• Article: Beta cell dynamics: beta cell replenishment, beta cell compensation and diabetes

  Cerf ME
  Endocrine 03/2013;
• Article: Fatigue as a window to the brain

  Donald Pfaff
  Endocrine 05/2012; 29(1):181-181.
• Article: Robert M. Carey, Hypertension and Hormone Mechanisms

  David A. Calhoun
  Endocrine 05/2012; 33(2):223-223.
• Article: Prostaglandin F2α-activated protein kinase Cα phosphorylates myristoylated alanine-rich C kinase substrate protein in bovine luteal cells

  Ugur Salli, Fredrick Stormshak
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  ABSTRACT: Prostaglandin F2α (PGF2α)-induced secretion of oxytocin by the bovine corpus luteum involves the phosphorylation of a unique protein kinase C (PKC) substrate, myristoylated alanine-rich C kinase substrate (MARCKS) protein. This study was conducted to determine the specific PKC isoform engaged in phosphorylation of MARCKS protein in bovine luteal cells. In experiment 1, dispersed luteal cells recovered from the corpus luteum on d 8 of the estrous cycle were preincubated with [32P] orthophosphate and then exposed to PGF2α alone or in combination with PKC inhibitors. Autoradiography and densitometry of Western blots revealed that MARCKS protein was phosphorylated by a conventional PKC (cPKC) isoform. Experiment 2 was conducted to identify the specific cPKC isoform that phosphorylates MARCKS protein in luteal cells. Corpora lutea were removed from control and PGF2α-treated heifers on d 8 of the cycle, and PKC isoforms associated with membrane and cytosolic fractions were determined. Treatment with PGF2α increased membrane concentrations of PKCα within 5 min after treatment (p<0.005). Collectively, these data suggest that phosphorylation of MARCKS protein coinciding with oxytocin secretion is mediated by PKCα.
  Endocrine 05/2012; 16(2):83-88.
• Article: Insulin-like growth factor (IGF)-I stimulates IGF-I and type 1 IGF receptor expression in cultured rat granulosa cells

  Marcos D. deMoura, Diran Chamoun, Carol E. Resnick, Eli Y. Adashi
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  ABSTRACT: A growing body of information documents the existence of a complete rat intrafollicular insulin-like growth factor (IGF)-I system replete with a ligand (IGF-I), a receptor (type 1 IGF receptor) IGF binding proteins (4 and 5), and IGFBP-directed endopeptidases (4 and 5). Previous studies have established the ability of IGF-I to promote the elaboration of granulosa cell-derived IGFBP-5 and to suppress the activity of granulosa cell-derived IGFBP-5-directed endopeptidase. It was the purpose of this article to examine the effects of treatment with IGF-I on the other components of the intrafollicular IGF system, i.e., IGF-I itself and the type 1 IGF-receptor. Granulosa cells, obtained by follicular puncture from 25-d-old estrogen-primed rats were cultured in polystyrene tubes for 72 h under serum-free conditions, in the absence or presence of the indicated agents. At the conclusion of each experiment, media were discarded, and RNA was extracted and subjected to an RNase protection assay. Treatment of cultured rat granulosa cells with IGF-I resulted in a significant 1.8-fold increase in the steady-state levels of IGF-I mRNA. No effect was noted on the total cellular DNA content thereby arguing against the possibility that the relative increase in IGF-I transcripts can be ascribed to a possible treatment-induced increase in cell number in culture. The IGF-I effect was apparent (p<0.05) at IGF-I doses as low as 1 ng/mL, minimal additional increments being noted thereafter. Treatment with insulin and des (1–3) IGF-I proved equally effective, producing 2.0- and 2.6-fold increases, respectively, thereby suggesting that the IGF-I effect may be mediated via the type 1 IGF receptor. Treatment with IGF-I also resulted in a significant (p <0.005) increase in type 1 IGF receptor expression (2.3-fold increase), the first significant effect being noted at the 30 ng/mL dose level. Similar results obtained for insulin and des (1–3) IGF-I thereby suggest that the ability of IGF-I to upregulate the expression of its own receptor is probably type 1 IGF receptor-mediated. Taken together, these findings indicate that treatment of estrogen-primed granulosa cells with IGF-I will result in upregulation of the steady-state levels of transcripts corresponding to IGF-I itself and to its type 1 IGF receptor. These observations emphasize the importance of positive autoregulatory phenomena as determinants of the intrafollicular content of IGF-I and its receptor.
  Endocrine 05/2012; 13(1):103-110.
• Article: Inhibition of rat granulosa cell differentiation by overexpression of Gαq

  Rosalba Escamilla-Hernandez, Lynda Little-Ihrig, Anthony J. Zeleznik
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  ABSTRACT: Activation of FSH and LH receptors in undifferentiated granulosa cells (i.e., no prior exposure to FSH) results in comparable induction of progesterone production, but activation of the LH receptor is less effective than FSH in inducing aromatase and the native LH receptor. Because the LH receptor can also activate the Gαq signaling pathway, we investigated whether activation of this pathway could be responsible for these differences. Overexpression of Gαq inhibited FSH induction of both the estradiol and progesterone biosynthetic pathways as well as mRNA levels for cholesterol side-chain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase (3β-HSD), LH receptor (LHr), and P450aromatase (aromatase). This suppression was associated with a reduction (P<0.05) in FSH-stimulated cAMP production. Lower cAMP levels were not due to reduced FSH receptor (FSHr) mRNA levels or reduced levels of Gαs. Phosphodiesterase (PDE) activity and regulator of G-protein signaling 2 (RGS2) mRNA levels were significantly (P<0.05) increased by Gαq, both of which could account for diminished cAMP levels. We conclude that Gαq signaling pathway inhibits both estradiol and progesterone production comparably and thus activation of this pathway does not seem to account for differences between FSH and LH in the regulation of aromatase and the LH receptor. KeywordsGranulosa cells-Gαq signaling-FSH-LH-RGS2
  Endocrine 04/2012; 33(1):21-31.
• Article: Effect of the Pro12Ala polymorphism of the PPARγ2 gene on serum adiponectin changes

  Firoozeh Mousavinasab, Tuula Tähtinen, Jari Jokelainen, Pentti Koskela, Mauno Vanhala, Jorma Oikarinen, Sirkka Keinänen-Kiukaanniemi, Markku Laakso
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  ABSTRACT: The Pro12Ala polymorphism of the peroxisome proliferator-activated receptor gamma 2 (PPARγ2) gene and adiponectin, a protein secreted from adipose tissue, have been associated with insulin sensitivity. The present The Pro12Ala polymorphism of the peroxisome proliferator-activated receptor gamma 2 (PPARγ2) gene and adiponectin, a protein secreted from adipose tissue, have been associated with insulin sensitivity. The present study demonstrates that in Finnish servicemen who were on a high-caloric diet for 6 mo only subjects with the Ala 12 allele study demonstrates that in Finnish servicemen who were on a high-caloric diet for 6 mo only subjects with the Ala 12 allele of PPARγ2 had a significant increase in adiponectin levels with weight loss induced by heavy exercise. This study demonstrates an interaction of PPARγ2 had a significant increase in adiponectin levels with weight loss induced by heavy exercise. This study demonstrates an interaction of genetic and environmental factors in the regulation of serum adiponectin concentrations. of genetic and environmental factors in the regulation of serum adiponectin concentrations.
  Endocrine 04/2012; 27(3):307-309.
• Article: Role of ketoconazole treatment in urinary-free cortisol-to-cortisone and tetrahydrocortisol-to-tetrahydrocortisone ratios in nonectopic cushing’s syndrome

  Pablo Stiefel, José S. García-Morillo, Luis Jimenez, Encarnación Pamies, María Luisa Miranda, Joaquín Carneado, José Villar, Alfonso Leal-Cerro
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  ABSTRACT: We hypothesized that in nonectopic Cushing syndrome there is an insufficient activity of type II (renal) 11β-hydroxysteroid dehydrogenase (11β-HSD2) that is related to cortisol excess, rather than to corticotropin (adrenocorticotropic hormone [ACTH]) levels. We measured plasma ACTH and urinary-free cortisol (UFF), urinary-free cortisone (UFE), tetrahydrocortisol (UTHF), and tetrahydrocortisone (UTHE) in 24-h urine samples of 24 healthy subjects and 15 patients diagnosed with nonectopic Cushing syndrome. Then, in the group of patients, a new 24-h urine sample was collected after treatment with 800 mg daily of ketoconazole. The UFF/UFE and UTHF/UTHE ratios were calculated as an estimation of 11β-HSD2 activity. The patients had an increase in both the UFF/UFE (19.95±10.3 vs 5.78±4.72 nmol/24 h; p<0.0001) and UTHF/UTHE ratios (5.36±5.23 vs 1.39±0.95 nmol/24 h; p<0.001). Both UFF/UFE and UTHF/UTHE ratios decreased after ketoconazole treatment (19.95±10.3 vs 12.2±6.9 nmol/24 h; p<0.005; and 5.36±5.23 vs 1.62 vs 1.21 nmol/24 h; p<0.001, respectively). The control subjects had a significant relationship between UFF and UFE (r=0.70, p<0.0001), and between UTHF and UTHE (r=0.75, p<0.0001) that did not exist in the patient group. After ketoconazole treatment, the decrease in cortisol excretion in the patient group allowed a positive and significant relation between UFF and UFE (r=0.64, p<0.01) and between UTHF and UTHE (r=0.56, p<0.05) to appear. There was not any significant relationship between either UFF/UFE or UTHF/UTHE ratios and plasma levels of ACTH.
  Endocrine 04/2012; 18(3):279-284.
• Article: Identification and functional analysis of mutations in FAD-binding domain of mitochondrial glycerophosphate dehydrogenase in caucasian patients with type 2 diabetes mellitus

  Mònica Gudayol, Josep Vidal, Elena F. Usac, Albert Morales, Marta E. Fabregat, José C. Fernández-Checa, Anna Novials, Ramon Gomis
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  ABSTRACT: Ca2+-responsive mitochondrial FAD-linked glycerophosphate dehydrogenase (mGPDH) is a key component of the pancreatic β-cell glucose-sensing device. The purpose of this study was to examine the association of mutations in the cDNA coding for the FAD-binding domain of mGPDH and to explore the functional consequences of these mutations in vitro. To investigate this association in type 2 diabetes mellitus, we studied a cohort of 168 patients with type 2 diabetes and 179 glucose-tolerant control subjects of Spanish Caucasian origin by single-stranded conformational polymorphism analysis. In vitro site-directed mutagenesis was performed in the mGPDH cDNA sequence to reproduce those mutations that produce amino acid changes in a patient with type 2 diabetes. We detected mutations in the mGPDH FAD-binding domain in a single patient, resulting in a Gly to Arg amino acid change at positions 77, 78, and 81 and a Thr to Pro at position 90. In vitro expression of the mutated constructs in Xenopus oocytes resulted in a significantly lower enzymatic activity than in cells expressing the wild-type form of the enzyme. Our results indicate that although mutations in the mGPDH gene do not appear to have a major role in type 2 diabetes mellitus, the reduction in mGPDH enzymatic activity associated with the newly described mGPDH mutations suggests that they may contribute to the disease in some patients.
  Endocrine 04/2012; 16(1):39-42.
• Article: Stimulation of FSHβ transcription by blockade of endogenous pituitary follistatin production

  Daniel J. Haisenleder, Kevin W. Aylor, Laura L. Burger, Alan C. Dalkin, John C. Marshall
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  ABSTRACT: This study investigated FSHβ transcriptional responses to the suppression of endogenous follistatin (FST) production using FST antisense RNA (FST-AS) expressing adenovirus constructs in female rat pituitary cells in vitro. Adenoviral delivery systems were characterized and optimized using an adenovirus-green fluorescent protein construct, and maximal infection (85–90% of cells) was seen 48 h post adenovirus treatment. A 424 bp fragment, which included the translational start site and exons 1–3 of the rat FST gene, was subcloned in the reverse orientation into an adenovirus vector. Construct efficacy was tested using cultured rat pituitary cells infected with the adenovirus—AS construct. Infection with adenovirus—FST-AS increased FST-AS mRNA expression in a dose-dependent manner, reduced FST protein expression to undetectable levels, and stimulated increases in FSHβ primary transcript and FSH secretion. Treatment with testosterone alone stimulated FSHβ primary transcript and FSH release, and responses were doubled in the presence of adenovirus—FST-AS. These results demonstrate the effectiveness of adenovirus FST-AS in suppressing pituitary FST protein expression and enhancing FSH biological responses at the transcriptional level. Thus, the FST-deficient rat gonadotrope cell is a model that allows for the investigation of factors regulating FSHβ expression, which might otherwise involve the autocrine/paracrine actions of FST.
  Endocrine 04/2012; 29(3):399-404.
• Article: Pancreatic islets from hypothalamic obese rats maintain KATP+ channel-dependent but not-independent pathways on glucose-induced insulin release process

  Sabrina Grassiolli, Maria Lúcia Bonfleur, Dionizia Xavier Scomparin, Paulo Cezar de Freitas Mathias
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  ABSTRACT: One of the main features of obesity is hyperinsulinemia, which is related to insulin oversecretion. Glucose is by far the major physiological stimulator of insulin secretion. Glucose promotes an increase in the ATP/ADP ratio, which inactivates ATP-sensitive K+ channels (K+ ATP) and induces beta cell depolarization with consequent calcium influx. Increased intracellular calcium concentration triggers insulin exocytosis. K+ ATP channel function is important for K+ ATP channel-dependent pathways involved in glucose-stimulated insulin secretion (GSIS). However, K+ ATP channel-independent pathway has been identified and it has been found that this pathway sustains GSIS. Both pathways are critical to better GSIS control. GSIS was studied in pancreatic islets from hyperinsulinemic adult obese rats obtained by monosodium l-glutamate (MSG) neonatal treatment. Islets from MSG-obese rats were more glucose responsive than control ones. Diazoxide, a drug which maintains the K+ ATP channels open without interfering with cell metabolism, blocked GSIS in islets from both groups. High extracellular potassium concentration plus diaz-oxide was used to study an alternative to the K+ ATP channel pathway; in these conditions islets from MSG-obese rats did not respond, while islets from control animals showed enhanced GSIS. Results indicate that MSG-obese rats oversecreted insulin, even though the K+ ATP channel-independent pathway is impaired in their beta cells.
  Endocrine 04/2012; 30(2):191-196.
• Article: Estrogen receptors beta4 and beta5 are full length functionally distinct ERβ isoforms

  Indira Poola, Jessy Abraham, Kate Baldwin, Alecia Saunders, Rakesh Bhatnagar
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  ABSTRACT: We describe here the cloning and functional characterization of two unique ER isoforms, ERβ4 and ERβ5. The full length ERβ4 and ERβ5 were identified by asymmetric PCR using human ovary cDNA, cloning, and sequence analyses. Both receptors share identical sequences with ERβ1 from exon 1 to exon 7. In the place of exon 8, ERβ4 has unique sequences arising from a region downstream of the ERβ gene and upstream of the SYNE2 gene. ERβ5 has sequences arising from retention of the 5′ end of the intron between exon 7 and 8. Both receptors bind promoter sequences on DNA but do not bind estrogen. They translocate to the nucleus and exhibit three to four times higher estrogen-independent transcriptional activity than ERβ1. When co-transfected with ERα, they predominantly form heterodimers and negatively regulate its transcriptional activity. Estrogen-independent transcriptional activity of ERβ5, but not ERβ4, was inhibited by ERα, demonstrating for the first time that ERα regulates ERβ. Tissue-specific expression of ERβ4 and ERβ5, together with their ligand-independent transcriptional properties and ERα modulating activities, could have a number of implications in seemingly unlinked biological processes regulated by estrogen.
  Endocrine 04/2012; 27(3):227-238.
• Article: Short-term effect of bezafibrate on the expression of adiponectin mRNA in the adipose tissues

  Yutaka Mori, Fumiki Oana, Akane Matsuzawa, Satoshi Akahane, Naoko Tajima
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  ABSTRACT: The effect of short-term bezafibrate (BF) administration over time on the expression of adiponectin mRNA in the tissues was examined in Otsuka Long Evans Tokushima Fatty (OLETF) rats. Eight-week-old rats were divided into the high-dose (100 mg/kg) BF group (n=15), the low-dose (10 mg/kg) BF group (n=15), or the control group (n=15) and followed up for 14 d. Triglyceride and free fatty acid levels significantly decreased in a dose-dependent manner in the high-dose BF group. The insulin levels increased with time, although they were significantly lower in the high-dose BF group on d 3 and 7 than the control group. Adiponectin levels significantly increased in the high-dose BF group. On d 14 of BF administration, the levels of VLDL and chylomicron were significantly lower in BF groups, and adiponectin mRNA expression in the white adipose tissue was significantly higher in the high-dose BF group. Findings from this study suggest that in type 2 diabetes with insulin resistance, hypertriglyceridemia is closely linked to adiponectin.
  Endocrine 04/2012; 25(3):247-251.
• Article: Distinct intracellular Ca2+ response to extracellular adenosine triphosphate in pancreatic β-cells in rats and mice

  Yu-Feng Zhao, Ruwei Xu, Maria Hernandez, Yunlong Zhu, Chen Chen
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  ABSTRACT: Extracellular adenosine triphosphate (ATP) has distinct effects on insulin secretion from pancreatic β-cells between rats and mice. Using a confocal microscope, we compared changes between rats and mice in cytosolic free calcium concentration ([Ca2+]c) in pancreatic β-cells stimulated by extracellular ATP. Extracellular ATP (50 µM) induced calcium release from intracellular calcium stores by activating P2Y receptors in both rat and mouse β-cells. The intracellular calcium release stimulated by extracellular ATP is significantly smaller in amplitude and longer in duration in rat β-cells than in mouse. In response to extracellular ATP, rat β-cells activate store-operated calcium entry following intracellular calcium release. This response is lacking in mouse β-cells. Rat and mouse β-cells both responded to 9 mM glucose by increasing [Ca2+]c. This increase, however, was pronounced only in the rat β-cells. In 9 mM glucose, extracellular ATP induced a pro-nounced calcium release above the increased level of [Ca2+]c in rat β-cells. In mouse β-cells, however, extracellular ATP did not exhibit calcium release on top of the increased level of [Ca2+]c in 9 mM glucose. These results demonstrate distinct responses between rat and mouse β-cells to extracellular ATP under the condition of low and high glucose. Considering that extracellular ATP inhibits insulin secretion from mouse β-cells but stimulates insulin secretion from rat β-cells, we suggest that store-operated Ca2+ entry may be related to exocytosis in pancreatic rat β-cells.
  Endocrine 04/2012; 22(3):185-192.
• Article: Chronic daily ethanol and withdrawal

  Dennis D. Rasmussen, Dipak K. Sarkar, James L. Roberts, Andrea C. Gore
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  ABSTRACT: Although ethanol has been repeatedly demonstrated to inhibit the hypothalamo-pituitary-testes axis by multiple mechanisms, plasma testosterone levels can be normal in alcoholics who do not exhibit severely compromised liver function and even increased in some abstinent alcoholics, suggesting that adaptive changes to chronic alcohol abuse may alter these regulatory mechanisms. To address this variability, we have investigated the effects of chronic ethanol and withdrawal on rat testosterone regulation using a well-characterized liquid diet model that we have previously demonstrated to (1) provide daily oral ethanol consumption that produces behaviorally relevant plasma ethanol levels during the active (awake) stage of the photoperiod; (2) establish physical dependence on ethanol; and (3) produce not only hypothalamo-pituitary-adrenal axis, but also behavioral (anxiety-like behavior, response to novelty, sucrose preference) changes consistent with those of actively drinking and subsequently abstinent alcoholics. The results demonstrate that chronic daily episodes of ethanol consumption and withdrawal by male Sprague-Dawley rats decreased (p<0.01) plasma testosterone levels late in the afternoon (by 70% relative to ad libitum-fed controls and 63% relative to pair-fed controls), but not in the morning. During gradual cessation of daily ethanol consumption, morning plasma testosterone levels increased, and this 90–115% (p<0.05) increase was maintained for 3 d after complete cessation of ethanol consumption. Three weeks after cessation of ethanol consumption, plasma testosterone levels were again increased by approx 100% (p<0.01). Plasma luteinizing hormone (LH) concentrations and anterior hypothalamus/preoptic area gonadotropin-releasing hormone (GnRH) mRNA levels were not altered at any of these time points. Thus, chronic daily ethanol consumption and daily withdrawal induced changes in circulating testosterone regulation that (a) were time of day dependent and (b) included adaptive changes persisting long after consumption of ethanol ceased. Accordingly, resolution of changes in testosterone regulation and their potential roles in alcohol abuse and relapse will require evaluating changes throughout the circadian cycle during, shortly after, and long after active alcohol abuse.
  Endocrine 04/2012; 22(2):143-150.
• Article: Site-specific control of rat preadipocyte adipose conversion by ovarian status

  Danièle Lacasa, Esther Garcia Dos Santos, Yves Giudicelli
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  ABSTRACT: The preadipocyte-adipocyte conversion process from two intraabdominal (parametrial and perirenal fat depots) is differently affected by ovarian status in the rat. We have tested the hypothesis that these sitespecific alterations of adipogenesis might be related to changes in the expression of the transcription factors c-myc and CCAAT/enhancer binding proteins (C/EBPα,-β, and-ζ) that regulate proliferation and differentiation. The increased proliferation rates observed in parametrial and perirenal preadipocytes after ovariectomy were not linked to variations in c-myc mRNA levels. Expression of the early marker of adipogenesis, lipoprotein lipase (LPL), remained insensitive to the ovarian status in early differentiated parametrial and perirenal preadipocytes. By contrast, LPL expression increased in early differentiated sc preadipocytes from ovariectomized rats, an, effect that was completely reversed by in vivo estradiol and progesterone treatment. Expression of C/EBPβ protein was unaffected by ovarian status whatever the anatomic origin of the preadipocytes. By contrast, the levels of p42 and p30 isoforms of C/EBPα were specifically decreased in parametrial preadipocytes, an alteration that was completely corrected by in vivo administration of estradiol and progesterone. C/EBPζ, a dominant inhibitor of C/EBPα and β, exhibited a strong site-specific expression since C/EBPζ content was fivefold higher in sc preadipocytes than in deep intraabdominal cells whatever the ovarian status. Furthermore, ovariectomy selectively decreased C/EBPζ levels in sc cells. In conclusion, our study suggests that some of the site-specific effects of ovariecaltered expressions of C/EBPα and ζ, both of which are important transcriptional regulators of fat cell differentiation and metabolism.
  Endocrine 04/2012; 15(1):103-110.
• Article: Effects of cortisol and estradiol on pituitary expression of proopiomelanocortin, prohormone convertase-1, prohormone convertase-2, and glucocorticoid receptor mRNA in fetal sheep

  Alison C. Holloway, Wendy L. Whittle, John R. G. Challis
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  ABSTRACT: We hypothesized that in the late-gestation sheep fetus there is an interaction between the prepartum rise in cortisol and the increase in placental estradiol production that allows expression of key components of the fetal hypothalamic-pituitary-adrenal (HPA) axis. Therefore, the goal of this study was to investigate the effects of cortisol on the fetal HPA axis in the presence and absence of increased placental estradiol production. We obtained fetal plasma samples and pituitary tissue from animals that had received an infusion of either cortisol, cortisol and 4-hydroxyandrostenedione (4OHA, an aromatase inhibitor), saline, or saline+4OHA conrols. Cortisol significantly decreased plasma adrenocorticotropic hormone concentrations, and in the presence of 4OHA reduced pituitary proopiomelanocortin (POMC) mRNA levels in the pars distalis. There was no effect of any treatment on the expression of the key POMC processing enzymes, prohormone convertase-1 or-2 in the fetal pituitary. Converely, levels of glucocorticoid receptor (GR) mRNA in the pituitary were increased with cortisol treatment in the absence of increased estradiol. We suggest that in the late-gestation sheep fetus, cortisol and estradiol have opposite effects on pituitary POMC and GR mRNA expression, and interact to regulate these key components of the fetal HPA axis.
  Endocrine 04/2012; 14(3):343-348.
• Article: Pancreatic β-cells from obese-hyperglycemic mice are characterized by excessive firing of cytoplasmic Ca2+ transients

  Meftun Ahmed, Eva Grapengiesser
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  ABSTRACT: Pancreatic β-cells from obese-hyperglycemic (ob/ob) mice are widely used for studying the mechanisms of insulin release, including its regulation by the cytoplasmic Ca2+ concentration ([Ca2+]i). In this study, we compared changes of [Ca2+]i in single β-cells isolated from ob/ob mice with those from lean mice using dual-wavelength microfluorometry and the indicator fura-2. There were no differences in the frequency, amplitude, and half-width of the slow oscillations induced by glucose. Most β-cells from the obese mice responded to 10 mM caffeine with transformation of the oscillations into sustained elevation of [Ca2+]i, a process counteracted by ryanodine. The β-cells from the obese mice were characterized by ample generation of [Ca2+]i transients, which increased in number in the presence of glucagon. The transients became less frequent when leptin was added at a concentration as low as 1 nM. It is suggested that the excessive firing of [Ca2+]i transients in the ob/ob mice is owing to the absence of leptin and is mediated by activation of the phospholipase C signaling pathway.
  Endocrine 04/2012; 15(1):73-78.
• Article: Dual role of glucocorticoids in suckling-induced prolactin secretion

  Katalin M. Horváth, Zsuzsanna Bánky, Béla E. Tóth, György M. Nagy, Béla Halász
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  ABSTRACT: The exact contribution of corticosteroids to the control of prolactin secretion in lactating rats is poorly understood. Therefore, the present studies were focused on the effect of adrenalectomy and dexamethasone treatment on the suckling-induced prolactin release. Animals were adrenalectomized on the 3rd day of lactation and tested on the 7th day of lactation. In adrenalectomized animals, the suckling stimulus failed to induce the characteristic increase in plasma prolactin levels. Dexamethasone pretreatment (400 µg/kg b.w. s.c. 24, 48, 72 h before testing) of adrenalectomized rats restored this prolactin response. The same treatment with dexamethasone given to control animals attenuated the suckling stimulus induced prolactin response. The present findings indicate that corticosteroids are essential for a basic prolactin response of lactating rats.
  Endocrine 04/2012; 15(3):287-290.