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Department of Physiology, Medical College of Georgia at Augusta University, Augusta, Georgia, USA
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Department of Physiology, Medical College of Georgia at Augusta University, Augusta, Georgia, USA
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Department of Orthopaedic Surgery, Medical College of Georgia at Augusta University, Augusta, Georgia, USA
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Department of Physiology, Medical College of Georgia at Augusta University, Augusta, Georgia, USA
Department of Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia, USA
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Department of Medicine, Medical College of Georgia at Augusta University, Augusta, Georgia, USA
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-induced experimental Parkinson’s-like disease . Journal of Neuroscience 6332 – 6351 . ( https://doi.org/10.1523/JNEUROSCI.0426-16.2016 ) Almeida M Han L Martin-Millan M Plotkin LI Stewart SA Roberson PK Kousteni S O'Brien CA Bellido T Parfitt
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We investigated the effect of the glucocorticoid receptor (GR) antagonist Org 34850 on fast and delayed inhibition of corticosterone secretion in response to the synthetic glucocorticoid methylprednisolone (MPL). Male rats were implanted with a catheter in the right jugular vein, for blood sampling and MPL administration, and with an s.c. cannula for Org 34850 administration. All experiments were conducted at the diurnal hormonal peak in the late afternoon. Rats were connected to an automated sampling system and blood samples were collected every 5 or 10 min. Org 34850 (10 mg/kg, s.c.) or vehicle (5% mulgofen in saline) was injected at 1630 h; 30 min later, rats received an injection of MPL (500 μg/rat, i.v.) or saline (0.1 ml/rat). We found that an acute administration of MPL rapidly decreased the basal corticosterone secretion and this effect was not prevented by acute pretreatment with Org 34850. However, blockade of GR with Org 34850 prevented delayed inhibition of MPL on corticosterone secretion measured between 4 and 12 h after MPL administration. Our data suggest an involvement of GR in modulating delayed, but not fast, inhibition induced by MPL on basal corticosterone secretion.
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Arginine vasopressin (AVP) and corticotropin-releasing hormone (CRH) have both been implicated in modulating insulin secretion from pancreatic β-cells. In the present study, we investigated the insulin-secreting activities of AVP and CRH in wild-type and AVP VIb receptor knockout mice. Both neuropeptides stimulated insulin secretion from isolated mouse pancreatic islets. The response of islets to CRH was increased fourfold by concomitant incubation with a subthreshold dose of AVP that alone did not stimulate insulin secretion. Activation of the endogenously expressed M3 receptor by the cholinergic agonist carbachol also potentiated CRH-induced insulin secretion, indicating that the phenomenon may be pathway specific (i.e. Ca2 +-phospholipase C) rather than agonist specific. The protein kinase C (PKC) inhibitors Ro-31-8425 and bisindolylmaleimide I attenuated the potentiating effect of AVP on CRH-stimulated insulin secretion and blocked AVP-stimulated insulin secretion. A possible interaction between the PKC and protein kinase A pathways was also investigated. The phorbol ester phorbol myristate acetate (PMA) stimulated insulin secretion, while the addition of both PMA and CRH enhanced insulin secretion over that measured with either PMA or CRH alone. Additionally, no AVP potentiation of CRH-stimulated insulin secretion was observed upon incubation in Ca2 +-free Krebs–Ringer buffer. Taken together, the present study suggests a possible synergism between AVP and CRH to release insulin from pancreatic β-cells that relies at least in part on activation of the PKC signaling pathway and is dependent on extracellular Ca2 +. This is the first example of a possible interplay between the AVP and CRH systems outside of the hypothalamic–pituitary–adrenal axis.
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Estradiol-17β (E2) and progesterone (P4) play critical roles in female reproductive physiology and behavior. Given the sensitivity of females to exogenous sources of these steroids, we examined the presence of E2 and P4 in conspecifics' excretions and the transfer of excreted steroids between conspecifics. We paired individual adult female mice with a stimulus male or female conspecific given daily injections of [3H]E2 or [3H]P4. Following 48 h of direct interaction with the stimulus animal, we measured radioactivity in the uterus, ovaries, muscle, olfactory bulbs, mesencephalon and diencephalon (MC+DC), and cerebral cortex of the untreated female cohabitant. Radioactivity was significantly present in all tissues of female subjects after individual exposure to a stimulus male or female given [3H]E2. In females exposed to males given [3H]P4, radioactivity was significantly present in the uterus, ovaries, and muscle, but not in other tissues. In females exposed to stimulus females given [3H]P4, radioactivity was significantly present in all tissues except the MC+DC. In mice directly administered [3H]steroids, greater radioactivity was found in the urine of females than of males. Among females directly administered [3H]steroids, greater radioactivity was found in urine of those given [3H]P4 than of those given [3H]E2. When females were administered unlabeled E2 before exposure to [3H]E2-treated females, less radioactivity was detected in most tissues than was detected in the tissues of untreated females exposed to [3H]E2-treated females. We suggest that steroid transfer among individuals has implications for the understanding of various forms of pheromonal activity.
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Early postnatal events can predispose to metabolic and endocrine disease in adulthood. In this study, we evaluated the programming effects of a single early postnatal oestradiol injection on insulin sensitivity in adult female rats. We also assessed the expression of genes involved in inflammation and glucose metabolism in skeletal muscle and adipose tissue and analysed circulating inflammation markers as possible mediators of insulin resistance. Neonatal oestradiol exposure reduced insulin sensitivity and increased plasma levels of monocyte chemoattractant protein-1 (MCP-1) and soluble intercellular adhesion molecule-1. In skeletal muscle, oestradiol increased the expression of genes encoding complement component 3 (C3), Mcp-1, retinol binding protein-4 (Rbp4) and transforming growth factor β1 (Tgfβ1). C3 and MCP-1 are both related to insulin resistance, and C3, MCP-1 and TGFβ1 are also involved in inflammation. Expression of genes encoding glucose transporter-4 (Glut 4), carnitine-palmitoyl transferase 1b (Cpt1b), peroxisome proliferator-activated receptor δ (Ppard) and uncoupling protein 3 (Ucp3), which are connected to glucose uptake, lipid oxidation, and energy uncoupling, was down regulated. Expression of several inflammatory genes in skeletal muscle correlated negatively with whole-body insulin sensitivity. In s.c. inguinal adipose tissue, expression of Tgfβ1, Ppard and C3 was decreased, while expression of Rbp4 and Cpt1b was increased. Inguinal adipose tissue weight was increased but adipocyte size was unaltered, suggesting an increased number of adipocytes. We suggest that early neonatal oestrogen exposure may reduce insulin sensitivity by inducing chronic, low-grade systemic and skeletal muscle inflammation and disturbances of glucose and lipid metabolism in skeletal muscle in adulthood.
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The neuropeptide GnRH-I is critical for the regulation of reproduction in all vertebrates. Study of the regulation of GnRH-I in passerine songbirds has been the focus of studies on subjects as diverse as photoperiodism, puberty, stress, nutrition, processing of auditory information, migration, global climate change, and evolutionary biology. Until now, analysis of GnRH-I in songbirds has been limited to measurement of immunoreactive peptide. Measurement of mRNA regulation has been impossible because of lack of knowledge of the GnRH gene sequence, despite many attempts in the last 20 years to identify it. Thus, the relative roles of environmental, social, physiological, and evolutionary influences upon passerine GnRH regulation have remained enigmatic. Here, we report the first cloning of GnRH-I cDNA from a songbird, Taeniopygia guttata, its localization and regulation. Although the homology of its translated precursor polypeptide between chicken GnRH-I precursor polypeptide was only 54%, zebra finch GnRH-I precursor contained an amino acid sequence that can be processed into chicken GnRH-I peptide (pEHWSYGLQPG-amide). In situ hybridization combined with immunocytochemistry showed co-localization of GnRH-I mRNA and immunoreactive peptide in the preoptic area of sexually mature birds. GnRH-I mRNA signal was greatly reduced in sexually immature birds. Ovary mass of female birds was positively correlated with GnRH-I mRNA level in the brain. These data will now permit molecular analysis of the regulation of songbird reproduction by physical, social, and physiological cues, along with fine scale analysis of selection pressures acting upon the reproductive system of songbirds. (244/250).
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We have used a direct, non-immunochemical and highly accurate method to quantify the effects of testosterone and oestrogen on mitotic and apoptotic activity in the young, male rat anterior pituitary in vivo. Surgical gonadectomy resulted in a 3-fold increase in mitotic activity by the fourth post-operative day, which returned gradually to levels seen in intact animals over the subsequent 3–4 weeks. Both a single dose of Sustanon, a mixture of long-acting testosterone esters in arachis oil, and the same dose divided over 7 days (starting 6 days after gonadectomy), initially suppressed mitotic activity to levels seen in intact animals, but was associated after 48–96 h with a wave of increased mitotic activity. The latter was blocked by co-administration of Sustanon with the non-steroidal aromatase inhibitor letrozole and was not seen when the non-aromatisable androgen dihydrotestosterone was substituted for Sustanon. Oestrogen alone in gonadectomised and intact rats produced a marked increase in mitosis as expected. With the exception of a transient increase in response to a single high-dose injection of Sustanon in gonadectomised animals, apoptotic activity was unaffected by all of the above. This study suggests that pituitary mitotic activity is tonically inhibited by gonadal hormone production (at least in the short term) in adult male rats. The study also suggests that supraphysiological testosterone treatment – while unable to reduce anterior pituitary mitotic activity in untreated, intact animals –suppresses the early increase in mitotic activity induced by gonadectomy. Oestrogen, either exogenous or generated locally by aromatisation, stimulates anterior pituitary mitotic activity in a time-dependent manner.
Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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Institut National de la Santé et de la Recherche Médicale U676, Hôpital Robert-Debré, 48 Boulevard Sérurier, F-75019 Paris, France
Department of Physiology and Pharmacology L334, Oregon Health & Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97201-3098, USA
Institut de Physiologie et Biologie Cellulaires, Centre National de la Recherche Scientifique-Unité Mixte de Recherche, 6187 Pôle Biologie Santé, 40 Avenue du Recteur Pineau, 86022 Poitiers, France
Mental Retardation Research Center, University of California, Neurosciences Research Building, 655 Charles Young Drive South, Los Angeles, California 90095-7088, USA
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. Neuroendocrinology 53 45 –51. Loren I , Emson PC, Fahrenkrug J, Bjorklund A, Alumets J, Hakanson R & Sundler F 1979 Distribution of vasoactive intestinal polypeptide in the rat and mouse brain. Neuroscience 4 1953 –1976
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College of Health and Biomedicine, The Florey Institute of Neuroscience and Mental Health, Department of Physiology, Centre for Chronic Disease Prevention and Management, Victoria University, St Albans Campus, PO Box 14428, Melbourne, Victoria 8001, Australia
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Modulation of the endocannabinoid system as an anti-obesity therapeutic is well established; however, the direct effects of cannabinoid receptor 1 (CB1) antagonism on renal function and structure in a model of diet-induced obesity (DIO) are unknown. The aim of this study was to characterise the renal effects of the CB1 antagonist AM251 in a model of DIO. Male Sprague–Dawley rats were fed a low- or high-fat diet (HFD: 40% digestible energy from lipids) for 10 weeks to elicit DIO (n=9). In a different cohort, rats were fed a HFD for 15 weeks. After 9 weeks consuming a HFD, rats were injected daily for 6 weeks with 3 mg/kg AM251 (n=9) or saline via i.p. injection (n=9). After 10 weeks consuming a HFD, CB1 and megalin protein expression were significantly increased in the kidneys of obese rats. Antagonism of CB1 with AM251 significantly reduced weight gain, systolic blood pressure, plasma leptin, and reduced albuminuria and plasma creatinine levels in obese rats. Importantly, there was a significant reduction in tubular cross-section diameter in the obese rats treated with AM251. An improvement in albuminuria was likely due to the reduction in tubular size, reduced leptinaemia and maintenance of megalin expression levels. In obese rats, AM251 did not alter diastolic blood pressure, sodium excretion, creatinine clearance or expression of the fibrotic proteins VEGFA, TGFB1 and collagen IV in the kidney. This study demonstrates that treatment with CB1 antagonist AM251 improves renal outcomes in obese rats.
Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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Novo Nordisk Foundation Center for Basic Metabolic Research, Department of Biomedical Sciences, Wellcome Trust – MRC Institute of Metabolic Science, Department of Neuroscience and Pharmacology, University of Copenhagen, Blegdamsvej 3b, 2200 Copenhagen, Denmark
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The incretin hormones glucagon-like peptide-1 (GLP1) and glucose-dependent insulinotropic polypeptide (GIP) are secreted from intestinal endocrine cells, the so-called L- and K-cells. The cells are derived from a common precursor and are highly related, and co-expression of the two hormones in so-called L/K-cells has been reported. To investigate the relationship between the GLP1- and GIP-producing cells more closely, we generated a transgenic mouse model expressing a fluorescent marker in GIP-positive cells. In combination with a mouse strain with fluorescent GLP1 cells, we were able to estimate the overlap between the two cell types. Furthermore, we used primary cultured intestinal cells and isolated perfused mouse intestine to measure the secretion of GIP and GLP1 in response to different stimuli. Overlapping GLP1 and GIP cells were rare (∼5%). KCl, glucose and forskolin+IBMX increased the secretion of both GLP1 and GIP, whereas bombesin/neuromedin C only stimulated GLP1 secretion. Expression analysis showed high expression of the bombesin 2 receptor in GLP1 positive cells, but no expression in GIP-positive cells. These data indicate both expressional and functional differences between the GLP1-producing ‘L-cell’ and the GIP-producing ‘K-cell’.
