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Daniel L. Marks - One of the best experts on this subject based on the ideXlab platform.
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Hypothalamic Regulation of muscle metabolism
Current Opinion in Clinical Nutrition and Metabolic Care, 2011Co-Authors: Theodore P. Braun, Daniel L. MarksAbstract:The interest in obesity research has produced a large body of data describing the impact of neuronal signaling in the hypothalamus and brainstem on metabolic Regulation in the periphery. Studies have historically focused on central Regulation of metabolism in adipose and hepatic tissue. Recent studies highlight an important role for these same central regulatory centers in the control of muscle metabolism. This review will focus on these new studies, and will highlight the implications of these new data for the study of muscle catabolism in disease states. The balance of anabolism and catabolism in muscle requires activation of the Hypothalamic-pituitary-adrenal axis as well as changes in energy-dependent signaling pathways in the muscle. It is now apparent that the sympathetic nervous system conveys much of this information between key metabolism-regulating nuclei in the hypothalamus and skeletal muscle. Peripheral signals conveying information regarding the metabolic status of the animal appear to alter the function of metabolic centers in the brain that in turn regulate energy partitioning in muscle via a sympathetic relay. Our understanding of how this system is regulated in normal physiological states and in obesity is providing important clues for understanding muscle catabolism in disease.
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Hypothalamic Regulation of muscle metabolism.
Current opinion in clinical nutrition and metabolic care, 2011Co-Authors: Theodore P. Braun, Daniel L. MarksAbstract:PURPOSE OF REVIEW The interest in obesity research has produced a large body of data describing the impact of neuronal signaling in the hypothalamus and brainstem on metabolic Regulation in the periphery. Studies have historically focused on central Regulation of metabolism in adipose and hepatic tissue. Recent studies highlight an important role for these same central regulatory centers in the control of muscle metabolism. This review will focus on these new studies, and will highlight the implications of these new data for the study of muscle catabolism in disease states. RECENT FINDINGS The balance of anabolism and catabolism in muscle requires activation of the Hypothalamic-pituitary-adrenal axis as well as changes in energy-dependent signaling pathways in the muscle. It is now apparent that the sympathetic nervous system conveys much of this information between key metabolism-regulating nuclei in the hypothalamus and skeletal muscle. SUMMARY Peripheral signals conveying information regarding the metabolic status of the animal appear to alter the function of metabolic centers in the brain that in turn regulate energy partitioning in muscle via a sympathetic relay. Our understanding of how this system is regulated in normal physiological states and in obesity is providing important clues for understanding muscle catabolism in disease.
Walton W Dickhoff - One of the best experts on this subject based on the ideXlab platform.
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in vitro thyrotropin releasing activity of corticotropin releasing hormone family peptides in coho salmon oncorhynchus kisutch
General and Comparative Endocrinology, 1998Co-Authors: Donald A Larsen, Penny Swanson, Jon T Dickey, Jean Rivier, Walton W DickhoffAbstract:Abstract Investigations of Hypothalamic Regulation of fish thyrotropin (TSH) secretion and subsequent thyroid activity have been impeded by the lack of a reliable assay for TSH. Using a recently developed radioimmunoassay (RIA) for coho salmon TSH we employed an in vitro pituitary cell culture technique to examine Regulation of TSH secretion by corticotropin-releasing hormone (CRH) family peptides [ovine CRH (oCRH), carp urotensin I (UI), and frog sauvagine (SV)] as well as thyrotropin-releasing hormone (TRH), salmon growth hormone-releasing hormone (sGHRH), and salmon gonadotropin-releasing hormone (sGnRH). At concentrations of 0.01 to 100 nM, TRH, sGHRH, and sGnRH did not stimulate TSH secretion from coho salmon pituitary cells. However, at these same concentrations, both oCRH and SV caused a significant and concentration-dependent increase in TSH secretion; whereas, UI was highly stimulatory at all concentrations tested. In a related experiment we examined the effect of α-helical CRF (9–41) on oCRH-stimulated TSH release by pituitary cells. α-Helical CRF (9–41) is an analogue of CRH that has been shown by others to antagonize the adrenocorticotropic hormone (ACTH)-releasing activity of CRH in goldfish. Preincubation of cells with 1 μM α-helical CRF (9–41) for 4 h caused a significant suppression of the TSH-releasing activity of oCRH at 1.0 and 10 nM concentrations. The results of these experiments demonstrate the potency of a CRH-like peptide in the Hypothalamic Regulation of TSH in fish and reveal similarities in the inhibition of the response of both the thyroid and interrenal axis of fish to α-helical CRF (9–41) .
Jérôme Leprince - One of the best experts on this subject based on the ideXlab platform.
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A potential role for the secretogranin II-derived peptide EM66 in the Hypothalamic Regulation of feeding behaviour
Journal of Neuroendocrinology, 2017Co-Authors: Fatima Trebak, Isabelle Dubuc, Aranud Arabo, Abdelilah Alaoui, Loubna Boukhzar, Julie Maucotel, Marie Picot, Salouan Cherifi, Céline Duparc, Jérôme LeprinceAbstract:EM66 is a conserved 66-amino acid peptide derived from secretogranin II (SgII), a member of the granin protein family. EM66 is widely distributed in secretory granules of endocrine and neuroendocrine cells, as well as in Hypothalamic neurones. Although EM66 is abundant in the hypothalamus, its physiological function remains to be determined. The present study aimed to investigate a possible involvement of EM66 in the Hypothalamic Regulation of feeding behaviour. We show that i.c.v. administration of EM66 induces a drastic dose-dependent inhibition of food intake in mice deprived of food for 18 hours, which is associated with an increase of Hypothalamic pro-opiomelanocortin (POMC) and melanocortin-3 receptor mRNA levels and c-Fos immunoreactivity in the POMC neurones of the arcuate nucleus. By contrast, i.c.v. injection of EM66 does not alter the Hypothalamic expression of neuropeptide Y (NPY), or that of its Y1 and Y5 receptors. A 3-month high-fat diet (HFD) leads to an important decrease of POMC and SgII mRNA levels in the hypothalamus, whereas NPY gene expression is not affected. Finally, we show that a 48 hours of fasting in HFD mice decreases the expression of POMC and SgII mRNA, which is not observed in mice fed a standard chow. Taken together, the present findings support the view that EM66 is a novel anorexigenic neuropeptide regulating Hypothalamic feeding behaviour, at least in part, by activating the POMC neurones of the arcuate nucleus.
T.j. Lam - One of the best experts on this subject based on the ideXlab platform.
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Hypothalamic Regulation of the Pituitary–Thyroid Axis in the TilapiaOreochromis mossambicus
General and comparative endocrinology, 1997Co-Authors: P. Sukumar, A.d. Munro, E.y.m. Mok, S. Subburaju, T.j. LamAbstract:Abstract Electrolytic lesioning of the preoptic area resulted in an increase in plasma thyroxine (T4) and reverse triiodothyronine (rT3) 10 days later; plasma triiodothyronine (T3) levels were not affected, so that there was also a significant decrease in the T3:T4, but not rT3:T4, ratios. No significant changes in T4, T3, or rT3levels were observed in fish with lesions in either the anterior or posterior portions of the lateral tuberal nucleus. The pituitary contents of growth hormone and the two prolactins were not affected by any lesion. This indicates that the preoptic area may play a role in the inhibitory Regulation of the pituitary–thyroid axis inOreochromis mossambicus, presumably by way of effects on thyrotropin secretion.
Pushpa S Kalra - One of the best experts on this subject based on the ideXlab platform.
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Hypothalamic Regulation of Appetite and Obesity
Encyclopedia of Endocrine Diseases, 2004Co-Authors: Satya P Kalra, Pushpa S KalraAbstract:All living organisms require food or energy fuel for growth and maintenance and are endowed with innateness to store excess energy in reserve to meet energy needs when food is scarce. In addition, the fascination with characterizing the elements that either evoke pleasurable indulgence or attenuate appetite dates back to antiquity. Pleasurable indulgence and its adverse consequences on health and well-being have drawn much attention from ancient to modern medicine. However, during recent times, few human diseases have spurred more public interest than obesity and the attendant metabolic syndrome that are now pandemic. Intimately linked with excess energy deposition is metabolic syndrome contributing to the high rate of mortality, attributable to increases in cardiovascular diseases such as stroke and hypertension, on the one hand, and to insulin resistance, dyspilipidemia, and glucose intolerance eventuating in type 2 diabetes, on the other. Chronic energy imbalance is also an etiological contributor to sleep apnea, osteoarthritis, neurodegenerative diseases such as Alzheimer's, infertility, and increased risk for several types of cancer. The escalating medical costs for treating this spectrum of diseases has spurred research to better understand the cellular and molecular bases of the intrinsic expression and termination of appetite and metabolism of the acquired energy fuel. Recent evidence clearly demonstrates that the pathophysiology of obesity is a consequence of subtle and progressive derangements in homeostatic mechanisms due largely to environmental factors that encourage overeating and/or a sedentary lifestyle rather than to predisposing genetic factors.
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interacting appetite regulating pathways in the Hypothalamic Regulation of body weight
Endocrine Reviews, 1999Co-Authors: Satya P Kalra, Michael G Dube, Shuye Pu, B Xu, Tamas L Horvath, Pushpa S KalraAbstract:I. Introduction II. Neuroanatomical Substrate for Appetite Regulation A. Arcuate nucleus B. Ventromedial nucleus and lateral hypothalamus C. Dorsomedial nucleus D. Paraventricular nucleus and perifornical hypothalamus E. Suprachiasmatic nucleus and the timing device F. Overview of the neuroanatomical substrate associated with appetite control III. Orexigenic Signals A. Neuropeptide Y B. Galanin C. Endogenous opioid peptides D. Melanin-concentrating hormone E. Amino acids: glutamate and γ-aminobutyric acid F. Hypocretins/orexins G. Morphological and functional links among orexigenic signals IV. Anorexigenic Signals A. Corticotropin-releasing hormone family of peptides B. Neurotensin C. Glucagon-like peptide-1 D. Melanocortin and agouti protein E. Cocaine and amphetamine-regulated transcript V. Leptin A. An adipocyte signal B. Site of action C. Is leptin a physiological satiety signal? D. Leptin signal transduction and leptin resistance VI. Summary
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interacting appetite regulating pathways in the Hypothalamic Regulation of body weight
Endocrine Reviews, 1999Co-Authors: Satya P Kalra, Michael G Dube, Tamas L Horvath, Pushpa S KalraAbstract:Various aspects of the complex spatio-temporal patterning of Hypothalamic signaling that leads to the development of synchronized nocturnal feeding in the rat are critically examined. Undoubtedly, as depicted in Fig. 7, a distinct ARN in the hypothalamus is involved in the control of nocturnal appetite. At least four basic elements operate within this ARN. These are: 1) A discrete appetite-driving or orexigenic network of NPY, NE, GABA, GAL, EOP, and orexin transduces and releases appetite-stimulating signals. 2) Similarly, anorexigenic signal-producing pathways (e.g., CRH, GLP-1, alpha MSH, and CART) orchestrate neural events for dissipation of appetite and to terminate feeding, possibly by interrupting NPY efflux and action at a postsynaptic level within the hypothalamus. It is possible that some of these may represent the physiologically relevant "off" switches under the influence of GABA alone, or AgrP alone, or in combination with NPY released from the NPY-, GABA-, and AgrP-coproducing neurons. 3) Recent evidence shows that neural elements in the VMN-DMN complex tonically restrain the orexigenic signals during the intermeal interval; the restraint is greatly aided by leptin's action via diminution of orexigenic (NPY) and augmentation of anorexigenic (GLP-1, alpha MSH, and CART) signals. Since interruption of neurotransmission in the VMN resulted in hyperphagia and development of leptin resistance, it seems likely that the VMN is an effector site for the restraint exercised by leptin. The daily rhythms in leptin synthesis and release are temporally dissociable because the onset of daily rise in leptin gene expression in adipocytes precedes that in leptin secretion. Nevertheless, these rhythms are in phase with daily ingestive behavior because the peak in circulating leptin levels occurs during the middle of the feeding period. These observations, coupled with the fact that circulating levels of leptin are directly related to adiposity, pose a new challenge for elucidating the precise role of leptin in daily patterning of feeding in the rat. 4) A neural timing mechanism also operates upstream from the ARN in the daily management of energy homeostasis. Although the precise anatomical boundaries are not clearly defined, this device is likely to be composed of a group of neurons that integrate incoming internal and external information for the timely onset of the drive to eat. Evidently, this network operates independently in primates, but it is entrained to the circadian time keeper in the SCN of rodents. Apart from its role in the onset of drive to eat, the circadian patterns of gene expression of NPY, GAL, and POMC denote independent control of the timing device on the synthesis and availability for release of orexigenic signals. The VMN-DMN-PVN complex is apparently an integrated constituent of the timing mechanism in this context, because lesions in each of these sites result in loss of regulated feeding. The accumulated evidence points to the PVN and surrounding neural sites within this framework as the primary sites of release and action of various orexigenic and anorexigenic signals. A novel finding is the identification of the interconnected wiring of the DMN-mPVN axis that may mediate leptin restraint on NPY-induced feeding. The chemical phenotypes of leptin and NPY target neurons in this axis remain to be identified. These multiple orexigenic and anorexigenic pathways in the Hypothalamic ARN appear to represent redundancy, a characteristic of regulated biological systems to provide a "fail-safe" neural mechanism to meet an organism's constant energy needs for growth and maintenance. Within this formulation, the coexisting orexigenic signals (NPY, NE, GAL, GABA, and AgrP) represent either another level of redundancy or it is possible that these signals operate within the ARN as reinforcing agents to varying degrees under different circumstances. (ABSTRACT TRUNCATED)