Steroid Levels, Steroid Metabolic
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Amphibolic Nature of Krebs Cycle
Amphibolic nature of Krebs Cycle How what we are is what we eat • In aerobic organisms, the citric acid cycle is an amphibolic pathway, one that serves in both catabolic and anabolic processes. • Since the citric acid does both synthesis (anabolic) and breakdown (catabolic) activities, it is called an amphibolic pathway • The citric acid cycle is amphibolic (i.e it is both anabolic and catabolic in its function). • It is said to be an AMPHIBOLIC pathway, because it functions in both degradative or catabolic and biosynthetic or anabolic reactions (amphi = both) A central metabolic pathway or amphibolic pathway is a set of reactions which permit the interconversion of several metabolites, and represents the end of the catabolism and the beginning of anabolism • The KREBS CYCLE or citric acid cycle is a series of reactions that degrades acetyl CoA to yield carbon dioxide, and energy, which is used to produce NADH, H+ and FADH. • The KREBS CYCLE connects the catabolic pathways that begin with the digestion and degradation of foods in stages 1 and 2 with the oxidation of substrates in stage 3 that generates most of the energy for ATP synthesis. • The citric acid cycle is the final common pathway in the oxidation of fuel molecules. In stage 3 of metabolism, citric acid is a final common catabolic intermediate in the form of acetylCoA. • This is why the citric acid cycle is called a central metabolic pathway. Anaplerosis and Cataplerosis Anaplerosis is a series of enzymatic reactions in which metabolic intermediates enter the citric acid cycle from the cytosol. Cataplerosis is the opposite, a process where intermediates leave the citric acid cycle and enter the cytosol. -
Fructose Metabolism from a Functional
SSE #174 Sports Science Exchange (2017) Vol. 28, No. 174, 1-5 FRUCTOSE METABOLISM FROM A FUNCTIONAL PERSPECTIVE: IMPLICATIONS FOR ATHLETES Luke Tappy, MD | Department of Physiology, Faculty of Biology and Medicine, University of Lausanne, Service of Endocrinology, Diabetes and Metabolism | Lausanne University Hospital, and Cardio-metabolic Center, Broye Hospital | Estavayer-le-lac, Switzerland • Fructose was originally a seasonal natural nutrient, mainly consumed in summer and fall in fruits and vegetables. In the industrial era, it became a permanent constituent of our diet, essentially a constituent of added sugars (sucrose, high-fructose corn syrup). • Fructose cannot be directly metabolized by most cells in our body. It has to be processed first in the gut, liver and kidneys, where it is converted into glucose, lactate and fatty acids. • Too much dietary fructose along with excess energy intake and low physical activity can cause hepatic insulin resistance, hypertriglyceridemia and increased hepatic fat content. GAT11LOGO_GSSI_vert_fc_grn • In exercising athletes, net carbohydrate oxidation increases with glucose ingestion in a dose-dependent manner until a plateau is reached at about 1g/min. The addition of fructose to glucose drinks can further increase carbohydrate oxidation. • During exercise, substantial amounts of fructose can be converted into lactate in splanchnic organs if available and released in the systemic circulation to be oxidized in contracting muscles. This “reverse fructose-lactate Cori cycle” provides additional energy substrate to muscle during exercise. • Conversion of fructose into glucose and lactate in splanchnic organs is associated with enhanced splanchnic energy expenditure, while muscle energy efficiency is minimally altered. • During recovery after exercise, glucose and fructose mutually enhance their gut absorption and their storage as glycogen in the liver. -
• Glycolysis • Gluconeogenesis • Glycogen Synthesis
Carbohydrate Metabolism! Wichit Suthammarak – Department of Biochemistry, Faculty of Medicine Siriraj Hospital – Aug 1st and 4th, 2014! • Glycolysis • Gluconeogenesis • Glycogen synthesis • Glycogenolysis • Pentose phosphate pathway • Metabolism of other hexoses Carbohydrate Digestion! Digestive enzymes! Polysaccharides/complex carbohydrates Salivary glands Amylase Pancreas Oligosaccharides/dextrins Dextrinase Membrane-bound Microvilli Brush border Maltose Sucrose Lactose Maltase Sucrase Lactase ‘Disaccharidase’ 2 glucose 1 glucose 1 glucose 1 fructose 1 galactose Lactose Intolerance! Cause & Pathophysiology! Normal lactose digestion Lactose intolerance Lactose Lactose Lactose Glucose Small Intestine Lactase lactase X Galactose Bacteria 1 glucose Large Fermentation 1 galactose Intestine gases, organic acid, Normal stools osmotically Lactase deficiency! active molecules • Primary lactase deficiency: อาการ! genetic defect, การสราง lactase ลด ลงเมออายมากขน, พบมากทสด! ปวดทอง, ถายเหลว, คลนไสอาเจยนภาย • Secondary lactase deficiency: หลงจากรบประทานอาหารทม lactose acquired/transient เชน small bowel เปนปรมาณมาก เชนนม! injury, gastroenteritis, inflammatory bowel disease! Absorption of Hexoses! Site: duodenum! Intestinal lumen Enterocytes Membrane Transporter! Blood SGLT1: sodium-glucose transporter Na+" Na+" •! Presents at the apical membrane ! of enterocytes! SGLT1 Glucose" Glucose" •! Co-transports Na+ and glucose/! Galactose" Galactose" galactose! GLUT2 Fructose" Fructose" GLUT5 GLUT5 •! Transports fructose from the ! intestinal lumen into enterocytes! -
Inhibition of Fructolytic Enzymes in Boar Spermatozoa by (S)-A-Chlorohydrin and L-Chloro-3-Hydroxypropanone
Aust. J. BioI. Sci., 1986, 39, 395-406 Inhibition of Fructolytic Enzymes in Boar Spermatozoa by (S)-a-Chlorohydrin and l-Chloro-3-hydroxypropanone A. R. Jones, W. A. Bubb, S. R. Murdoch, and D. A. Stevenson Department of Biochemistry, The University of Sydney, New South Wales 2006. Abstract When boar spermatozoa were incubated with the (S)-isomer of the male antifertility agent a-chlorohydrin the activity of glyceraldehyde-3-phosphate dehydrogenase was inhibited. The (R)-isomer had no significant effect on the activity of this enzyme whereas (R,S)-3-chlorolactaldehyde caused an inhibition of its activity and also in that of lactate dehydrogenase. The in vitro production of (S)-3-chlorolactaldehyde, the active metabolite of (S)-a-chlorohydrin, was attempted by incubating boar spermatozoa with l-chloro-3- hydroxypropanone. Preliminary results lead us to propose that this compound is converted into (S)-3- chlorolactaldehyde as well as to another metabolite which is an inhibitor of other enzymes within the fructolytic pathway. Introduction Of the many non-steroidal chemicals which are known to elicit an antifertility response in the male (Jackson 1966), only one compound has most of the attributes of an ideal male contraceptive. This compound, (S)-a-chlorohydrin [(S)-3-chloro propan-l,2-diol, I (Fig. 1)], affects the metabolic activity of mature spermatozoa by inhibiting the activity of the glycolytic or fructolytic enzyme glyceraldehyde- 3-phosphate dehydrogenase (Ee 1.2.1.12) thereby causing a decrease in the fructolytic flux. This limits the capability of the spermatozoa to synthesize ATP so that when CHpH I c=o I CH2C1 III Fig. -
Energy Metabolism: Gluconeogenesis and Oxidative Phosphorylation
International Journal for Innovation Education and Research www.ijier.net Vol:-8 No-09, 2020 Energy metabolism: gluconeogenesis and oxidative phosphorylation Luis Henrique Almeida Castro ([email protected]) PhD in the Health Sciences Graduate Program, Federal University of Grande Dourados Dourados, Mato Grosso do Sul – Brazil. Leandro Rachel Arguello Dom Bosco Catholic University Campo Grande, Mato Grosso do Sul – Brazil. Nelson Thiago Andrade Ferreira Motion Science Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. Geanlucas Mendes Monteiro Heath and Development in West Central Region Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. Jessica Alves Ribeiro Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. Juliana Vicente de Souza Motion Science Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. Sarita Baltuilhe dos Santos Motion Science Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. Fernanda Viana de Carvalho Moreto MSc., Nutrition, Food and Health Graduate Program, Federal University of Grande Dourados Dourados, Mato Grosso do Sul – Brazil. Ygor Thiago Cerqueira de Paula Motion Science Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. International Educative Research Foundation and Publisher © 2020 pg. 359 International Journal for Innovation Education and Research ISSN 2411-2933 September 2020 Vanessa de Souza Ferraz Motion Science Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. Tayla Borges Lino Motion Science Graduate Program, Federal University of Mato Grosso do Sul Campo Grande, Mato Grosso do Sul – Brazil. -
Detection of Estrogen Receptor Endocrine Disruptor Potency of Commonly Used Organochlorine Pesticides Using the LUMI-CELL ER Bioassay
DEVELOPMENTAL AND REPRODUCTIVE TOXICITY Detection of Estrogen Receptor Endocrine Disruptor Potency of Commonly Used Organochlorine Pesticides Using The LUMI-CELL ER Bioassay John D. Gordon1, Andrew C: Chu1, Michael D. Chu2, Michael S. Denison3, George C. Clark1 1Xenobiotic Detection Systems, Inc., 1601 E. Geer St., Suite S, Durham, NC 27704, USA 2Alta Analytical Perspectives, 2714 Exchange Drive, Wilmington, NC 28405, USA 3Dept. of Environmental Toxicology, Meyer Hall, Univ. of California, Davis; Davis, CA 95616 USA Introduction Organochlorine pesticides are found in many ecosystems worldwide as result of agricultural and industrial activities and exist as complex mixtures. The use of these organochlorine pesticides has resulted in the contamination of lakes and streams, and eventually the animal and human food chain. Many of these pesticides, such as pp ’-DDT, pp ’-DDE, Kepone, Vinclozolin, and Methoxychlor (a substitute for the banned DDT), have been described as putative estrogenic endocrine disruptors, and act by mimicking endogenous estrogen 1-3 . Estrogenic compounds can have a significant detrimental effect on the endocrine and reproductive systems of both human and other animal populations 4 . Previous studies have shown a strong association between several EDCs (17p-Estradiol, DES, Zeralanol, Zeralenone, Coumestrol, Genistein, Biochanin A, Diadzein, Naringenin, Tamoxifin) and estrogenic activity via uterotropic assay, cell height, gland number, increased lactoferrin, and a transcriptional activity assay using BG1Luc4E2 cells4 . Some other examples of the effects of these EDCs are: decreased reproductive success and feminization of males in several wildlife species; increased hypospadias along with reductions in sperm counts in men; increase in the incidence of human breast and prostate cancers; and endometriosis 3-5 . -
Endocrine Disruptors
Endocrine disruptors Afke Groen & Christine Neuhold The RECIPES project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 824665 Authors Afke Groen, Maastricht University* Christine Neuhold, Maastricht University * currently works at the think tank Mr. Hans van Mierlo Stichting With thanks to our two anonymous interviewees Manuscript completed in April 2020 Document title WP2 Case study: Endocrine disruptors Work Package WP2 Document Type Deliverable Date 13 April 2020 Document Status Final version Acknowledgments & Disclaimer This project has received funding from the European Union’s Horizon 2020 research and innovation programme under grant agreement No 824665. Neither the European Commission nor any person acting on behalf of the Commission is responsible for the use which might be made of the following information. The views expressed in this publication are the sole responsibility of the author and do not necessarily reflect the views of the European Commission. Reproduction and translation for non-commercial purposes are authorised, provided the source is acknowledged and the publisher is given prior notice and sent a copy. WP2 Case study: Endocrine disruptors i Abstract Endocrine disrupting chemicals (EDCs) are at the centre stage of a scientific and regulatory controversy. Given the complexities, ambiguities and particularly the uncertainties surrounding the hazards of EDCs, the precautionary principle is of utmost relevance to the case. Even the definition of EDCs remains much contested, as do the scientific processes and methods through which to identify them. On the one hand, there is considerable societal pressure to regulate ECDs ‘now’. On the other hand, this quick regulation is often impossible as the limited evidence available does not suffice in the context of traditional EU scientific risk assessment. -
Development of in Vivo Flux Analysis of Hepatic Glucose Production in Type 2 Diabetes
Gluconeogenesis as a System: Development of in vivo Flux Analysis of Hepatic Glucose Production in Type 2 Diabetes By José Orlando Alemán B.S. Chemical Engineering Cornell University, 2001 SUBMITTED TO THE HARVARD-MIT DIVISION OF HEALTH SCIENCES AND TECHNOLOGY IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF DOCTOR OF PHILOSOPHY IN MEDICAL ENGINEERING AT THE MASSACHUSETTS INSTITUTE OF TECHNOLOGY February 2008 © 2008 Massachusetts Institute of Technology All rights reserved Signature of Author_________________________________________________________ Harvard-MIT Division of Health Sciences and Technology September 24, 2007 Certified by________________________________________________________________ Gregory Stephanopoulos, PhD Willard Henry Dow Professor of Chemical Engineering and Biotechnology Massachusetts Institute of Technology Thesis Supervisor Accepted by_______________________________________________________________ Martha L. Gray, Ph.D. Edward Hood Taplin Professor of Medical and Electrical Engineering Co-Director, Harvard-MIT Division of Health Sciences and Technology Gluconeogenesis as a System: Development of in vivo Flux Analysis of Hepatic Glucose Production in Type 2 Diabetes by José O. Alemán Submitted to the Division of Health Sciences and Technology on September 24, 2007 in partial fulfillment of the requirements for the degree of Doctor of Philosophy in Medical Engineering ABSTRACT Metabolic diseases are an increasing health concern in the developed world. Type 2 Diabetes, (T2D) affects over 100 million people worldwide and significantly contributes to chronic diseases such as atherosclerosis and kidney failure. This condition is characterized by deregulation of glucose homeostasis through the development of insulin resistance, manifested as increased glucose production in the liver. Hepatic gluconeogenesis provides de novo formation of glucose from three- carbon precursors such as glycerol, lactate, pyruvate and alanine. The upregulation of this pathway underlies the persistent hyperglycemia observed in diabetic patients. -
ORGANIZING and COMPUTING METABOLIC PATHWAY DATA in TERMS of BINARY RELATIONS 1 Introduction
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Fermentation and Cellular Respiration 1. Define: Glycolysis – Glycolysis Is
Fermentation and Cellular Respiration 1. Define: Glycolysis – Glycolysis is a metabolic pathway allowing for the partial catabolism of glucose. During glycolysis, each glucose molecule is split into two pyruvic acid molecules with the associated production of two molecules of ATP and the reduction of two molecules of NAD to form NADH + H+ (also known as the Embden-Meyerhof-Parnas pathway). Fermentation – Fermentation is the anaerobic decomposition of organic compounds (especially carbohydrates) that involves an organic compound (usually) as the final electron acceptor. For those examples used in class, pyruvic acid serves as the final electron acceptor, but some organisms use other compounds. Heterofermentative – The term heterofermentative applies to organisms that produce a variety of end products (more than one) as the result of their fermentation activities. For example, Saccharomyces cerevisiae produces both ethanol and CO2 during its fermentation activities, so is heterofermentative. Krebs cycle – The Krebs cycle, also known as the tricarboxylic acid (TCA) cycle or citric acid cycle, is a cyclic series of chemical reactions that plays a central role in metabolism. When functioning catabolically, it involves the decarboxylation of organic acids (isocitric acid and a-ketoglutaric acid). The carboxyl groups removed form carbon dioxide, a waste gas. Most of the energy released during the cycle is captured in the form of reduced + coenzymes (NADH + H and FADH2). A small amount of energy is captured in the form of GTP or ATP. When functioning anabolically, the TCA cycle provides precursors for various biosynthetic pathways. In eukaryotic cells, the enzymes involved in this cycle are found in the matrix of mitochondria, while in prokaryotic cells they are found in the cytoplasm. -
EPA Method 525.2
METHOD 525.2 DETERMINATION OF ORGANIC COMPOUNDS IN DRINKING WATER BY LIQUID-SOLID EXTRACTION AND CAPILLARY COLUMN GAS CHROMATOGRAPHY/MASS SPECTROMETRY Revision 2.0 J.W. Eichelberger, T.D. Behymer, W.L. Budde - Method 525, Revision 1.0, 2.0, 2.1 (1988) J.W. Eichelberger, T.D. Behymer, and W.L. Budde - Method 525.1 Revision 2.2 (July 1991) J.W. Eichelberger, J.W. Munch, and J.A. Shoemaker Method 525.2 Revision 1.0 (February, 1994) J.W. Munch - Method 525.2, Revision 2.0 (1995) NATIONAL EXPOSURE RESEARCH LABORATORY OFFICE OF RESEARCH AND DEVELOPMENT U.S. ENVIRONMENTAL PROTECTION AGENCY CINCINNATI, OHIO 45268 525.2-1 METHOD 525.2 DETERMINATION OF ORGANIC COMPOUNDS IN DRINKING WATER BY LIQUID-SOLID EXTRACTION AND CAPILLARY COLUMN GAS CHROMATOGRAPHY/MASS SPECTROMETRY 1.0 SCOPE AND APPLICATION 1.1 This is a general purpose method that provides procedures for determination of organic compounds in finished drinking water, source water, or drinking water in any treatment stage. The method is applicable to a wide range of organic compounds that are efficiently partitioned from the water sample onto a C18 organic phase chemically bonded to a solid matrix in a disk or cartridge, and sufficiently volatile and thermally stable for gas chromatog-raphy. Single-laboratory accuracy and precision data have been determined with two instrument systems using both disks and cartridges for most of the following compounds: Chemical Abstract Services Analyte MW1 Registry Number Acenaphthylene 152 208-96-8 Alachlor 269 15972-60-8 Aldrin 362 309-00-2 Ametryn 227 -
Production of Butyric Acid and Hydrogen by Metabolically Engineered Mutants of Clostridium Tyrobutyricum
PRODUCTION OF BUTYRIC ACID AND HYDROGEN BY METABOLICALLY ENGINEERED MUTANTS OF CLOSTRIDIUM TYROBUTYRICUM DISSERTATION Presented in Partial Fulfillment of the Requirements for the Degree Doctor of Philosophy in the Graduate School of The Ohio State University By Xiaoguang Liu, M.S. ***** The Ohio State University 2005 Dissertation committee: Approved by Professor Shang-Tian Yang, Adviser Professor Barbara E Wyslouzil Adviser Professor Hua Wang Department of Chemical Engineering ABSTRACT Butyric acid has many applications in chemical, food and pharmaceutical industries. The production of butyric acid by fermentation has become an increasingly attractive alternative to current petroleum-based chemical synthesis. Clostridium tyrobutyricum is an anaerobic bacterium producing butyric acid, acetic acid, hydrogen and carbon dioxide as its main products. Hydrogen, as an energy byproduct, can add value to the fermentation process. The goal of this project was to develop novel bioprocess to produce butyric acid and hydrogen economically by Clostridial mutants. Conventional fermentation technologies for butyric acid and hydrogen production are limited by low reactor productivity, product concentration and yield. In this project, novel engineered mutants of C. tyrobutyricum were created by gene manipulation and cell adaptation. Fermentation process was also optimized using immobilizing cells in the fibrous-bed bioreactor (FBB) to enhance butyric acid and hydrogen production. First, metabolic engineered mutants with knocked-out acetate formation pathway were created and characterized. Gene inactivation technology was used to delete the genes of phosphotransacetylase (PTA) and acetate kinase (AK), two key enzymes in the acetate-producing pathway of C. tyrobutyricum, through homologous recombination. The metabolic engineered mutants were characterized by Southern hybridization, enzyme assay, protein expression and metabolites production.