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Dexamethasone sodium phosphate ( 0.339 ) Melengestrol acetate ( 0.282 ) 17beta−Trenbolone ( 0.252 ) 17alpha−Estradiol ( 0.24 ) 17alpha−Hydroxyprogesterone ( 0.238 ) Triamcinolone ( 0.233 ) Zearalenone ( 0.216 ) CP−634384 ( 0.21 ) 17alpha−Ethinylestradiol ( 0.203 ) Raloxifene hydrochloride ( 0.203 ) Volinanserin ( 0.2 ) Tiratricol ( 0.197 ) trans−Retinoic acid ( 0.192 ) Chlorpromazine hydrochloride ( 0.191 ) PharmaGSID_47315 ( 0.185 ) Apigenin ( 0.183 ) Diethylstilbestrol ( 0.178 ) 4−Dodecylphenol ( 0.161 ) 2,2',6,6'−Tetrachlorobisphenol A ( 0.156 ) o,p'−DDD ( 0.155 ) Progesterone ( 0.152 ) 4−Hydroxytamoxifen ( 0.151 ) SSR150106 ( 0.149 ) Equilin ( 0.3 ) 3,5,3'−Triiodothyronine ( 0.256 ) 17−Methyltestosterone ( 0.242 ) 17beta−Estradiol ( 0.24 ) 5alpha−Dihydrotestosterone ( 0.235 ) Mifepristone ( 0.218 ) Norethindrone ( 0.214 ) Spironolactone ( 0.204 ) Farglitazar ( 0.203 ) Testosterone propionate ( 0.202 ) meso−Hexestrol ( 0.199 ) Mestranol ( 0.196 ) Estriol ( 0.191 ) 2,2',4,4'−Tetrahydroxybenzophenone ( 0.185 ) 3,3,5,5−Tetraiodothyroacetic acid ( 0.183 ) Norgestrel ( 0.181 ) Cyproterone acetate ( 0.164 ) GSK232420A ( 0.161 ) N−Dodecanoyl−N−methylglycine ( 0.155 ) Pentachloroanisole ( 0.154 ) HPTE ( 0.151 ) Biochanin A ( 0.15 ) Dehydroepiandrosterone ( 0.149 ) PharmaCode_333941 ( 0.148 ) Prednisone ( 0.146 ) Nordihydroguaiaretic acid ( 0.145 ) p,p'−DDD ( 0.144 ) Diphenhydramine hydrochloride ( 0.142 ) Forskolin ( 0.141 ) Perfluorooctanoic acid ( 0.14 ) Oleyl sarcosine ( 0.139 ) Cyclohexylphenylketone ( 0.138 ) Pirinixic acid ( 0.137 ) -
Nutrition 102 – Class 3
Nutrition 102 – Class 3 Angel Woolever, RD, CD 1 Nutrition 102 “Introduction to Human Nutrition” second edition Edited by Michael J. Gibney, Susan A. Lanham-New, Aedin Cassidy, and Hester H. Vorster May be purchased online but is not required for the class. 2 Technical Difficulties Contact: Erin Deichman 574.753.1706 [email protected] 3 Questions You may raise your hand and type your question. All questions will be answered at the end of the webinar to save time. 4 Review from Last Week Vitamins E, K, and C What it is Source Function Requirement Absorption Deficiency Toxicity Non-essential compounds Bioflavonoids: Carnitine, Choline, Inositol, Taurine, and Ubiquinone Phytoceuticals 5 Priorities for Today’s Session B Vitamins What they are Source Function Requirement Absorption Deficiency Toxicity 6 7 What Is Vitamin B1 First B Vitamin to be discovered 8 Vitamin B1 Sources Pork – rich source Potatoes Whole-grain cereals Meat Fish 9 Functions of Vitamin B1 Converts carbohydrates into glucose for energy metabolism Strengthens immune system Improves body’s ability to withstand stressful conditions 10 Thiamine Requirements Groups: RDA (mg/day): Infants 0.4 Children 0.7-1.2 Males 1.5 Females 1 Pregnancy 2 Lactation 2 11 Thiamine Absorption Absorbed in the duodenum and proximal jejunum Alcoholics are especially susceptible to thiamine deficiency Excreted in urine, diuresis, and sweat Little storage of thiamine in the body 12 Barriers to Thiamine Absorption Lost into cooking water Unstable to light Exposure to sunlight Destroyed -
Guidelines on Food Fortification with Micronutrients
GUIDELINES ON FOOD FORTIFICATION FORTIFICATION FOOD ON GUIDELINES Interest in micronutrient malnutrition has increased greatly over the last few MICRONUTRIENTS WITH years. One of the main reasons is the realization that micronutrient malnutrition contributes substantially to the global burden of disease. Furthermore, although micronutrient malnutrition is more frequent and severe in the developing world and among disadvantaged populations, it also represents a public health problem in some industrialized countries. Measures to correct micronutrient deficiencies aim at ensuring consumption of a balanced diet that is adequate in every nutrient. Unfortunately, this is far from being achieved everywhere since it requires universal access to adequate food and appropriate dietary habits. Food fortification has the dual advantage of being able to deliver nutrients to large segments of the population without requiring radical changes in food consumption patterns. Drawing on several recent high quality publications and programme experience on the subject, information on food fortification has been critically analysed and then translated into scientifically sound guidelines for application in the field. The main purpose of these guidelines is to assist countries in the design and implementation of appropriate food fortification programmes. They are intended to be a resource for governments and agencies that are currently implementing or considering food fortification, and a source of information for scientists, technologists and the food industry. The guidelines are written from a nutrition and public health perspective, to provide practical guidance on how food fortification should be implemented, monitored and evaluated. They are primarily intended for nutrition-related public health programme managers, but should also be useful to all those working to control micronutrient malnutrition, including the food industry. -
Dietary Reference Intakes (Dris): Recommended Dietary Allowances and Adequate Intakes, Vitamins Food and Nutrition Board, Institute of Medicine, National Academies
Dietary Reference Intakes (DRIs): Recommended Dietary Allowances and Adequate Intakes, Vitamins Food and Nutrition Board, Institute of Medicine, National Academies Life Stage Vitamin A Vitamin C Vitamin D Vitamin E Vitamin K Thiamin Riboflavin Niacin Vitamin B6 Folate Vitamin B12 Pantothenic Biotin Choline Group (µg/d)a (mg/d) (µg/d)b,c (mg/d) d (µg/d) (mg/d) (mg/d) (mg/d)e (mg/d) (µg/d)f (µg/d) Acid (mg/d) (µg/d) (mg/d)g Infants 0 to 6 mo 400* 40* 10 4* 2.0* 0.2* 0.3* 2* 0.1* 65* 0.4* 1.7* 5* 125* 6 to 12 mo 500* 50* 10 5* 2.5* 0.3* 0.4* 4* 0.3* 80* 0.5* 1.8* 6* 150* Children 1–3 y 300 15 15 6 30* 0.5 0.5 6 0.5 150 0.9 2* 8* 200* 4–8 y 400 25 15 7 55* 0.6 0.6 8 0.6 200 1.2 3* 12* 250* Males 9–13 y 600 45 15 11 60* 0.9 0.9 12 1.0 300 1.8 4* 20* 375* 14–18 y 900 75 15 15 75* 1.2 1.3 16 1.3 400 2.4 5* 25* 550* 19–30 y 900 90 15 15 120* 1.2 1.3 16 1.3 400 2.4 5* 30* 550* 31–50 y 900 90 15 15 120* 1.2 1.3 16 1.3 400 2.4 5* 30* 550* 51–70 y 900 90 15 15 120* 1.2 1.3 16 1.7 400 2.4h 5* 30* 550* > 70 y 900 90 20 15 120* 1.2 1.3 16 1.7 400 2.4h 5* 30* 550* Females 9–13 y 600 45 15 11 60* 0.9 0.9 12 1.0 300 1.8 4* 20* 375* 14–18 y 700 65 15 15 75* 1.0 1.0 14 1.2 400i 2.4 5* 25* 400* 19–30 y 700 75 15 15 90* 1.1 1.1 14 1.3 400i 2.4 5* 30* 425* 31–50 y 700 75 15 15 90* 1.1 1.1 14 1.3 400i 2.4 5* 30* 425* 51–70 y 700 75 15 15 90* 1.1 1.1 14 1.5 400 2.4h 5* 30* 425* > 70 y 700 75 20 15 90* 1.1 1.1 14 1.5 400 2.4h 5* 30* 425* Pregnancy 14–18 y 750 80 15 15 75* 1.4 1.4 18 1.9 600j 2.6 6* 30* 450* 19–30 y 770 85 15 15 90* 1.4 1.4 18 1.9 600j 2.6 6* 30* 450* 31–50 y 770 85 15 15 90* 1.4 1.4 18 1.9 600j 2.6 6* 30* 450* Lactation 14–18 y 1,200 115 15 19 75* 1.4 1.6 17 2.0 500 2.8 7* 35* 550* 19–30 y 1,300 120 15 19 90* 1.4 1.6 17 2.0 500 2.8 7* 35* 550* 31–50 y 1,300 120 15 19 90* 1.4 1.6 17 2.0 500 2.8 7* 35* 550* NOTE: This table (taken from the DRI reports, see www.nap.edu) presents Recommended Dietary Allowances (RDAs) in bold type and Adequate Intakes (AIs) in ordinary type followed by an asterisk (*). -
Biotinidase Deficiency: a Survey of 10 Cases
Arch Dis Child: first published as 10.1136/adc.63.10.1244 on 1 October 1988. Downloaded from Archives of Disease in Childhood, 1988, 63, 1244-1249 Biotinidase deficiency: a survey of 10 cases H J WASTELL,* K BARTLET,t G DALE,* AND A SHEIN *Department of Clinical Biochemistry, Newcastle General Hospital, and tDepartments of Child Health and Clinical Biochemistry, Newcastle University Medical School, Newcastle upon Tyne SUMMARY Ten patients with biotinidase deficiency were studied. Clinical findings at presenta- tion varied with dermatological signs (dermatitis and alopecia), neurological abnormalities (fits, hypotonia, and ataxia), and recurrent infections being the most common features, although none of these occurred in every case. Biochemically the disease is characterised by metabolic acidosis and organic aciduria. Treatment with biotin results in pronounced, rapid, clinical and biochemical improvement, but some patients have residual neurological damage comprising neurosensory hearing loss, visual pathway defects, ataxia, and mental retardation. The cause of this permanent damage remains obscure and it is not clear if the early introduction of treatment will prevent it. Biotin is a cofactor required by acetyl CoA carboxy- a functional biotin deficiency (biotinidase deficiency) lase (ACC) [EC 6.4.1.2], pyruvate carboxylase (PC) caused by failure to recycle endogenous biotin and [EC 6.4.1.1], propionyl CoA carboxylase (PCC) to liberate dietary biotin, or by defective biotinylation copyright. [EC 6.4.1.3] and 3 methylcrotonyl CoA carboxylase of apocarboxylase because of a mutant holocarboxy- (MCC) [EC 6.4.1.4.].' It is covalently attached to lase synthetase that has an increased Km with the apocarboxylases by the epsilon amino group of a respect to biotin. -
Bone Disorder and Reduction of Ascorbic Acid Concentration Induced by Biotin Deficiency in Osteogenic Disorder Rats Unable to Synthesize Ascorbic Acid
J. Clin. Biochem. Nutr., 12, 171-182, 1992 Bone Disorder and Reduction of Ascorbic Acid Concentration Induced by Biotin Deficiency in Osteogenic Disorder Rats Unable to Synthesize Ascorbic Acid Yuji FURUKAWA,1,* Akiko KINOSHITA,1,•õ1 Hiroichi SATOH,1,•õ2 Hiroko KIKUCHI,1, •õ3 Shoko OHKOSHI,1,•õ4 Masaru MAEBASHI,2 Yoshio MAKINO,3 Takao SATO,4 Michiko ITO,1 and Shuichi KIMURA1 1 Laboratory of Nutrition, Department of Food Chemistry, Faculty of Agriculture, Tohoku University, Aoba-ku, Sendai 981, Japan 2 The Second Department of Internal Medicine, School of Medicine, Tohoku University, Aoba-ku, Sendai 980, Japan 3 Makino Dermatology Clinic, Aoba-ku, Sendai 981, Japan 4 Division of Internal Medicine, National Sendai Hospital, Miyagino-ku, Sendai 983, Japan (Received January 13, 1992) Summary The developmental mechanism of the bone disorder in- duced by biotin deficiency was studied in osteogenic disorder rats, animals that have a hereditary defect in ascorbic acid-synthesizing ability. The osteogenic disorder rats fed a biotin-deficient diet containing raw egg white were afflicted with bone abnormality including a hunch in the vertebral column. In the case of biotin deficiency, although the ascorbic acid content in the diet was in excess of the required amount, ascorbic acid levels of the plasma and the organs in the rats were significant lower than those of control rats. This suggests that the bone disorder induced by biotin deficiency in the rats may result from the promotion of ascorbic acid consumption or the impairment of ascorbic acid incorporation in the animal tissues. Key Words: osteogenic disorder rat, biotin deficiency, ascorbic acid, bone disorder, acetyl-CoA carboxylase Biotin serves as an essential cofactor for four carboxylases, namely, acetyl- *To whom correspondence should be addressed . -
DRIDIETARY REFERENCE INTAKES Thiamin, Riboflavin, Niacin, Vitamin
Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline http://www.nap.edu/catalog/6015.html DIETARY REFERENCE INTAKES DRI FOR Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline A Report of the Standing Committee on the Scientific Evaluation of Dietary Reference Intakes and its Panel on Folate, Other B Vitamins, and Choline and Subcommittee on Upper Reference Levels of Nutrients Food and Nutrition Board Institute of Medicine NATIONAL ACADEMY PRESS Washington, D.C. Copyright © National Academy of Sciences. All rights reserved. Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6, Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline http://www.nap.edu/catalog/6015.html NATIONAL ACADEMY PRESS • 2101 Constitution Avenue, N.W. • Washington, DC 20418 NOTICE: The project that is the subject of this report was approved by the Governing Board of the National Research Council, whose members are drawn from the councils of the National Academy of Sciences, the National Academy of Engineering, and the Institute of Medicine. The members of the committee responsible for the report were chosen for their special competences and with regard for appropriate balance. This project was funded by the U.S. Department of Health and Human Services Office of Disease Prevention and Health Promotion, Contract No. 282-96-0033, T01; the National Institutes of Health Office of Nutrition Supplements, Contract No. N01-OD-4-2139, T024, the Centers for Disease Control and Prevention, National Center for Chronic Disease Preven- tion and Health Promotion, Division of Nutrition and Physical Activity; Health Canada; the Institute of Medicine; and the Dietary Reference Intakes Corporate Donors’ Fund. -
Biotin Fact Sheet for Consumers
Biotin Fact Sheet for Consumers What is biotin and what does it do? Biotin is a B-vitamin found in many foods. Biotin helps turn the carbohydrates, fats, and proteins in the food you eat into the energy you need. How much biotin do I need? The amount of biotin you need each day depends on your age. Average daily recommended amounts are listed below in micrograms (mcg). Life Stage Recommended Amount Birth to 6 months 5 mcg Infants 7–12 months 6 mcg Children 1–3 years 8 mcg Children 4–8 years 12 mcg Biotin is naturally present in some Children 9–13 years 20 mcg foods, such as salmon and eggs. Teens 14–18 years 25 mcg Adults 19+ years 30 mcg Pregnant teens and women 30 mcg Breastfeeding teens and women 35 mcg What foods provide biotin? Many foods contain some biotin. You can get recommended amounts of biotin by eating a variety of foods, including the following: • Meat, fish, eggs, and organ meats (such as liver) • Seeds and nuts • Certain vegetables (such as sweet potatoes, spinach, and broccoli) What kinds of biotin dietary supplements are available? Biotin is found in some multivitamin/multimineral supplements, in B-complex supplements, and in supplements containing only biotin. Am I getting enough biotin? Most people get enough biotin from the foods they eat. However, certain groups of people are more likely than others to have trouble getting enough biotin: • People with a rare genetic disorder called “biotinidase deficiency” • People with alcohol dependence • Pregnant and breastfeeding women 2 • BIOTIN FACT SHEET FOR CONSUMERS What happens if I don’t get enough biotin? Biotin and healthful eating Biotin deficiency is very rare in the United States. -
Case Report Biotinidase Deficiency: Early Presentation
Scholars Journal of Applied Medical Sciences (SJAMS) ISSN 2320-6691 (Online) Sch. J. App. Med. Sci., 2016; 4(2D):614-617 ISSN 2347-954X (Print) ©Scholars Academic and Scientific Publisher (An International Publisher for Academic and Scientific Resources) www.saspublisher.com Case Report Biotinidase Deficiency: Early Presentation Saumya Chaturvedi, Jayashree Nadkarni*, Rashmi Randa, Shweta Sharma, Rajesh Tikkas Department of Paediatrics, Gandhi Medical College and Associated Kamla Nehru and Hamidia Hospital, Bhopal (M.P.) India *Corresponding author Dr. Jayashree Nadkarni Email: [email protected] Abstract: A 2 month old male child presented with fever, seizures, metabolic acidosis, alopecia and dermatitis. Diagnosed to be case of biotinidase enzyme deficiency. Identification of this disorder is important as it is easily treatable and the patients show dramatic response to therapy. It can prove fatal if not diagnosed. Keywords: alopecia, dermatitis, biotinidase enzyme deficiency. INTRODUCTION and needed ventilation. He was diagnosed as having Biotinidase recycles the vitamin biotin. meningitis after CSF examination. Biotinidase deficiency is a rare metabolic disorder with autosomal recessive inheritance which can cause On examination, patient was found to have dermatological manifestations and lead to severe loss of eyelashes, excessive hair fall, and multiple neurological sequelae if untreated. The symptoms can episodes of myoclonic jerks, dermatitis and be successfully treated or prevented by administering conjunctivitis which the mother had noticed since pharmacological doses of biotin. Holocarboxylase around 1 month of life. He was treated synthetase deficiency also has similar manifestations symptomatically, followed by anticonvulsant therapy and needs to be differentiated. with phenytoin. Convulsions improved and after two days he was removed from ventilator and put on It was first described by Wolf and colleagues intranasal oxygen. -
Medium Composition Influence on Biotin and Riboflavin Production by Newly Isolated Candida Sp
Brazilian Journal of Microbiology (2011) 42: 1093-1100 ISSN 1517-8382 MEDIUM COMPOSITION INFLUENCE ON BIOTIN AND RIBOFLAVIN PRODUCTION BY NEWLY ISOLATED CANDIDA SP. Gaby Tiemi Suzuki, Juliana Alves Macedo*, Gabriela Alves Macedo Departamento de Ciência de Alimentos, Faculdade de Engenharia de Alimentos, Universidade Estadual de Campinas, Campinas, SP, Brasil. Submitted: October 16, 2009; Returned to authors for corrections: December 10, 2010; Approved: May 16, 2011. ABSTRACT Complex B vitamins as Biotin and Riboflavin are required by living organisms, not only for growth but also for metabolite production, and the feed market classifies them as growth promoters. Since Brazil will soon be one of the world’s biggest animal protein producers, feed production is a large consumer of vitamins and micronutrients. The industry requires 10 mg riboflavin/0.2 mg biotin per kilogram of feed; a ratio of 40 ~ 50:1. Although few studies have been conducted specifically on riboflavin production using factorial design and surface response method as an optimization strategy, it is a common practice in biotechnology with many research reports available. However, there are no reports on the use of statistical design for biotin production. This study set out to evaluate medium composition influence on biotin and riboflavin production using a statistical design. There are no studies relating biotin and riboflavin production by Candida sp LEB 130. In this preliminary study to improve the simultaneous production of biotin and riboflavin, the maximum riboflavin/biotin ratio of 8.3 µg/mL was achieved with medium component concentrations of: sucrose 30 g/L, KH2PO4 2 g/L, MgSO4 1 g/L and ZnSO4 0.5mL/L. -
Human Vitamin and Mineral Requirements
Human Vitamin and Mineral Requirements Report of a joint FAO/WHO expert consultation Bangkok, Thailand Food and Agriculture Organization of the United Nations World Health Organization Food and Nutrition Division FAO Rome The designations employed and the presentation of material in this information product do not imply the expression of any opinion whatsoever on the part of the Food and Agriculture Organization of the United Nations concerning the legal status of any country, territory, city or area or of its authorities, or concern- ing the delimitation of its frontiers or boundaries. All rights reserved. Reproduction and dissemination of material in this information product for educational or other non-commercial purposes are authorized without any prior written permission from the copyright holders provided the source is fully acknowledged. Reproduction of material in this information product for resale or other commercial purposes is prohibited without written permission of the copyright holders. Applications for such permission should be addressed to the Chief, Publishing and Multimedia Service, Information Division, FAO, Viale delle Terme di Caracalla, 00100 Rome, Italy or by e-mail to [email protected] © FAO 2001 FAO/WHO expert consultation on human vitamin and mineral requirements iii Foreword he report of this joint FAO/WHO expert consultation on human vitamin and mineral requirements has been long in coming. The consultation was held in Bangkok in TSeptember 1998, and much of the delay in the publication of the report has been due to controversy related to final agreement about the recommendations for some of the micronutrients. A priori one would not anticipate that an evidence based process and a topic such as this is likely to be controversial. -
Vitamin B2 (Riboflavin)
EXCERPTED FROM: Vitamin and Mineral Safety 3rd Edition (2013) Council for Responsible Nutrition (CRN) www.crnusa.org Vitamin B2 (Riboflavin) Introduction Riboflavin, like thiamin and some other B vitamins, is essential for normal development, growth, reproduction, lactation, physical performance, and well-being. It is involved in a wide array of essential biochemical oxidation-reduction reactions, especially those that yield energy and metabolize carbohydrates, fats, and proteins. Riboflavin is widely distributed in small amounts in many foods, and milk is one important dietary source. Similar to many members of the water- soluble B-complex family of vitamins, riboflavin is easily lost from grains or vegetables during milling, heating, canning, blanching, and storage. Riboflavin is especially sensitive to light. It is readily absorbed in small amounts from the intestine and readily excreted through the kidneys (McCormick 1999). Safety Considerations Riboflavin consumed orally has no reported toxicity (Miller and Hayes 1982; Institute of Medicine [IOM] 1998; Expert Group on Vitamins and Minerals [EVM] 2003). Reports of adverse effects all relate to animal studies or cell culture research involving either drugs with phototoxicity, intense exposure of lens tissue to ultraviolet light, or both in combination with high levels of riboflavin (Floersheim 1994; Spector et al. 1995). There are no reports of adverse reactions that can be attributed to riboflavin consumed orally from foods or dietary supplements. Official Reviews Institute of Medicine (IOM 1998). The IOM found no evidence of adverse effects associated with excess intake of riboflavin from food or supplements, that is, no toxicity data on which to base a LOAEL or a NOAEL.