Editing Hypoglycemia (section)

==== Inborn errors of metabolism ====
Briefly, [[inborn errors of metabolism]] are a group of rare [[genetic disorder]]s that are associated with the improper breakdown or storage of [[protein]]s, [[carbohydrate]]s, or [[fatty acid]]s.<ref name=":11">{{Cite book |title=StatPearls |vauthors=Jeanmonod R, Asuka E, Jeanmonod D |date=2022 |publisher=StatPearls Publishing |location=Treasure Island (FL) |chapter=Inborn Errors Of Metabolism |pmid=29083820 |access-date=24 January 2022 |chapter-url=http://www.ncbi.nlm.nih.gov/books/NBK459183/ |archive-url=https://web.archive.org/web/20211013135517/https://www.ncbi.nlm.nih.gov/books/NBK459183/ |archive-date=13 October 2021 |url-status=live}}</ref> Inborn errors of metabolism may cause infant hypoglycemia, and much less commonly adult hypoglycemia.<ref name=":11" />

Disorders that are related to the breakdown of glycogen, called [[Glycogen storage disease|''glycogen storage diseases'']], may cause hypoglycemia.<ref name="Jameson_2018" /><ref name=":11" /> Normally, breakdown of glycogen leads to increased glucose levels, particularly in a fasting state.<ref name="Jameson_2018" /> In glycogen storage diseases, however, glycogen cannot be properly broken down, leading to inappropriately decreased glucose levels in a fasting state, and thus hypoglycemia.<ref name="Jameson_2018" /> The glycogen storage diseases associated with hypoglycemia include [[Glycogen storage disease type 0|type 0]], [[Glycogen storage disease type I|type I]], [[Glycogen storage disease type III|type III]], and [[Glycogen storage disease type IV|type IV]], as well as [[Fanconi syndrome]].<ref name="Jameson_2018" />

Some [[Organic acidemia|organic]] and amino acid acidemias, especially those involving the [[Fatty-acid metabolism disorder|oxidation of fatty acids]], can lead to the symptom of intermittent hypoglycemia,<ref name=":14">{{Cite journal |last=Ozand |first=Pinar T. |date=2000 |title=Hypoglycemia in association with various organic and amino acid disorders |url=https://linkinghub.elsevier.com/retrieve/pii/S0146000500800324 |journal=Seminars in Perinatology |language=en |volume=24 |issue=2 |pages=172–193 |doi=10.1053/sp.2000.6367 |pmid=10805172}}</ref><ref>{{Cite journal |last=Baker |first=Joshua J |last2=Burton |first2=Barbara K |date=November 2021 |title=Diagnosis and Clinical Management of Long-chain Fatty-acid Oxidation Disorders: A Review |journal=TouchREVIEWS in Endocrinology |volume=17 |issue=2 |pages=108–111 |doi=10.17925/EE.2021.17.2.108 |issn=2752-5457 |pmc=8676101 |pmid=35118456}}</ref> as for example in [[combined malonic and methylmalonic aciduria]] (CMAMMA),<ref>{{Cite journal |last=NIH Intramural Sequencing Center Group |last2=Sloan |first2=Jennifer L |last3=Johnston |first3=Jennifer J |last4=Manoli |first4=Irini |last5=Chandler |first5=Randy J |last6=Krause |first6=Caitlin |last7=Carrillo-Carrasco |first7=Nuria |last8=Chandrasekaran |first8=Suma D |last9=Sysol |first9=Justin R |last10=O'Brien |first10=Kevin |last11=Hauser |first11=Natalie S |last12=Sapp |first12=Julie C |last13=Dorward |first13=Heidi M |last14=Huizing |first14=Marjan |last15=Barshop |first15=Bruce A |date=2011 |title=Exome sequencing identifies ACSF3 as a cause of combined malonic and methylmalonic aciduria |journal=Nature Genetics |language=en |volume=43 |issue=9 |pages=883–886 |doi=10.1038/ng.908 |issn=1061-4036 |pmc=3163731 |pmid=21841779}}</ref><ref>{{Cite journal |last=Wehbe |first=Zeinab |last2=Behringer |first2=Sidney |last3=Alatibi |first3=Khaled |last4=Watkins |first4=David |last5=Rosenblatt |first5=David |last6=Spiekerkoetter |first6=Ute |last7=Tucci |first7=Sara |date=2019 |title=The emerging role of the mitochondrial fatty-acid synthase (mtFASII) in the regulation of energy metabolism |url=https://linkinghub.elsevier.com/retrieve/pii/S1388198119301349 |journal=Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids |language=en |volume=1864 |issue=11 |pages=1629–1643 |doi=10.1016/j.bbalip.2019.07.012 |pmid=31376476 |s2cid=199404906}}</ref><ref>{{Cite journal |last=Levtova |first=Alina |last2=Waters |first2=Paula J. |last3=Buhas |first3=Daniela |last4=Lévesque |first4=Sébastien |last5=Auray-Blais |first5=Christiane |author-link5=Christiane Auray |last6=Clarke |first6=Joe T.R. |last7=Laframboise |first7=Rachel |last8=Maranda |first8=Bruno |last9=Mitchell |first9=Grant A. |last10=Brunel-Guitton |first10=Catherine |last11=Braverman |first11=Nancy E. |date=2019 |title=Combined malonic and methylmalonic aciduria due to ACSF3 mutations: Benign clinical course in an unselected cohort |url=https://onlinelibrary.wiley.com/doi/10.1002/jimd.12032 |journal=Journal of Inherited Metabolic Disease |language=en |volume=42 |issue=1 |pages=107–116 |doi=10.1002/jimd.12032 |issn=0141-8955 |pmid=30740739 |s2cid=73436689}}</ref> [[propionic acidemia]]<ref name=":15">{{Citation |last=Ozand |first=Pinar T. |title=Disorders of Organic Acid and Amino Acid Metabolism |date=2012 |work=Textbook of Clinical Pediatrics |pages=451–514 |editor-last=Elzouki |editor-first=Abdelaziz Y. |editor-last2=Harfi |editor-first2=Harb A. |editor-last3=Nazer |editor-first3=Hisham M. |editor-last4=Stapleton |editor-first4=F. Bruder |url=http://link.springer.com/10.1007/978-3-642-02202-9_38 |place=Berlin, Heidelberg |publisher=Springer Berlin Heidelberg |language=en |doi=10.1007/978-3-642-02202-9_38 |isbn=978-3-642-02201-2 |last2=Al-Essa |first2=Mohammed }}</ref><ref name=":14" /> or isolated [[methylmalonic acidemia]].<ref name=":15" /><ref name=":14" />