Editing Hyperglycemia (section)

===Endocrine===
Chronic, persistent hyperglycaemia is most often a result of [[diabetes]].{{Citation needed|date=November 2020}} Several hormones act to increase blood glucose levels and may thus cause hyperglycaemia when present in excess, including: cortisol, catecholamines, growth hormone, glucagon,<ref>{{cite journal |last1=Umpierrez |first1=Guillermo E. |last2=Pasquel |first2=Francisco J. |date=April 2017 |title=Management of Inpatient Hyperglycemia and Diabetes in Older Adults |journal=Diabetes Care |volume=40 |issue=4 |pages=509–517 |issn=0149-5992 |pmid=28325798 |doi=10.2337/dc16-0989 |pmc=5864102}}</ref> and [[thyroid hormones]].<ref name=":0">{{cite journal |last1=Hage |first1=Mirella |last2=Zantout |first2=Mira S. |last3=Azar |first3=Sami T. |date=2011-07-12 |title=Thyroid Disorders and Diabetes Mellitus |journal=Journal of Thyroid Research |volume=2011 |page=439463 |issn=2042-0072 |pmid=21785689 |doi=10.4061/2011/439463 |doi-access=free |pmc=3139205}}</ref> Hyperglycaemia may thus be seen in: [[Cushing's syndrome]],<ref>{{cite journal |last1=Scaroni |first1=Carla |last2=Zilio |first2=Marialuisa |last3=Foti |first3=Michelangelo |last4=Boscaro |first4=Marco |date=2017-06-01 |title=Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management |journal=Endocrine Reviews |language=en |volume=38 |issue=3 |pages=189–219 |issn=0163-769X |pmid=28368467 |doi=10.1210/er.2016-1105 |doi-access=free |s2cid=3985558}}</ref> [[pheochromocytoma]],<ref>{{citation |last1=Mubarik |first1=Ateeq |title=Chromaffin Cell Cancer |date=2020 |work=StatPearls |place=Treasure Island (FL) |publisher=StatPearls Publishing |last2=Aeddula |first2=Narothama R. |pmid=30570981 |url=http://www.ncbi.nlm.nih.gov/books/NBK535360/ |access-date=2020-11-22 |url-status=live |archive-url=https://web.archive.org/web/20220126212649/https://www.ncbi.nlm.nih.gov/books/NBK535360/ |archive-date=2022-01-26}}</ref> [[acromegaly]],<ref>{{cite book |title=Oxford desk reference. Endocrinology |others=Turner, Helen E., 1967-, Eastell, R. (Richard), Grossman, Ashley |year=2018 |isbn=978-0-19-967283-7 |edition=First |publisher=Oxford University Press |oclc=1016052167 |url=https://www.worldcat.org/oclc/1016052167}}</ref> [[hyperglucagonemia]],<ref>{{cite journal |last1=Wewer Albrechtsen |first1=Nicolai J. |last2=Kuhre |first2=Rune E. |last3=Pedersen |first3=Jens |last4=Knop |first4=Filip K. |last5=Holst |first5=Jens J. |date=November 2016 |title=The biology of glucagon and the consequences of hyperglucagonemia |journal=Biomarkers in Medicine |volume=10 |issue=11 |pages=1141–1151 |issn=1752-0371 |pmid=27611762 |doi=10.2217/bmm-2016-0090 |doi-access=free}}</ref> and [[hyperthyroidism]].<ref name=":0"/>

====Diabetes mellitus====
Chronic hyperglycemia that persists even in fasting states is most commonly caused by [[diabetes mellitus]]. In fact, chronic hyperglycemia is the defining characteristic of the disease. Intermittent hyperglycemia may be present in prediabetic states. Acute episodes of hyperglycemia without an obvious cause may indicate developing diabetes or a predisposition to the disorder.{{Citation needed|date=November 2020}}

In diabetes mellitus, hyperglycemia is usually caused by low [[insulin]] levels ([[diabetes mellitus type 1]]) and/or by resistance to insulin at the cellular level ([[diabetes mellitus type 2]]), depending on the type and state of the disease.<ref>{{cite web |title=Hyperglycemia in diabetes |publisher=Mayo Clinic |url=https://www.mayoclinic.org/diseases-conditions/hyperglycemia/symptoms-causes/syc-20373631 |access-date=22 Sep 2020 |url-status=live |archive-url=https://web.archive.org/web/20220126212703/https://www.mayoclinic.org/diseases-conditions/hyperglycemia/symptoms-causes/syc-20373631 |archive-date=26 January 2022}}</ref> Low insulin levels and/or [[insulin resistance]] prevent the body from converting glucose into [[glycogen]] (a starch-like source of energy stored mostly in the liver), which in turn makes it difficult or impossible to remove excess glucose from the blood. With normal glucose levels, the total amount of glucose in the blood at any given moment is only enough to provide energy to the body for 20–30 minutes, and so glucose levels must be precisely maintained by the body's internal control mechanisms. When the mechanisms fail in a way that allows glucose to rise to abnormal levels, hyperglycemia is the result.{{Citation needed|date=November 2020}}

Ketoacidosis may be the first symptom of immune-mediated diabetes, particularly in children and adolescents. Also, patients with immune-mediated diabetes can change from modest fasting hyperglycemia to severe hyperglycemia and even ketoacidosis as a result of stress or an infection.<ref name="ADA"/>

====Insulin resistance====
Obesity has been contributing to increased [[insulin resistance]] in the global population. Insulin resistance increases hyperglycemia because the body becomes over saturated by glucose. Insulin resistance desensitizes insulin receptors, preventing insulin from lowering blood sugar levels.<ref>{{cite journal |date=2019 |title=Adipose Tissue Insulin Resistance in Youth on the Spectrum From Normal Weight to Obese and From Normal Glucose Tolerance to Impaired Glucose Tolerance to Type 2 Diabetes |journal=Diabetes Care |volume=42 |issue=2 |pages=265–272 |last1=Kim |first1=J. Y. |last2=Bacha |first2=F. |last3=Tfayli |first3=H. |last4=Michaliszyn |first4=S. F. |last5=Yousuf |first5=S. |last6=Arslanian |first6=S. |pmid=30455334 |doi=10.2337/dc18-1178 |pmc=6341282}}</ref>

The leading cause of hyperglycemia in [[type 2 diabetes]] is the failure of insulin to suppress glucose production by [[glycolysis]] and [[gluconeogenesis]] due to insulin resistance.<ref name="pmid30370538">{{cite journal |vauthors=Swe MT, Pongchaidecha A, Chatsudthipong V, Chattipakorn N, Lungkaphin A |title=Molecular signaling mechanisms of renal gluconeogenesis in nondiabetic and diabetic conditions |journal=[[Journal of Cellular Physiology]] |volume=234 |issue=6 |pages=8134–8151 |year=2019 |pmid=30370538 |doi=10.1002/jcp.27598 |s2cid=53097552}}</ref> Insulin normally inhibits glycogenolysis, but fails to do so in a condition of insulin resistance, resulting in increased glucose production.<ref name="pmid31377934">{{cite journal |vauthors=Sargsyan A, Herman MA |title=Regulation of Glucose Production in the Pathogenesis of Type 2 Diabetes |journal=[[Current Diabetes Reports]] |volume=19 |issue=9 |pages=77 |year=2019 |pmid=31377934 |doi=10.1007/s11892-019-1195-5 |pmc=6834297}}</ref> In the liver, [[FOXO6]] normally promotes gluconeogenesis in the fasted state, but insulin blocks Fox06 upon feeding.<ref name="pmid28213398">{{cite journal |vauthors=Lee S, Dong HH |title=FoxO integration of insulin signaling with glucose and lipid metabolism |journal=[[Journal of Endocrinology]] |volume=233 |issue=2 |pages=R67–R79 |year=2017 |pmid=28213398 |doi=10.1530/JOE-17-0002 |pmc=5480241}}</ref> In a condition of insulin resistance insulin fails to block Fox06, resulting in continued gluconeogenesis even upon feeding.<ref name="pmid28213398"/>