Editing Glucose (section)

===Uptake===
Ingested glucose initially binds to the receptor for sweet taste on the tongue in humans. This complex of the proteins [[T1R2]] and [[T1R3]] makes it possible to identify glucose-containing food sources.<ref name="fca">{{cite web | url=https://foodb.ca/compounds/FDB012530 | title=Showing Compound D-Glucose (FDB012530) - FooDB | access-date=18 March 2024 | archive-date=6 December 2022 | archive-url=https://web.archive.org/web/20221206084746/https://www.foodb.ca/compounds/FDB012530 | url-status=live }}</ref><ref name="Löffler/Petrides 404"/> Glucose mainly comes from food—about {{cvt|300|g}} per day is produced by conversion of food,<ref name="Löffler/Petrides 404">Peter C. Heinrich: ''Löffler/Petrides Biochemie und Pathobiochemie''. Springer-Verlag, 2014, {{ISBN|978-3-642-17972-3}}, p.&nbsp;404.</ref> but it is also synthesized from other metabolites in the body's cells. In humans, the breakdown of glucose-containing polysaccharides happens in part already during [[chewing]] by means of [[amylase]], which is contained in [[saliva]], as well as by [[maltase]], [[lactase]], and [[sucrase]] on the [[brush border]] of the [[small intestine]]. Glucose is a building block of many carbohydrates and can be split off from them using certain enzymes. [[Glucosidases]], a subgroup of the glycosidases, first catalyze the hydrolysis of long-chain glucose-containing polysaccharides, removing terminal glucose. In turn, disaccharides are mostly degraded by specific glycosidases to glucose. The names of the degrading enzymes are often derived from the particular poly- and disaccharide; inter alia, for the degradation of polysaccharide chains there are amylases (named after amylose, a component of starch), cellulases (named after cellulose), chitinases (named after chitin), and more. Furthermore, for the cleavage of disaccharides, there are maltase, lactase, sucrase, [[trehalase]], and others. In humans, about 70 genes are known that code for glycosidases. They have functions in the digestion and degradation of glycogen, [[sphingolipid]]s, [[mucopolysaccharides]], and poly([[Adenosine diphosphate ribose|ADP-ribose]]). Humans do not produce cellulases, chitinases, or trehalases, but the bacteria in the [[gut microbiota]] do.

In order to get into or out of cell membranes of cells and membranes of cell compartments, glucose requires special transport proteins from the [[major facilitator superfamily]]. In the small intestine (more precisely, in the [[jejunum]]),<ref name="Harper 641">Harold A. Harper: ''Medizinische Biochemie'' {{In lang|de}}. Springer-Verlag, 2013, {{ISBN|978-3-662-22150-1}}, p.&nbsp;641.</ref> glucose is taken up into the intestinal [[epithelium]] with the help of [[glucose transporter]]s<ref>{{Cite journal |doi=10.1007/s12551-015-0186-2 |pmc=5425736 |pmid=28510148|year=2016 |last1=Navale |first1=A. M. |title=Glucose transporters: Physiological and pathological roles |journal=Biophysical Reviews |volume=8 |issue=1 |pages=5–9 |last2=Paranjape |first2=A. N. }}</ref> via a [[secondary active transport]] mechanism called sodium ion-glucose [[symport]] via [[sodium/glucose cotransporter 1]] (SGLT1).<ref name="Löffler/Petrides 199" /> Further transfer occurs on the [[basolateral]] side of the intestinal epithelial cells via the glucose transporter [[GLUT2]],<ref name="Löffler/Petrides 199" /> as well uptake into [[hepatocyte|liver cells]], kidney cells, cells of the [[Pancreatic islets|islets of Langerhans]], [[neuron]]s, [[astrocyte]]s, and [[tanycyte]]s.<ref>{{Cite journal|doi=10.1007/s00125-014-3451-1|pmid=25421524|year=2015|last1=Thorens|first1=B.|title=GLUT2, glucose sensing and glucose homeostasis|journal=Diabetologia|volume=58|issue=2|pages=221–32|doi-access=free|url=http://doc.rero.ch/record/331705/files/125_2014_Article_3451.pdf|access-date=18 March 2024|archive-date=2 December 2023|archive-url=https://web.archive.org/web/20231202190651/http://doc.rero.ch/record/331705/files/125_2014_Article_3451.pdf|url-status=live}}</ref> Glucose enters the liver via the [[portal vein]] and is stored there as a cellular glycogen.<ref name="Löffler/Petrides 214" /> In the liver cell, it is [[Phosphorylation|phosphorylated]] by [[glucokinase]] at position 6 to form [[glucose 6-phosphate]], which cannot leave the cell. [[Glucose 6-phosphatase]] can convert glucose 6-phosphate back into glucose exclusively in the liver, so the body can maintain a sufficient blood glucose concentration. In other cells, uptake happens by passive transport through one of the 14 GLUT proteins.<ref name="Löffler/Petrides 199" /> In the other cell types, phosphorylation occurs through a [[hexokinase]], whereupon glucose can no longer diffuse out of the cell.

The glucose transporter [[GLUT1]] is produced by most cell types and is of particular importance for nerve cells and pancreatic [[Beta cell|β-cell]]s.<ref name="Löffler/Petrides 199" /> [[GLUT3]] is highly expressed in nerve cells.<ref name="Löffler/Petrides 199" /> Glucose from the bloodstream is taken up by [[GLUT4]] from [[muscle cell]]s (of the [[skeletal muscle]]<ref>{{Cite journal |doi=10.1016/j.cmet.2007.03.006 |pmid=17403369|year=2007|last1=Huang| first1=S.|title=The GLUT4 glucose transporter|journal=Cell Metabolism|volume=5|issue=4|pages=237–52|last2=Czech|first2=M. P.|doi-access=free}}</ref> and [[heart muscle]]) and [[fat cell]]s.<ref>{{Cite book |pmid=25344989|date=2014| last1=Govers|first1=R.|title=Cellular regulation of glucose uptake by glucose transporter GLUT4|series=Advances in Clinical Chemistry|volume=66|pages=173–240|publisher=Elsevier |doi=10.1016/B978-0-12-801401-1.00006-2|isbn=978-0-12-801401-1}}</ref> [[GLUT14]] is expressed exclusively in [[testicle]]s.<ref>{{cite journal |last1=Wu |first1=Xiaohua |last2=Freeze |first2=Hudson H. |title=GLUT14, a Duplicon of GLUT3, is Specifically Expressed in Testis as Alternative Splice Forms |journal=Genomics |date=December 2002 |volume=80 |issue=6 |pages=553–7 |doi=10.1006/geno.2002.7010 |pmid=12504846}}</ref> Excess glucose is broken down and converted into fatty acids, which are stored as [[triglyceride]]s. In the [[kidney]]s, glucose in the urine is absorbed via SGLT1 and [[SGLT2]] in the apical cell membranes and transmitted via GLUT2 in the basolateral cell membranes.<ref>{{Cite journal |doi=10.1007/s00125-018-4656-5 |pmid=30132032|pmc=6133168|year=2018|last1=Ghezzi|first1=C.|title=Physiology of renal glucose handling via SGLT1, SGLT2, and GLUT2|journal=Diabetologia|volume=61|issue=10|pages=2087–2097|author2=Loo DDF|last3=Wright|first3=E. M.}}</ref> About 90% of kidney glucose reabsorption is via SGLT2 and about 3% via SGLT1.<ref>{{Cite journal |doi=10.1097/MNH.0000000000000152 |pmc=5364028 |pmid=26125647|year=2015 |last1=Poulsen |first1=S. B. |title=Sodium-glucose cotransport |journal=Current Opinion in Nephrology and Hypertension |volume=24 |issue=5 |pages=463–9 |last2=Fenton |first2=R. A. |last3=Rieg |first3=T. }}</ref>