Galactan is a polymeric form of galactose found in hemicellulose, and forming the core of the galactans, a class of natural polymeric carbohydrates.[4]
D-Galactose is also known as brain sugar since it is a component of glycoproteins (oligosaccharide-protein compounds) found in nerve tissue.[5]
Etymology
The word galactose was coined by Charles Weissman[6] in the mid-19th century and is derived from Greek γαλακτος, galaktos, (of milk) and the generic chemical suffix for sugars -ose.[7] The etymology is comparable to that of the word lactose in that both contain roots meaning "milk sugar". Lactose is a disaccharide of galactose plus glucose.
Structure and isomerism
Galactose exists in both open-chain and cyclic form. The open-chain form has a carbonyl at the end of the chain.
Four isomers are cyclic, two of them with a pyranose (six-membered) ring, two with a furanose (five-membered) ring. Galactofuranose occurs in bacteria, fungi and protozoa,[8][9] and is recognized by a putative chordate immune lectin intelectin through its exocyclic 1,2-diol. In the cyclic form there are two anomers, named alpha and beta, since the transition from the open-chain form to the cyclic form involves the creation of a new stereocenter at the site of the open-chain carbonyl.[10]
The IR spectra for galactose shows a broad, strong stretch from roughly wavenumber 2500 cm−1 to wavenumber 3700 cm−1.[11]
The Proton NMR spectra for galactose includes peaks at 4.7 ppm (D2O), 4.15 ppm (−CH2OH), 3.75, 3.61, 3.48 and 3.20 ppm (−CH2 of ring), 2.79–1.90 ppm (−OH).[11]
Cyclic forms of galactoseChair conformation of D-galactopyranose
In nature, lactose is found primarily in milk and milk products. Consequently, various food products made with dairy-derived ingredients can contain lactose.[13] Galactose metabolism, which converts galactose into glucose, is carried out by the three principal enzymes in a mechanism known as the Leloir pathway. The enzymes are listed in the order of the metabolic pathway: galactokinase (GALK), galactose-1-phosphate uridyltransferase (GALT), and UDP-galactose-4’-epimerase (GALE).[citation needed]
In human lactation, galactose is required in a 1 to 1 ratio with glucose to enable the mammary glands to synthesize and secrete lactose. In a study where women were fed a diet containing galactose, 69 ± 6% of glucose and 54 ± 4% of galactose in the lactose they produced were derived directly from plasma glucose, while 7 ± 2% of the glucose and 12 ± 2% of the galactose in the lactose, were derived directly from plasma galactose. 25 ± 8% of the glucose and 35 ± 6% of the galactose was synthesized from smaller molecules such as glycerol or acetate in a process referred to in the paper as hexoneogenesis. This suggests that the synthesis of galactose is supplemented by direct uptake and of use of plasma galactose when present.[14]
Metabolism
Metabolism of common monosaccharides and some biochemical reactions of glucose
Galactose metabolism
Glucose is more stable than galactose and is less susceptible to the formation of nonspecific glycoconjugates, molecules with at least one sugar attached to a protein or lipid. Many speculate that it is for this reason that a pathway for rapid conversion from galactose to glucose has been highly conserved among many species.[15]
The main pathway of galactose metabolism is the Leloir pathway; humans and other species, however, have been noted to contain several alternate pathways, such as the De Ley Doudoroff Pathway. The Leloir pathway consists of the latter stage of a two-part process that converts β-D-galactose to UDP-glucose. The initial stage is the conversion of β-D-galactose to α-D-galactose by the enzyme, mutarotase (GALM). The Leloir pathway then carries out the conversion of α-D-galactose to UDP-glucose via three principal enzymes: Galactokinase (GALK) phosphorylates α-D-galactose to galactose-1-phosphate, or Gal-1-P; Galactose-1-phosphate uridyltransferase (GALT) transfers a UMP group from UDP-glucose to Gal-1-P to form UDP-galactose; and finally, UDP galactose-4’-epimerase (GALE) interconverts UDP-galactose and UDP-glucose, thereby completing the pathway.[16]
The above mechanisms for galactose metabolism are necessary because the human body cannot directly convert galactose into energy, and must first go through one of these processes in order to utilize the sugar.[17]
Galactosemia is an inability to properly break down galactose due to a genetically inherited mutation in one of the enzymes in the Leloir pathway. As a result, the consumption of even small quantities is harmful to galactosemics.[18]
Chronic systemic exposure of mice, rats, and Drosophila to D-galactose causes the acceleration of senescence (aging). It has been reported that high dose exposure of D-galactose (120 mg/kg) can cause reduced sperm concentration and sperm motility in rodents and has been extensively used as an aging model when administered subcutaneously.[19][20][21]
Two studies have suggested a possible link between galactose in milk and ovarian cancer.[22][23] Other studies show no correlation, even in the presence of defective galactose metabolism.[24][25] More recently, pooled analysis done by the Harvard School of Public Health showed no specific correlation between lactose-containing foods and ovarian cancer, and showed statistically insignificant increases in risk for consumption of lactose at 30 g/day.[26] More research is necessary to ascertain possible risks.[citation needed]
Some ongoing studies suggest galactose may have a role in treatment of focal segmental glomerulosclerosis (a kidney disease resulting in kidney failure and proteinuria).[27] This effect is likely to be a result of binding of galactose to FSGS factor.[28]
Galactose is a component of the antigens (chemical markers) present on blood cells that distinguish blood type within the ABO blood group system. In O and A antigens, there are two monomers of galactose on the antigens, whereas in the B antigens there are three monomers of galactose.[29]
Galactose in sodium saccharin solution has also been found to cause conditioned flavor avoidance in adult female rats within a laboratory setting when combined with intragastric injections.[31] The reason for this flavor avoidance is still unknown, however it is possible that a decrease in the levels of the enzymes required to convert galactose to glucose in the liver of the rats could be responsible.[31]
History
In 1855, E. O. Erdmann noted that hydrolysis of lactose produced a substance besides glucose.[32][33]
Galactose was first isolated and studied by Louis Pasteur in 1856 and he called it "lactose".[34] In 1860, Berthelot renamed it "galactose" or "glucose lactique".[35][36] In 1894, Emil Fischer and Robert Morrell determined the configuration of galactose.[37]
^Fridovich-Keil JL, Walter JH. "Galactosemia". In Valle D, Beaudet AL, Vogelstein B, Kinzler KW, Antonarakis SE, Ballabio A, Gibson KM, Mitchell G (eds.). The Online Metabolic and Molecular Bases of Inherited Disease. Archived from the original on 2018-06-26. Retrieved 2018-06-25. a 4 b 21 c 22 d 22
^Pourmemar E, Majdi A, Haramshahi M, Talebi M, Karimi P, Sadigh-Eteghad S (January 2017). "Intranasal Cerebrolysin Attenuates Learning and Memory Impairments in D-galactose-Induced Senescence in Mice". Experimental Gerontology. 87 (Pt A): 16–22. doi:10.1016/j.exger.2016.11.011. PMID27894939. S2CID40793896.
^Cui X, Zuo P, Zhang Q, Li X, Hu Y, Long J, Packer L, Liu J (August 2006). "Chronic systemic D-galactose exposure induces memory loss, neurodegeneration, and oxidative damage in mice: protective effects of R-alpha-lipoic acid". Journal of Neuroscience Research. 84 (3): 647–54. doi:10.1002/jnr.20899. PMID16710848. S2CID13641006.
^Cramer DW (November 1989). "Lactase persistence and milk consumption as determinants of ovarian cancer risk". American Journal of Epidemiology. 130 (5): 904–10. doi:10.1093/oxfordjournals.aje.a115423. PMID2510499.
^Cramer DW, Harlow BL, Willett WC, Welch WR, Bell DA, Scully RE, Ng WG, Knapp RC (July 1989). "Galactose consumption and metabolism in relation to the risk of ovarian cancer". Lancet. 2 (8654): 66–71. doi:10.1016/S0140-6736(89)90313-9. PMID2567871. S2CID34304536.
^Fung WL, Risch H, McLaughlin J, Rosen B, Cole D, Vesprini D, Narod SA (July 2003). "The N314D polymorphism of galactose-1-phosphate uridyl transferase does not modify the risk of ovarian cancer". Cancer Epidemiology, Biomarkers & Prevention. 12 (7): 678–80. PMID12869412.
^Genkinger JM, Hunter DJ, Spiegelman D, Anderson KE, Arslan A, Beeson WL, et al. (February 2006). "Dairy products and ovarian cancer: a pooled analysis of 12 cohort studies". Cancer Epidemiology, Biomarkers & Prevention. 15 (2): 364–72. doi:10.1158/1055-9965.EPI-05-0484. PMID16492930.
^Pasteur L (1856). "Note sur le sucre de lait" [Note on milk sugar]. Comptes rendus (in French). 42: 347–351. From page 348: Je propose de le nommer lactose. (I propose to name it lactose.)
