Phlorizin - CAS 60-81-1
Catalog number: 60-81-1
Category: Inhibitor
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Molecular Formula:
C21H24O10
Molecular Weight:
436.41
COA:
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Targets:
SGLT
Description:
Phlorizin is a 2'-glucoside of phloretin. It belongs to the group of dihydrochalcones, a type of flavonoids.
Purity:
>98%
Synonyms:
Phloridzin
MSDS:
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InChIKey:
IOUVKUPGCMBWBT-QNDFHXLGSA-N
InChI:
InChI=1S/C21H24O10/c22-9-16-18(27)19(28)20(29)21(31-16)30-15-8-12(24)7-14(26)17(15)13(25)6-3-10-1-4-11(23)5-2-10/h1-2,4-5,7-8,16,18-24,26-29H,3,6,9H2/t16-,18-,19+,20-,21-/m1/s1
Canonical SMILES:
C1=CC(=CC=C1CCC(=O)C2=C(C=C(C=C2OC3C(C(C(C(O3)CO)O)O)O)O)O)O
1.Phlorizin Supplementation Attenuates Obesity, Inflammation, and Hyperglycemia in Diet-Induced Obese Mice Fed a High-Fat Diet.
Shin SK1, Cho SJ2,3, Jung UJ4, Ryu R5,6, Choi MS7,8. Nutrients. 2016 Feb 16;8(2). pii: E92. doi: 10.3390/nu8020092.
Obesity, along with its related complications, is a serious health problem worldwide. Many studies reported the anti-diabetic effect of phlorizin, while little is known about its anti-obesity effect. We investigated the beneficial effects of phlorizin on obesity and its complications, including diabetes and inflammation in obese animal. Male C57BL/6J mice were divided into three groups and fed their respective experimental diets for 16 weeks: a normal diet (ND, 5% fat, w/w), high-fat diet (HFD, 20% fat, w/w), or HFD supplemented with phlorizin (PH, 0.02%, w/w). The findings revealed that the PH group had significantly decreased visceral and total white adipose tissue (WAT) weights, and adipocyte size compared to the HFD. Plasma and hepatic lipids profiles also improved in the PH group. The decreased levels of hepatic lipids in PH were associated with decreased activities of enzymes involved in hepatic lipogenesis, cholesterol synthesis and esterification.
2.Bile Diversion in Roux-en-Y Gastric Bypass Modulates Sodium-Dependent Glucose Intestinal Uptake.
Baud G1, Daoudi M2, Hubert T1, Raverdy V1, Pigeyre M1, Hervieux E1, Devienne M1, Ghunaim M1, Bonner C1, Quenon A1, Pigny P3, Klein A4, Kerr-Conte J1, Gmyr V1, Caiazzo R1, Pattou F5. Cell Metab. 2016 Mar 8;23(3):547-53. doi: 10.1016/j.cmet.2016.01.018. Epub 2016 Feb 25.
Gastro-intestinal exclusion by Roux-en-Y gastric bypass (RYGB) improves glucose metabolism, independent of weight loss. Although changes in intestinal bile trafficking have been shown to play a role, the underlying mechanisms are unclear. We performed RYGB in minipigs and showed that the intestinal uptake of ingested glucose is blunted in the bile-deprived alimentary limb (AL). Glucose uptake in the AL was restored by the addition of bile, and this effect was abolished when active glucose intestinal transport was blocked with phlorizin. Sodium-glucose cotransporter 1 remained expressed in the AL, while intraluminal sodium content was markedly decreased. Adding sodium to the AL had the same effect as bile on glucose uptake. It also increased postprandial blood glucose response in conscious minipigs following RYGB. The decrease in intestinal uptake of glucose after RYGB was confirmed in humans. Our results demonstrate that bile diversion affects postprandial glucose metabolism by modulating sodium-glucose intestinal cotransport.
3.SGLT1 activity in lung alveolar cells of diabetic rats modulates airway surface liquid glucose concentration and bacterial proliferation.
Oliveira TL1,2, Candeia-Medeiros N1, Cavalcante-Araújo PM1, Melo IS1, Fávaro-Pípi E3, Fátima LA4, Rocha AA2, Goulart LR5,6, Machado UF4, Campos RR2, Sabino-Silva R7. Sci Rep. 2016 Feb 23;6:21752. doi: 10.1038/srep21752.
High glucose concentration in the airway surface liquid (ASL) is an important feature of diabetes that predisposes to respiratory infections. We investigated the role of alveolar epithelial SGLT1 activity on ASL glucose concentration and bacterial proliferation. Non-diabetic and diabetic rats were intranasally treated with saline, isoproterenol (to increase SGLT1 activity) or phlorizin (to decrease SGLT1 activity); 2 hours later, glucose concentration and bacterial proliferation (methicillin-resistant Sthaphylococcus aureus, MRSA and Pseudomonas aeruginosa, P. aeruginosa) were analyzed in bronchoalveolar lavage (BAL); and alveolar SGLT1 was analyzed by immunohistochemistry. BAL glucose concentration and bacterial proliferation increased in diabetic animals: isoproterenol stimulated SGLT1 migration to luminal membrane, and reduced (50%) the BAL glucose concentration; whereas phlorizin increased the BAL glucose concentration (100%). These regulations were accompanied by parallel changes of in vitro MRSA and P.
4.Phlorizin Supplementation Attenuates Obesity, Inflammation, and Hyperglycemia in Diet-Induced Obese Mice Fed a High-Fat Diet.
Shin SK1, Cho SJ2,3, Jung UJ4, Ryu R5,6, Choi MS7,8. Nutrients. 2016 Feb 16;8(2). pii: E92. doi: 10.3390/nu8020092.
Obesity, along with its related complications, is a serious health problem worldwide. Many studies reported the anti-diabetic effect of phlorizin, while little is known about its anti-obesity effect. We investigated the beneficial effects of phlorizin on obesity and its complications, including diabetes and inflammation in obese animal. Male C57BL/6J mice were divided into three groups and fed their respective experimental diets for 16 weeks: a normal diet (ND, 5% fat, w/w), high-fat diet (HFD, 20% fat, w/w), or HFD supplemented with phlorizin (PH, 0.02%, w/w). The findings revealed that the PH group had significantly decreased visceral and total white adipose tissue (WAT) weights, and adipocyte size compared to the HFD. Plasma and hepatic lipids profiles also improved in the PH group. The decreased levels of hepatic lipids in PH were associated with decreased activities of enzymes involved in hepatic lipogenesis, cholesterol synthesis and esterification.
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CAS 60-81-1 Phlorizin

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