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Antidiabetic Principle in Cucumis sativus L.

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Ibitoye Oluwayemisi Beatrice, Ajiboye Taofeek Olakunle, Abdulazeez Azeemat Titilola, Oyegoke Rukayat Abiodun, Muritala Hamdalat Folake and Abubakar Fatimah Aluko

Submitted: October 21st, 2020 Reviewed: February 3rd, 2021 Published: June 7th, 2021

DOI: 10.5772/intechopen.96393

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Diabetes is one of the leading cause of death globally. One of the strategies towards managing diabetes is the antidiabetic drugs which has recorded a huge success but accompanied with different degrees of side effect, hence, the use of natural plants products is encouraged. Several reports of antidiabetic medicinal plants have flooded literature but few has led to identification of active ingredient in such. Cucumis sativus is one of such plants reported to have antidiabetic property but there is little or no data on the active agent. This chapter therefore provides report on the active principle and mechanism of action underlying the antidiabetic activity of C. sativus.


  • diabetes
  • Cucumis sativus
  • flavonoids
  • kaempferol

1. Introduction

Diabetes is a disorder where the body cells cannot use glucose effectively due to low insulin (Type 1 diabetes) or insulin insensitivity (Type 2 diabetes), therefore the blood glucose level increases [1]. It is characterized by a fasting blood glucose level higher than 126 mg/dL. It is one of the top 10 causes of death globally. About 463 million adults are living with diabetes; by 2045 this will rise to 700 million and Diabetes caused 4.2 million deaths in 2019 [2].

In 2017, total estimated cost of diagnosed diabetes in the U.S. was $327 billion [3].

Some complications of diabetes are oxidative stress, dyslipidaemia, endoplasmic reticulum (ER) stress [4, 5], retinopathy [6], neuropathy [7], nephropathy [8], cardiovascular complications [9], and ulcerations [10].

The management of diabetes has involved many approaches in order to enhance the availability of insulin, boost insulin sensitivity and reduce alpha glucosidase activity [11].

From research, people with excess weight can greatly manage diabetes by engaging in moderate and considerate weight loss plan, also exercise can help control blood sugar levels, reduce glycated hemoglobin and reduce insulin resistance.

Antidiabetic drugs are pharmacological substances that are employed in treating hyperglycemia when life style modifications do not bring desired effects [12]. They are categorized into different classes and they work either to enhance synthesis of insulin or reduce blood glucose level using different strategies. These antidiabetic drugs are very effective in treating hyperglycemia, but despite this success, there has been increased side effects accompanying their use. Therefore, there is increased search for antidiabetic agents from medicinal plants with little or no adverse effects. Experimental reports have validated the presence of antidiabetic substances in medicinal plants [13, 14, 15]. One of such plants reported to have antidiabetic property is Cucumis sativus. Saidu et al.’s study reported the hypoglycemic property of methanolic fruit pulp extract of Cucumis sativus [16].

This chapter focuses on the antidiabetic principle identified in Cucumis sativus L.


2. Flavonoids

Flavonoids are a class of plants secondary metabolites made up of polyphenolic structures that contribute to the color and fragrance of fruits and flowers, therefore, they constitute a significant part of the human diet [17]. As a large class, flavonoids are subdivided into groups based on the structure of their carbon rings and these include flavanols, flavones, chalcones, flavonones, flavanonols and isoflavones. They are abundantly distributed in vegetables, fruits and some beverages. Flavonoids possess a wide range of health-promoting properties like the antioxidant effect, anti-carcinogenic, anti-inflammatory and antidiabetic capabilities. They display these properties by modulating the functions of some cellular enzymes as well as inhibition of different enzymes like lipo-oxygenase, cyclo-oxygenase, phosphoinositide 3-kinase and xanthine oxidase [18, 19]. Therefore, they are indispensable components in various pharmaceutical, cosmetics and medicinal applications. One of the flavonoids that possesses antidiabetic property is kaempferol.


3. Cucumis sativus L.

Cucumis sativus L. also known as Cucumber is a creeping plant in the family Cucurbitaceae. It is a fruit native to India and widely cultivated around the world. It is consumed fresh in salads, fermented (pickles) and as cooked vegetable [20]. Cucumis sativus L. as a fruit, in addition to its nutritional value, has been reported to have some biological activities as anti-aging [21], antioxidant [22], and antidiabetic [23]. These properties have been linked to the presence of some phytochemical substances detected in Cucumis sativus L. like cucurbitacins [24], ascorbic acid [25], cucumerin, apigenin [26], lutein [27], quercetin 3-O-glucoside and kaempferol 3-O-glucoside [28].

Recent studies validated the presence of antidiabetic agents in Cucumis sativus L.

Ibitoye et al [29] identified the antidiabetic agent in Cucumis sativus L. as a flavonoid called kaempferol using HPLC (Figure 1).

Figure 1.

High pressure liquid chromatographic profiling of the antidiabetic principle derived from Cucumis sativus fruit juice.


4. Kaempferol

Kaempferol (3,5,7-trihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one also known as kaempferol-3, Figure 2) is a yellow crystalline flavonoid having a molecular weight of 286.23 with a melting point of 276–278 °C. It is soluble in hot ethanol and slightly soluble in water.

Figure 2.

Structure of Kaempferol.

It has been isolated from different parts of different plants. Yang et al. separated kaempferol and its derivatives from the methanolic crude extract of Neocheiropteris palmatopedata by repeated column chromatography, using a Sephadex LH-20 column [30]. Orhan et al. reported the bioactivity-guided fractionation of Calluna vulgaris and isolated kaempferol galactoside using successive column chromatography techniques [31]. Ibitoye et al. also reported the bioactivity guided isolation of kaempferol from Cucumis sativus L. [26].


5. Biosynthesis of kaempferol

Kaempferol and its derivatives are synthesized in plants by different types of enzymes. Kaempferol is synthesized by condensation of 4-coumaroyl-CoA with tripropionyl-CoA to produce naringenin chalcone, this reaction is catalyzed by chalcone synthase [32]. Naringenin chalcone is then converted into a flavanone called naringenin, which is thereafter hydroxylated by flavanone 3-dioxygenase to produce dihydrokaempferol [33]. Finally, the introduction of a double bond at the C2-C3 position of dihydrokaempferol produces kaempferol.

There is no much data on the pharmacokinetics of Kaempferol, however, flavonoids are extensively metabolized by the colonic microflora [34, 35]. Intestinal permeability study of kaempferol shows it undergoes significant biotransformation, with only a small fraction of the unchanged kaempferol able to cross the intestinal barrier [36].

It has been isolated from tea as well as common vegetables and fruits like beans, broccoli, cabbage, grapes, strawberries, tomatoes, apples and grapefruit [37].

Kaempferol has anti-inflammatory and anti-cancer properties, protects the liver and prevent metabolic diseases (Figure 3). The most well-known of its properties are its anti-inflammatory effects by decreasing lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1) expression and also by increasing the number of activated macrophages [38]. Kaempferol is a dietary flavonoids that occur in fruits, vegetables, beverages, chocolates, herbs and plants [39] and reported to possess anti-diabetic property.

Figure 3.

Biological roles of Kaempferol.


6. Mechanism of antidiabetic action of kaempferol

Kaempferol has been reported to lower blood glucose [40], inhibit α -amylase and α -glucosidase [41]. This section addresses the mechanism of action of Kaempferol under the following headings.


7. Inhibition of α-amylase and α-glucosidase enzymes.

α-Amylase and α-glucosidase are carbohydrate hydrolyzing enzymes located in the digestive tract. α- amylase in the duodenum initiates digestion and catalyzes the hydrolysis of α-1, 4 glycosidic linkages in starch resulting into sugars such as maltose, maltotriose and branched oligosaccharides. Then, α-glucosidase present in the brush border of the intestinal epithelium (enterocytes) is responsible for the final step of carbohydrates digestion, prior to their absorption. This enzyme cleaves terminal non-reducing 1, 4 linkages and converts the disaccharides and oligosaccharides into glucose, which is then transported by sodium/glucose co-transporter 1 (SGLT1) from the intestinal lumen to the cytosol of enterocytes. In turn, glucose transporter 2 (GLUT2), found in the basolateral membrane of enterocytes, transports glucose from cytosol to blood via facilitated diffusion.

One of the approaches to managing diabetes is to delay the absorption of glucose by the inhibition of carbohydrate hydrolyzing enzymes in the digestive tract of humans [42, 43].

Controlling the activity of these enzymes slows glucose production in the postprandial stage and this could be a therapeutic approach for people with diabetes. Hence, the search for inhibitors from medicinal plants is a great development [44].

Ibitoye et al. identified that kaempferol from Cucumis sativus L. lowers blood glucose and inhibited the activity of α -amylase and α glucosidase at IC50 of 51.24 and 29.37 μg/mL respectively [29]. This inhibition means reduction in blood glucose in the postprandial stage of alloxan-induced diabetic rats when given 165 mg/kg body weight of kaempferol from Cucumis sativus fruits. This evidently supports that kaempferol lowers blood glucose and inhibit α-amylase and α -glucosidase.

It may be possible that the glucose lowering activity of C. sativus fruits is through inhibition of α -amylase and α -glucosidase through kaempferol.


8. Maintaining glucose homeostasis

Diabetes features dysregulated glucose metabolism characterized by increased hepatic glucose production and decreased glucose oxidation. This eventually leads to deterioration in glucose control. Alkhalidy et al reported that kaempferol ameliorate hyperglycemia and enhance glucose tolerance in insulin deficient mice [45]. Diabetic mice displayed significantly higher pyruvate carboxylase activity. Kaempferol treatment suppressed the elevated pyruvate carboxylase activity and glucose-6 phosphatase activity in the liver suggesting that kaempferol may improve glycemic control in diabetes in part through suppressing gluconeogenesis in the liver via the regulation of pyruvate carboxylase, the first and critical step in gluconeogenesis [45]. It could therefore be a strategy for maintaining glucose homeostasis by targeting the glucose production and metabolic pathways.


9. Modulation of antioxidant profile

Generation of reactive oxygen species and free radicals contributes to the pathogenesis of diabetes [46]. This increased ROS production overruns the cellular antioxidant defense system leading to oxidative stress and damage [47]. Some diabetes research confirm this phenomenon in different diabetes model [48, 49]. Catalase, superoxide dismutase and glutathione are reduced significantly in diabetes [50]. Kaempferol reversed the alterations on oxidative stress markers in alloxan-induced diabetic rats [29].


10. Reversal of lipid profile alterations

One of the complications in diabetes is dyslipidemia, where the lipid profile is disturbed. It is usually presented with elevated levels of total cholesterol TC, triacylglycerol TAG, and low-density lipoprotein cholesterol LDLc and a reduction of high density lipoprotein cholesterol HDLc [51]. These alterations could predispose to developing atherosclerosis and cardiovascular diseases. Reversal of these alterations in alloxan-diabetic rats suggests its anti-dyslipidemic capability [29]. Alkhalidy et al. observed that untreated diabetic mice had lower total cholesterol, HDL-cholesterol, and LDL-cholesterol levels when compared to non-diabetic mice [45]. Kaempferol treatment reversed these changes to the levels similar to those seen in non-diabetic mice.

11. Maintenance of glycoprotein content

Glycoproteins are carbohydrate-containing proteins found on the cell membrane. They play important roles in membrane transport, cell differentiation and recognition, adhesion of macromolecules to cell surface and also in the secretion and absorption of macromolecules [52]. Impaired metabolism of glycoproteins contributes to the pathogenesis of diabetes [53]. Studies have reported that alterations in concentrations of various glycoproteins contribute to human diabetes [54]. Elevated levels of glycoproteins in diabetic condition could be a consequence of impaired carbohydrate metabolism [55]. Chandramohan et al. reported that kaempferol reversed elevated level of hexoses, hexosamines, fucose and sialic acid (glycoprotein componets) in streptozotocin-induced diabetic rats which may be due to the activation of glucose transport mechanism and also alters insulin binding receptor specificity [56].


  1. 1. Zimmet, P., Alberti, K. G., & Shaw, J. (2001). Global and societal implications of the diabetes epidemic. Nature, 414, 782-787
  2. 2. The International Diabetes Federation Diabetes Atlas Ninth edition 2019. Diabetes facts & figures
  3. 3. American Diabetes Association, The cost of Diabetes Updated 02/2020. Accessed January 12, 2021
  4. 4. Ozcan, U., Cao, Q., Yilmaz, E., Lee, A.-H., Iwakoshi, N. N., Ozdelen, E., & Hotamisligil, G. S. (2004). Endoplasmic reticulum stress links obesity, insulin action, and type 2 diabetes. Science, 306, 457-461
  5. 5. Poitout, V., & Robertson, R. P. (2008). Glucolipotoxicity: Fuel excess and cell dysfunction. Endocrine Reviews, 29(3), 351-366
  6. 6. Hove, M. N., Kristensen, J. K., Lauritzen, T., & Bek, T. (2004). The prevalence of retinopathy in an unselected population of type 2 diabetes patients from Arhus County, Denmark. Acta Ophthalmologica Scandinavica, 82, 443-448
  7. 7. Moran, A., Palmas, W., Field, L., Bhattarai, J., Schwartz, J. E., Weinstock, R. S., & Shea, S. (2004). Cardiovascular autonomic neuropathy is associated with microalbuminuria in older patients with type 2 diabetes. Diabetes Care, 27, 972-977
  8. 8. Huang, C., Kim, Y., Caramori, M. L., Fish, A. J., Rich, S. S., Miller, M. E., & Mauer, M. (2002). Cellular basis of diabetic nephropathy: II. The transforming growth factor-beta system and diabetic nephropathy lesions in type 1 diabetes. Diabetes, 51, 3577-3581
  9. 9. Saely, C. H., Aczel, S., Marte, T., Langer, P., & Drexel, H. (2004). Cardiovascular complications in Type 2 diabetes mellitus depend on the coronary angiographic state rather than on the diabetic state. Diabetologia, 47, 145-146
  10. 10. Wallace, C., Reiber, G. E., LeMaster, J., Smith, D. G., Sullivan, K., Hayes, S., & Vath, C. (2002). Incidence of falls, risk factors for falls, and fallrelated fractures in individuals with diabetes and a prior foot ulcer. Diabetes Care, 25, 1983-1986
  11. 11. Ajiboye, T. O., Uwazie, J., Haliru, F., Ibitoye, O., & Sunmonu, T. O. (2017). Mechanisms of action of columbamine, jatrorrhizine and magnoflorine as antidiabetic agents. In J. N. Govil (Ed.), Recent progress in medicinal plant (Vol. 45, pp. 221-232). USA: Studium Press LLC
  12. 12. Antidiabetic drugs. Updated: October 5, 2020. Accessed: November 22, 2020
  13. 13. Marles, R. J., & Farnsworth, N. R. (1995). Antidiabetic plants and their active constituents. Phytomedicine: International Journal of Phytotherapy and Phytopharmacology, 2: 137-189
  14. 14. Sharma, N., & Garg, V. (2009). Antidiabetic and antioxidant potential of ethanolic extract of Butea monosperma leaves in alloxan-induced diabetic mice. Indian Journal of Biochemistry & Biophysics, 46: 99-105
  15. 15. Sun, H., Fang, W., Wang, W., & Hu, C. (2006). Structure-activity relationships of oleanane- and ursane-type triterpenoids. Botanical Studies, 47: 339-368
  16. 16. Saidu, A. N., Oibiokpa, F. I. & Olukotun, I. O. (2014). Phytochemical screening and hypoglycemic effect of methanolic fruit pulp extract of Cucumis sativus in alloxan induced diabetic rats. Journal of Medicinal Plants Research, 8(39): 1173-1178
  17. 17. Wojdyo A, Oszmianski J, Czemerys R. (2007). Antioxidant activity and phenolic compounds in 32 selected herbs. Food Chemistry, 105:940-949
  18. 18. Panche, A., Diwan, A.D. & Chandra, S.R. (2016). Flavonoids: An overview. Journal of Nutrition Science, 5, 5
  19. 19. Metodiewa, D., Kochman, A. & Karolczak, S. (1997). Evidence for antiradical and antioxidant properties of four biologically active N, N-Diethylaminoethyl ethers of flavaone oximes: A comparison with natural polyphenolic flavonoid rutin action. IUBMB Life, 41, 1067-1075
  20. 20. Sotiroudis, G., Melliou, E., Sotiroudis, T. G., & Chinou, I. (2010). Chemical analysis, antioxidant and antimicrobial activity of three Greek cucumber (Cucumis sativus) cultivars. Journal of Food Biochemistry, 34: 61-78
  21. 21. Mukherjee, P. K., Maity, N., Nema, N. K., & Sarkar, B. K. (2011). Bioactive compounds from natural resources against skin aging. Phytomedicine, 19(1): 64-73
  22. 22. Nema, N. K., Maity, N., Sarkar, B., & Mukherjee, P. K. (2011). Cucumis sativus fruit-potential antioxidant, anti-hyaluronidase, and antielastase agent. Archives of Dermatological Research, 303: 247-252
  23. 23. Roman-Ramos, R., Flores-Saenz, J. L., & Alarcon-Aguilar, F. J. (1995). Anti-hyperglycemic effect of some edible plants. Journal of Ethnopharmacology, 48: 25-32
  24. 24. Enslin, P. R., Joubert, F. J., & Rehm, S. (1956). Bitter principles of the Cucurbitaceae. III.—Elaterase, an active enzyme for the hydrolysis of bitter principle glycosides. Journal of the Science of Food and Agriculture, 7: 646-655
  25. 25. Chu, Y.-F., Sun, J., Wu, X., & Liu, R. H. (2002). Antioxidant and anti-proliferative activities of common vegetables. Journal of Agricultural and Food Chemistry, 50: 6910-6916
  26. 26. McNally, D. J., Wurms, K. V., Labbe, C., Quideau, S., & Belanger, R. R. (2003). Complex C-glycosyl flavonoid phytoalexins from Cucumis sativus. Journal of Natural Products, 66: 1280-1283
  27. 27. Kai, H., Baba, M., & Okuyama, T. (2007). Two new megastigmanes from the leaves of Cucumis sativus. Chemical & Pharmaceutical Bulletin, 55: 133-136
  28. 28. Krauze-Baranowska, M., & Cisowski, W. (2001). Flavonoids from some species of the genus Cucumis, Biochemical Systematics and Ecology, 29(3), 321-324
  29. 29. Ibitoye, O. B., Uwazie, J. N., & Ajiboye, T. O. (2017). Bioactivity-guided isolation of kaempferol as the antidiabetic principle from Cucumis sativus L. fruits. Journal of Food Biochemistry, 12479
  30. 30. Yang, J.H., Kondratyuk, T.P., Marler, L.E., Qiu, X., Choi, Y., Cao, H., Yu, R., Sturdy, M., Pegan, S. & Liu, Y. (2010). Isolation and evaluation of kaempferol glycosides from the fern Neocheiropteris palmatopedata. Phytochemistry, 71, 641-647
  31. 31. Orhan, I., Küpeli, E., Terzioglu, S. & Yesilada, E. (2007). Bioassay-guided isolation of kaempferol-3-O-β-d-galactoside with anti inflammatory and antinociceptive activity from the aerial part of Calluna vulgaris L. Journal of Ethnopharmacology, 114, 32-37
  32. 32. Devi, K. P., Malar, D. S., Nabavi, S. F., Sureda, A., Xiao, J., Nabavi, S. M. & Daglia, M. (2015). Kaempferol and inflammation: From chemistry to medicine. Pharmacology Research, 99:1-10
  33. 33. Tsao, R. (2010). Chemistry and biochemistry of dietary polyphenols. Nutrients, 2:1231-1246
  34. 34. Hollman, P.C.H. (2004). Absorption, bioavailability, and metabolism of flavonoids, Pharm. Biol. 42: 74-83
  35. 35. Van Duynhoven, J., Vaughan, E.E., Jacobs, D.M., Kemperman, R.A., Van Velzen, E.J.J., Gross, G., Roger, L.C., Possemiers, S., Smilde, A.K., Doré, J., Westerhuis, J.A. & Van de Wiele, T. (2011) . Metabolic fate of polyphenols in the human superorganism, Proc. Natl. Acad. Sci. U. S. A. 108: 4531-4538
  36. 36. Moradi-Afrapoli, F. Oufir, M., Walter, F.R., Deli, M.A., Smiesko, M., Zabela, V., Butterweck, .V. & Hamburger, M. (2016). Validation of UHPLC-MS/MS methods for the determination of kaempferol and its metabolite 4-hydroxyphenyl acetic acid, and application to in vitro blood-brain barrier and intestinal drug permeability studies, J. Pharm. Biomed. Anal. 128 264-274
  37. 37. Calderón-Montaño, J. M., Burgos-Morón, E., Pérez-Guerrero, C. & López-Lázaro M. (2011). A review on the dietary flavonoid kaempferol. Mini Review on Medicinal Chemistry, 11: 298-344
  38. 38. Ramachandran, V. and Baojun, X. (2015). Antidiabetic properties of dietary flavonoids: A cellular mechanism review, Nutr Metabol, 12: 60
  39. 39. Lin, M. K., Yu, Y. L., Chen, K. C., Chang, W. T., Lee, M. S., Yang, M. J., Cheng, H. C., Liu, C. H., Chen, D.C. & Chu, C. L. (2011). Kaempferol from Semen cuscutae attenuates the immune function of dendritic cells. Immunobiology, 216:1103-1109
  40. 40. Alkhalidy, H., Moore, W., Zhang, Y., McMillan, R., Wang, A., Ali, M. & Liu, D. (2015). Small molecule kaempferol promotes insulin sensitivity and preserved pancreatic b-cell mass in middle-aged obese diabetic mice. Journal of Diabetes Research, 532984
  41. 41. Peng, X., Zhang, G., Liao, Y. & Gong, D. (2016). Inhibitory kinetics and mechanism of kaempferol on α -glucosidase. Food Chemistry, 190207-190215
  42. 42. Hara, Y. & Honda, M. (1990). The Inhibition of α-Amylase by Tea Polyphenols. Agricultural and Biological Chemistry, 54, (8):1939-1945
  43. 43. Deshpande, M. C., Venkateswarlu, V., Babu, R. K. & Trivedi, R. K. (2009). Design and evaluation of oral bioadhesive controlled release formulations of miglitol, intended for prolonged inhibition of intestinal α-glucosidases and enhancement of plasma glucagon like peptide-1 levels. International Journal of Pharmaceutics, 380, (1-2): 16-24
  44. 44. Yin, Z., Zhang, W., Feng, F., Zhang, Y. & Kang, W. (2014). α-Glucosidase inhibitors isolated from medicinal plants. Food Science and Human Wellness, 33-4, 136-174
  45. 45. Alkhalidy, H., Moore, W., Wang, Y., Luo, J., McMillan, R. P., Zhen, W., Zhou, K. & Liu, D. (2018). The Flavonoid Kaempferol Ameliorates Streptozotocin-Induced Diabetes by Suppressing Hepatic Glucose Production. Molecules, 23, 2338
  46. 46. Rains, J. L., & Jain, S. K. (2011). Oxidative stress, insulin signaling, and diabetes. Free Radical Biology & Medicine, 50, 567-575
  47. 47. Sies, H. (1991). Oxidative stress: From basic research to clinical application. The American Journal of Medicine, 91, 31S–38S
  48. 48. Oloyede, H. O. B., Ajiboye, T. O., Abdussalam, A. F., &. Adeleye, A. O. (2014). Blighia sapida leaves halt elevated blood glucose, dyslipidemia and oxidative stress in alloxan-induced diabetic rats. Journal of Ethnopharmacology, 157, 309-319
  49. 49. Oloyede, H. O. B., Bello, T. O., Ajiboye, T. O., & Salawu, M. O. (2015). Antidiabetic and antidyslipidemic activities of aqueous leaf extract of Dioscoreophyllum cumminsii (Stapf) Diels in alloxan-induced diabetic rats. Journal of Ethnopharmacology, 166, 313-322
  50. 50. Ajiboye, T. O., Akinpelu, S. A., Muritala, H. F., Ogunbode, S. M., Adeleye, A. O., Oladiji, A. T., & Oloyede, O. B. (2014). Trichosanthes cucumerina fruit extenuates dyslipidemia, protein oxidation, lipid peroxidation and DNA fragmentation in the liver of high-fat diet-fed rats. Journal of Food Biochemistry, 38, 480-490
  51. 51. Mittal, N., Keaur, J. & Mahmood, A. (1996). Changes in tubular membrane glycosylation in diabetic insulin and thyroxin treated rat kidneys. Indian Journal of Experimental Biology, 34: 782-785
  52. 52. Knecht KT, Bradford BU, Mason RP & Thurman RG. (1990). In vivo formation of free radicals metabolite of ethanol. Molecular Pharmacology, 38: 26-30
  53. 53. Sharma, C., Dalferes, F. R., Radhakrishnamurthy, B., De-Paolo, C. J. & Berenson, G. S. (1987). Hepatic glycoprotein synthesis in streptozotocin diabetic rats. Biochem Int, 1987; 36: 15-19
  54. 54. Chandramohan, G., Al-Numair, K. S., Alsaif, M. A. & Veeramani, C. (2015). Antidiabetic effect of kaempferol a flavonoid compound, on streptozotocin-induced diabetic rats with special reference to glycoprotein components. Progress in Nutrition, Vol. 17, N. 1: 50-57
  55. 55. Peppa, M., Stavroulakis, P. & Raptis, S. A. (2009). Advanced glycoxidation products and impaired diabetic wound healing. Wound Repair Regeneration, 17; 461-472
  56. 56. Marshall, S., Bacote, V. & Traxinger, R. R. (1991). Discovery of metabolic pathway mediating glucose induced desensitization of glucose transport system: role of hexosamine biosynthesis in the induction of insulin resistance. J Biol Chem 1991; 266: 4706-4712

Written By

Ibitoye Oluwayemisi Beatrice, Ajiboye Taofeek Olakunle, Abdulazeez Azeemat Titilola, Oyegoke Rukayat Abiodun, Muritala Hamdalat Folake and Abubakar Fatimah Aluko

Submitted: October 21st, 2020 Reviewed: February 3rd, 2021 Published: June 7th, 2021