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Effect of Swimming Exercise on Levels of Blood Glucose, Adiponectin, Glucose-6-Phosphatase and Lipid Profile in Diabetic Wistar Rats

Received: 20 June 2024     Accepted: 8 July 2024     Published: 23 July 2024
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Abstract

Diabetes mellitus is a chronic metabolic condition that causes persistent hyperglycemia due to insulin action or secretion. Regular physical exercise has been reported to improve glycemia and lipid profile in diabetes. However, literature is scare on the effects of swimming exercise on the serum levels of adiponectin and glucose 6 phosphatase in Wister rats with diabetes This study therefore, investigated the effects of swimming exercise on adiponectin, glucose 6-phosphatase and lipid profile in male Wistar rats with streptozotocin-induced diabetes. This study was carried out on 25 male Wistar rats grouped into five groups (n=5/group): group 1=control, group 2=diabetes, group 3=diabetes treated with metformin, group 4=non-diabetes and swimming exercise, group 5=diabetes and swimming exercise. Animals in groups 2, 3, and 5 were induced with Streptozotocin (STZ) 50 mg/kg intraperitoneally. After 72 hours of diabetes induction, animals with a blood glucose level of ≥ 200 mg/dl were confirmed diabetics and used for the study. Group 3 animals were treated with metformin 200mg/kg giving orally for 28 days. Animals in groups 4 and 5 were subjected to swimming exercises for 5-10 minutes during the first week until they could swim freely for 30 minutes. The animals were then allowed to swim 5 days per week for 28 days. Swimming exercise for 28 days significantly reduced blood glucose, glucose-6-phosphatase (G6Ppase), Lactate dehydrogenase (LDH), Total cholesterol (TC), and Low-density lipoprotein (LDL) levels but caused significant increase in adiponectin and High-density lipoprotein (HDL) levels in diabetic rats compared with untreated diabetic rats. There was a significant decrease in triglyceride (TG) of diabetic animals caused by swimming for 28 days. This study demonstrated that swimming exercise for 28 days may help lower glucose level and improve insulin sensitivity by increasing adiponectin level and decreasing G6Pase activity in diabetic rats. Also, swimming exercise may help improve lipid profile in diabetic rats.

Published in Advances in Applied Physiology (Volume 9, Issue 1)
DOI 10.11648/j.aap.20240901.12
Page(s) 13-20
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2024. Published by Science Publishing Group

Keywords

Diabetes, Swimming, Blood Glucose, Lactate Dehydrogenase, Adiponectin, Glucose-6-Phosphatase, Lipid Profile

References
[1] J. S. Omar, N. Jaradat, M. Qadoumi, and A. N. Qadoumi, “Regular swimming exercise improves metabolic syndrome risk factors: a quasi-experimental study,” BMC Sports Sci. Med. Rehabil., vol. 13, pp. 1–7, 2021.
[2] B.-A. Lee and D.-J. Oh, “Effect of regular swimming exercise on the physical composition, strength, and blood lipid of middle-aged women.,” J. Exerc. Rehabil., vol. 11, no. 5, pp. 266–271, Oct. 2015,
[3] D. CDC, “National Diabetes Statistics Report,” May 2024. [Online]. Available:
[4] L. Kumar et al., “Knowledge and Awareness About Diabetes Mellitus Among Urban and Rural Population Attending a Tertiary Care Hospital in Haryana,” Cureus, vol. 15, no. 4, 2023.
[5] H. Tanaka, D. R. J. Bassett, and E. T. Howley, “Effects of swim training on body weight, carbohydrate metabolism, lipid and lipoprotein profile.,” Clin. Physiol. Oxf. Engl., vol. 17, no. 4, pp. 347–359, Jul. 1997,
[6] B. K. Pedersen and B. Saltin, “Evidence for prescribing exercise as therapy in chronic disease,” Scand. J. Med. Sci. Sports, vol. 16, no. S1, pp. 3–63, 2006.
[7] J. B. Farinha et al., “Glycemic, inflammatory and oxidative stress responses to different high-intensity training protocols in type 1 diabetes: A randomized clinical trial,” J. Diabetes Complications, vol. 32, no. 12, pp. 1124–1132, 2018.
[8] Z. Punthakee et al., “Adiponectin, adiposity, and insulin resistance in children and adolescents,” J. Clin. Endocrinol. Metab., vol. 91, no. 6, pp. 2119–2125, 2006.
[9] W. M. Denning, E. Bressel, D. Dolny, M. Bressel, and M. K. Seeley, “A review of biophysical differences between aquatic and land-based exercise,” Int. J. Aquat. Res. Educ., vol. 6, no. 1, p. 7, 2012.
[10] R. L. McNeal, “Aquatic therapy for patients with rheumatic disease.,” Rheum. Dis. Clin. North Am., vol. 16, no. 4, pp. 915–929, Nov. 1990.
[11] M. Ussher, R. West, A. McEwen, A. Taylor, and A. Steptoe, “Efficacy of exercise counselling as an aid for smoking cessation: a randomized controlled trial.,” Addict. Abingdon Engl., vol. 98, no. 4, pp. 523–532, Apr. 2003,
[12] M. G. Flynn et al., “Fat storage in athletes: metabolic and hormonal responses to swimming and running,” Int. J. Sports Med., vol. 11, no. 06, pp. 433–440, 1990.
[13] Y. Sengoku, K. Nakamura, T. Takeda, Y. Nabekura, and S. Tsubakimoto, “Glucose response after a ten-week training in swimming,” Int. J. Sports Med., vol. 32, no. 11, pp. 835–838, 2011.
[14] D. X. Scomparin et al., “Low-Intensity swimming training after weaning improves glucose and lipid homeostasis in MSG hypothalamic obese mice.,” Endocr. Res., vol. 36, no. 2, pp. 83–90, 2011,
[15] F. Zahedmanesh, A. Zafari, and F. Zahedmanesh, “Lipid profiles changes induced by swimming combined training in academic level athlete’s women,” Eur. J. Exp. Biol., vol. 3, pp. 223–227, Jan. 2013.
[16] L.-K. Wang, H. Wang, X.-L. Wu, L. Shi, R.-M. Yang, and Y.-C. Wang, “Relationships among resistin, adiponectin, and leptin and microvascular complications in patients with type 2 diabetes mellitus.,” J. Int. Med. Res., vol. 48, no. 4, p. 300060519870407, Apr. 2020,
[17] J. F. Clapp and W. Kiess, “Effects of pregnancy and exercise on concentrations of the metabolic markers tumor necrosis factor alpha and leptin.,” Am. J. Obstet. Gynecol., vol. 182, no. 2, pp. 300–306, Feb. 2000,
[18] Y. R. Jung et al., “Adiponectin signaling regulates lipid production in human sebocytes,” PLoS One, vol. 12, no. 1, p. e0169824, 2017.
[19] C. Lara-Castro, Y. Fu, B. H. Chung, and W. T. Garvey, “Adiponectin and the metabolic syndrome: mechanisms mediating risk for metabolic and cardiovascular disease,” Curr. Opin. Lipidol., vol. 18, no. 3, pp. 263–270, 2007.
[20] L. Qiao et al., “Adiponectin deficiency impairs maternal metabolic adaptation to pregnancy in mice,” Diabetes, vol. 66, no. 5, pp. 1126–1135, 2017.
[21] J. Y. Xia et al., “Acute loss of adipose tissue-derived adiponectin triggers immediate metabolic deterioration in mice.,” Diabetologia, vol. 61, no. 4, pp. 932–941, Apr. 2018,
[22] J. Ventura-Sobrevilla et al., “Effect of varying dose and administration of streptozotocin on blood sugar in male CD1 mice.,” Proc. West. Pharmacol. Soc., vol. 54, pp. 5–9, 2011.
[23] N. A. Qinna and A. A. Badwan, “Impact of streptozotocin on altering normal glucose homeostasis during insulin testing in diabetic rats compared to normoglycemic rats,” Drug Des. Devel. Ther., pp. 2515–2525, 2015.
[24] E. U. Etuk, “Animals models for studying diabetes mellitus,” Agric Biol JN Am, vol. 1, no. 2, pp. 130–134, 2010.
[25] N. Sakata, G. Yoshimatsu, H. Tsuchiya, S. Egawa, and M. Unno, “Animal models of diabetes mellitus for islet transplantation,” J. Diabetes Res., vol. 2012, no. 1, p. 256707, 2012.
[26] S. Rahimi et al., “Long-term exercise from adolescence to adulthood reduces anxiety- and depression-like behaviors following maternal immune activation in offspring.,” Physiol. Behav., vol. 226, p. 113130, Nov. 2020,
[27] A. Ghasemi, S. Khalifi, and S. Jedi, “Streptozotocin-nicotinamide-induced rat model of type 2 diabetes,” Acta Physiol. Hung., vol. 101, no. 4, pp. 408–420, 2014.
[28] P. Trinder, “Determination of blood glucose using 4-amino phenazone as oxygen acceptor.,” J. Clin. Pathol., vol. 22, no. 2, p. 246, Mar. 1969,
[29] H. Zhou et al., “Adiponectin represses gluconeogenesis independent of insulin in hepatocytes,” Biochem. Biophys. Res. Commun., vol. 338, no. 2, p. 793-799, Dec. 2005,
[30] M. Esfahani, A. Movahedian, M. Baranchi, and M. T. Goodarzi, “Adiponectin: an adipokine with protective features against metabolic syndrome,” Iran. J. Basic Med. Sci., vol. 18, no. 5, p. 430, 2015.
[31] O. M. Ahmed, A. M. Mahmoud, A. Abdel-Moneim, and M. B. Ashour, “Antidiabetic effects of hesperidin and naringin in type 2 diabetic rats.,” 2012.
[32] A. M. Mahmoud, O. M. Ahmed, A. Abdel-Moneim, and M. B. Ashour, “Upregulation of PPARγ mediates the antidiabetic effects of citrus flavonoids in type 2 diabetic rats,” Int. J. Bioassays, vol. 2, no. 5, pp. 756–761, 2013.
[33] J. Kawano and R. Arora, “The role of adiponectin in obesity, diabetes, and cardiovascular disease,” J. Cardiometab. Syndr., vol. 4, no. 1, pp. 44–49, 2009.
[34] X. Li et al., “Mechanisms by which adiponectin reverses high fat diet-induced insulin resistance in mice,” Proc. Natl. Acad. Sci., vol. 117, no. 51, pp. 32584–32593, 2020.
[35] D. Stensel, “Exercise, appetite and appetite-regulating hormones: implications for food intake and weight control,” Ann. Nutr. Metab., vol. 57, no. Suppl. 2, pp. 36–42, 2011.
[36] R. Polito, I. Di Meo, M. Barbieri, A. Daniele, G. Paolisso, and M. R. Rizzo, “Adiponectin role in neurodegenerative diseases: focus on nutrition review,” Int. J. Mol. Sci., vol. 21, no. 23, p. 9255, 2020.
[37] M. Izadi, M. T. Goodarzi, H. S. Khalaj, D. Khorshidi, and H. Doali, “Serum adiponectin levels are inversely correlated with insulin resistance in obese men with type 2 diabetes,” Int. J. Endocrinol. Metab., vol. 9, no. 1, 2011.
[38] C. Bouche, S. Serdy, C. R. Kahn, and A. B. Goldfine, “The cellular fate of glucose and its relevance in type 2 diabetes,” Endocr. Rev., vol. 25, no. 5, pp. 807–830, 2004.
[39] K. L. Kavanagh, R. A. Elling, and D. K. Wilson, “Structure of Toxoplasma gondii LDH1: active-site differences from human lactate dehydrogenases and the structural basis for efficient APAD+ use,” Biochemistry, vol. 43, no. 4, pp. 879–889, 2004.
[40] E. K. Ainscow, C. Zhao, and G. A. Rutter, “Acute overexpression of lactate dehydrogenase-A perturbs beta-cell mitochondrial metabolism and insulin secretion.,” Diabetes, vol. 49, no. 7, pp. 1149–1155, 2000.
[41] P. Palsamy and S. Subramanian, “Modulatory effects of resveratrol on attenuating the key enzymes activities of carbohydrate metabolism in streptozotocin–nicotinamide-induced diabetic rats,” Chem. Biol. Interact., vol. 179, no. 2–3, pp. 356–362, 2009.
[42] G. S. Prasath and S. P. Subramanian, “Modulatory effects of fisetin, a bioflavonoid, on hyperglycemia by attenuating the key enzymes of carbohydrate metabolism in hepatic and renal tissues in streptozotocin-induced diabetic rats.,” Eur. J. Pharmacol., vol. 668, no. 3, pp. 492–496, Oct. 2011,
[43] E. van Schaftingen and I. Gerin, “The glucose-6-phosphatase system.,” Biochem. J., vol. 362, no. Pt 3, pp. 513–532, Mar. 2002,
[44] S. Srinivasan, G. Sathish, M. Jayanthi, J. Muthukumaran, U. Muruganathan, and V. Ramachandran, “Ameliorating effect of eugenol on hyperglycemia by attenuating the key enzymes of glucose metabolism in streptozotocin-induced diabetic rats,” Mol. Cell. Biochem., vol. 385, pp. 159–168, 2014.
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    Olufunmilayo, I. G., Mojirade, L. N. (2024). Effect of Swimming Exercise on Levels of Blood Glucose, Adiponectin, Glucose-6-Phosphatase and Lipid Profile in Diabetic Wistar Rats. Advances in Applied Physiology, 9(1), 13-20. https://doi.org/10.11648/j.aap.20240901.12

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    Olufunmilayo, I. G.; Mojirade, L. N. Effect of Swimming Exercise on Levels of Blood Glucose, Adiponectin, Glucose-6-Phosphatase and Lipid Profile in Diabetic Wistar Rats. Adv. Appl. Physiol. 2024, 9(1), 13-20. doi: 10.11648/j.aap.20240901.12

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    AMA Style

    Olufunmilayo IG, Mojirade LN. Effect of Swimming Exercise on Levels of Blood Glucose, Adiponectin, Glucose-6-Phosphatase and Lipid Profile in Diabetic Wistar Rats. Adv Appl Physiol. 2024;9(1):13-20. doi: 10.11648/j.aap.20240901.12

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  • @article{10.11648/j.aap.20240901.12,
      author = {Isehunwa Grace Olufunmilayo and Layonu Naheemat Mojirade},
      title = {Effect of Swimming Exercise on Levels of Blood Glucose, Adiponectin, Glucose-6-Phosphatase and Lipid Profile in Diabetic Wistar Rats
    },
      journal = {Advances in Applied Physiology},
      volume = {9},
      number = {1},
      pages = {13-20},
      doi = {10.11648/j.aap.20240901.12},
      url = {https://doi.org/10.11648/j.aap.20240901.12},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.aap.20240901.12},
      abstract = {Diabetes mellitus is a chronic metabolic condition that causes persistent hyperglycemia due to insulin action or secretion. Regular physical exercise has been reported to improve glycemia and lipid profile in diabetes. However, literature is scare on the effects of swimming exercise on the serum levels of adiponectin and glucose 6 phosphatase in Wister rats with diabetes This study therefore, investigated the effects of swimming exercise on adiponectin, glucose 6-phosphatase and lipid profile in male Wistar rats with streptozotocin-induced diabetes. This study was carried out on 25 male Wistar rats grouped into five groups (n=5/group): group 1=control, group 2=diabetes, group 3=diabetes treated with metformin, group 4=non-diabetes and swimming exercise, group 5=diabetes and swimming exercise. Animals in groups 2, 3, and 5 were induced with Streptozotocin (STZ) 50 mg/kg intraperitoneally. After 72 hours of diabetes induction, animals with a blood glucose level of ≥ 200 mg/dl were confirmed diabetics and used for the study. Group 3 animals were treated with metformin 200mg/kg giving orally for 28 days. Animals in groups 4 and 5 were subjected to swimming exercises for 5-10 minutes during the first week until they could swim freely for 30 minutes. The animals were then allowed to swim 5 days per week for 28 days. Swimming exercise for 28 days significantly reduced blood glucose, glucose-6-phosphatase (G6Ppase), Lactate dehydrogenase (LDH), Total cholesterol (TC), and Low-density lipoprotein (LDL) levels but caused significant increase in adiponectin and High-density lipoprotein (HDL) levels in diabetic rats compared with untreated diabetic rats. There was a significant decrease in triglyceride (TG) of diabetic animals caused by swimming for 28 days. This study demonstrated that swimming exercise for 28 days may help lower glucose level and improve insulin sensitivity by increasing adiponectin level and decreasing G6Pase activity in diabetic rats. Also, swimming exercise may help improve lipid profile in diabetic rats.
    },
     year = {2024}
    }
    

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  • TY  - JOUR
    T1  - Effect of Swimming Exercise on Levels of Blood Glucose, Adiponectin, Glucose-6-Phosphatase and Lipid Profile in Diabetic Wistar Rats
    
    AU  - Isehunwa Grace Olufunmilayo
    AU  - Layonu Naheemat Mojirade
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    JO  - Advances in Applied Physiology
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    EP  - 20
    PB  - Science Publishing Group
    SN  - 2471-9714
    UR  - https://doi.org/10.11648/j.aap.20240901.12
    AB  - Diabetes mellitus is a chronic metabolic condition that causes persistent hyperglycemia due to insulin action or secretion. Regular physical exercise has been reported to improve glycemia and lipid profile in diabetes. However, literature is scare on the effects of swimming exercise on the serum levels of adiponectin and glucose 6 phosphatase in Wister rats with diabetes This study therefore, investigated the effects of swimming exercise on adiponectin, glucose 6-phosphatase and lipid profile in male Wistar rats with streptozotocin-induced diabetes. This study was carried out on 25 male Wistar rats grouped into five groups (n=5/group): group 1=control, group 2=diabetes, group 3=diabetes treated with metformin, group 4=non-diabetes and swimming exercise, group 5=diabetes and swimming exercise. Animals in groups 2, 3, and 5 were induced with Streptozotocin (STZ) 50 mg/kg intraperitoneally. After 72 hours of diabetes induction, animals with a blood glucose level of ≥ 200 mg/dl were confirmed diabetics and used for the study. Group 3 animals were treated with metformin 200mg/kg giving orally for 28 days. Animals in groups 4 and 5 were subjected to swimming exercises for 5-10 minutes during the first week until they could swim freely for 30 minutes. The animals were then allowed to swim 5 days per week for 28 days. Swimming exercise for 28 days significantly reduced blood glucose, glucose-6-phosphatase (G6Ppase), Lactate dehydrogenase (LDH), Total cholesterol (TC), and Low-density lipoprotein (LDL) levels but caused significant increase in adiponectin and High-density lipoprotein (HDL) levels in diabetic rats compared with untreated diabetic rats. There was a significant decrease in triglyceride (TG) of diabetic animals caused by swimming for 28 days. This study demonstrated that swimming exercise for 28 days may help lower glucose level and improve insulin sensitivity by increasing adiponectin level and decreasing G6Pase activity in diabetic rats. Also, swimming exercise may help improve lipid profile in diabetic rats.
    
    VL  - 9
    IS  - 1
    ER  - 

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