Background: Excess caloric intake expands adipose tissue resulting in a higher risk of metabolic disease. Lipocalin 2 (LCN2) is an adipokine having a role in innate immunity and energy metabolism. It is an acute phase protein that was recently correlated with potential effects on obesity and inflammation. The reaction of this protein to progressive exercise in animals has limited studies. Exercise encourages weight loss and improves insulin sympathy. However, the molecular mechanisms mediating its beneficial effects are not fully understood. Obesity associates with increased production of inflammatory cytokines, which in turn, subsidizes to systemic insulin resistance. LCN2 has been shown to have a significant association with body mass index (BMI). However, only few of the LCN2-related studies have investigated whether LCN2 constitutes a causal factor of the metabolic conditions in animals. One of the best strategies to prevent obesity and its associated inflammation is participation in regular physical activity. Objective: This study was designed to test the hypothesis that exercise mitigates this inflammatory response, thereby improving insulin sensitivity, we tested whether there is an insulin-sensitizing effect of exercise is associated with related changes in circulating LCN2 levels in rats. Design: A total number of 24 adult healthy male albino rats were used. Rats were divided into three groups: group I (control, C), group II (model of pre-diabetic obese rats without exercise, PD) and group III (model of pre-diabetic obese rats with acute voluntary exercise, PDE). Results: This study revealed that after a 2 days acute exercise program, insulin sensitivity was improved, as indicated by a significant decrease in serum insulin (1.98±0.04), serum glucose (121.75±2.85) and Homeostasis Model Assessment for Insulin Resistance Index (HOMA-IR) (0.59±0.02) in PDE in comparison to corresponding values in PD group (3.94±0.08), (159±1.49) and (1.44±0.11) respectively. Also, Serum LCN2 concentrations were significantly decreased (62.88±1.79) in PDE group in comparison to PD group (94.75±3.36). Conclusion: We concluded that exercise has an insulin sensitizing effect in the pre-diabetic stage and its mechanism could involve a reduction in LCN2 levels in exercise-trained group.
| Published in | American Journal of Clinical and Experimental Medicine (Volume 3, Issue 3) |
| DOI | 10.11648/j.ajcem.20150303.16 |
| Page(s) | 105-109 |
| 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), 2015. Published by Science Publishing Group |
Insulin Resistance, Lipocalin 2, Glucose, Adipocytes, Exercise, HOMA-IR, Rats
| [1] | Yan, Q.W., et al., The adipokine lipocalin 2 is regulated by obesity and promotes insulin resistance. Diabetes, 2007. 56(10): p. 2533-40. |
| [2] | Zhang, J., et al., The role of lipocalin 2 in the regulation of inflammation in adipocytes and macrophages. Mol Endocrinol, 2008. 22(6): p. 1416-26. |
| [3] | Guo, H., et al., Lipocalin-2 deficiency impairs thermogenesis and potentiates diet-induced insulin resistance in mice. Diabetes, 2010. 59(6): p. 1376-85. |
| [4] | Zhang, Y., et al., Lipocalin 2 expression and secretion is highly regulated by metabolic stress, cytokines, and nutrients in adipocytes. PLoS One, 2014. 9(5): p. e96997. |
| [5] | Teixeira-Lemos, E., et al., Regular physical exercise training assists in preventing type 2 diabetes development: focus on its antioxidant and anti-inflammatory properties. Cardiovasc Diabetol, 2011. 10: p. 12. |
| [6] | Conn, V.S., et al., Metabolic effects of interventions to increase exercise in adults with type 2 diabetes. Diabetologia, 2007. 50(5): p. 913-21. |
| [7] | Saely, C.H., K. Geiger, and H. Drexel, Brown versus white adipose tissue: a mini-review. Gerontology, 2012. 58(1): p. 15-23. |
| [8] | Kiess, W., et al., Adipocytes and adipose tissue. Best Pract Res Clin Endocrinol Metab, 2008. 22(1): p. 135-53. |
| [9] | Seneff, S., G. Wainwright, and L. Mascitelli, Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet? Arch Med Sci, 2011. 7(1): p. 8-20. |
| [10] | Coelho, M., T. Oliveira, and R. Fernandes, Biochemistry of adipose tissue: an endocrine organ. Archives of Medical Science : AMS, 2013. 9(2): p. 191-200. |
| [11] | Sun, K., C.M. Kusminski, and P.E. Scherer, Adipose tissue remodeling and obesity. The Journal of Clinical Investigation, 2011. 121(6): p. 2094-2101. |
| [12] | Roupas, N.D., et al., The effect of prolonged aerobic exercise on serum adipokine levels during an ultra-marathon endurance race. Hormones (Athens), 2013. 12(2): p. 275-82. |
| [13] | Guo, H., et al., Evidence for the Regulatory Role of Lipocalin 2 in High-Fat Diet-Induced Adipose Tissue Remodeling in Male Mice. Endocrinology, 2013. 154(10): p. 3525-3538. |
| [14] | Alwahsh, S.M., et al., Diet high in fructose leads to an overexpression of lipocalin-2 in rat fatty liver. World J Gastroenterol, 2014. 20(7): p. 1807-21. |
| [15] | Lopes, L.R., et al., Reduced inflammatory response in rats fed fat-rich diets: Role of leukotrienes. Life Sciences, 2000. 67(1): p. 13-21. |
| [16] | Ropelle, E.R., et al., Acute exercise modulates the Foxo1/PGC-1α pathway in the liver of diet-induced obesity rats. The Journal of Physiology, 2009. 587(9): p. 2069-2076. |
| [17] | Nayak, Y. and V. Hillemane, Antidiabetic activity of benzopyrone analogues in nicotinamide-streptozotocin induced type 2 diabetes in rats. 2014. 2014: p. 854267. |
| [18] | Bonora, E., et al., Homeostasis model assessment closely mirrors the glucose clamp technique in the assessment of insulin sensitivity: studies in subjects with various degrees of glucose tolerance and insulin sensitivity. Diabetes Care, 2000. 23(1): p. 57-63. |
| [19] | Catalan, V., et al., Increased adipose tissue expression of lipocalin-2 in obesity is related to inflammation and matrix metalloproteinase-2 and metalloproteinase-9 activities in humans. J Mol Med (Berl), 2009. 87(8): p. 803-13. |
| [20] | Sommer, G., et al., Lipocalin-2 is induced by interleukin-1beta in murine adipocytes in vitro. J Cell Biochem, 2009. 106(1): p. 103-8. |
| [21] | Luciano, E., et al., Endurance training improves responsiveness to insulin and modulates insulin signal transduction through the phosphatidylinositol 3-kinase/Akt-1 pathway. Eur J Endocrinol, 2002. 147(1): p. 149-57. |
| [22] | Aoi, W., et al., Effect of exercise on hepatic gene expression in rats: a microarray analysis. Life Sci, 2004. 75(26): p. 3117-28. |
| [23] | Flores, M.B., et al., Exercise improves insulin and leptin sensitivity in hypothalamus of Wistar rats. Diabetes, 2006. 55(9): p. 2554-61. |
| [24] | Pauli, J.R., et al., Acute physical exercise reverses S-nitrosation of the insulin receptor, insulin receptor substrate 1 and protein kinase B/Akt in diet-induced obese Wistar rats. J Physiol, 2008. 586(2): p. 659-71. |
| [25] | Peres, S.B., et al., Endurance exercise training increases insulin responsiveness in isolated adipocytes through IRS/PI3-kinase/Akt pathway. J Appl Physiol (1985), 2005. 98(3): p. 1037-43. |
| [26] | Ropelle, E.R., et al., Reversal of diet-induced insulin resistance with a single bout of exercise in the rat: the role of PTP1B and IRS-1 serine phosphorylation. J Physiol, 2006. 577(Pt 3): p. 997-1007. |
| [27] | Law, I.K., et al., Lipocalin-2 deficiency attenuates insulin resistance associated with aging and obesity. Diabetes, 2010. 59(4): p. 872-82. |
| [28] | Jun, L.S., C.P. Siddall, and E.D. Rosen, A minor role for lipocalin 2 in high-fat diet-induced glucose intolerance. Am J Physiol Endocrinol Metab, 2011. 301(5): p. E825-35. |
| [29] | Guo, H., et al., Evidence for the regulatory role of lipocalin 2 in high-fat diet-induced adipose tissue remodeling in male mice. Endocrinology, 2013. 154(10): p. 3525-38. |
| [30] | Paton, C.M., et al., Lipocalin-2 increases fat oxidation in vitro and is correlated with energy expenditure in normal weight but not obese women. Obesity (Silver Spring), 2013. 21(12): p. E640-8. |
| [31] | DeFronzo, R.A., From the Triumvirate to the Ominous Octet: A New Paradigm for the Treatment of Type 2 Diabetes Mellitus. Diabetes, 2009. 58(4): p. 773-795. |
APA Style
Rania Reafaat Abdelkader Atia, Khaled Abdelfattah Abdelhamid Abulfadle. (2015). Serum Lipocalin 2 Levels in Acute Exercised Prediabetic Rat Model in Comparison to Normal Healthy Control. American Journal of Clinical and Experimental Medicine, 3(3), 105-109. https://doi.org/10.11648/j.ajcem.20150303.16
ACS Style
Rania Reafaat Abdelkader Atia; Khaled Abdelfattah Abdelhamid Abulfadle. Serum Lipocalin 2 Levels in Acute Exercised Prediabetic Rat Model in Comparison to Normal Healthy Control. Am. J. Clin. Exp. Med. 2015, 3(3), 105-109. doi: 10.11648/j.ajcem.20150303.16
AMA Style
Rania Reafaat Abdelkader Atia, Khaled Abdelfattah Abdelhamid Abulfadle. Serum Lipocalin 2 Levels in Acute Exercised Prediabetic Rat Model in Comparison to Normal Healthy Control. Am J Clin Exp Med. 2015;3(3):105-109. doi: 10.11648/j.ajcem.20150303.16
Share This Article
Twitter
Linked In
Facebook
Copy
Download@article{10.11648/j.ajcem.20150303.16,
author = {Rania Reafaat Abdelkader Atia and Khaled Abdelfattah Abdelhamid Abulfadle},
title = {Serum Lipocalin 2 Levels in Acute Exercised Prediabetic Rat Model in Comparison to Normal Healthy Control},
journal = {American Journal of Clinical and Experimental Medicine},
volume = {3},
number = {3},
pages = {105-109},
doi = {10.11648/j.ajcem.20150303.16},
url = {https://doi.org/10.11648/j.ajcem.20150303.16},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ajcem.20150303.16},
abstract = {Background: Excess caloric intake expands adipose tissue resulting in a higher risk of metabolic disease. Lipocalin 2 (LCN2) is an adipokine having a role in innate immunity and energy metabolism. It is an acute phase protein that was recently correlated with potential effects on obesity and inflammation. The reaction of this protein to progressive exercise in animals has limited studies. Exercise encourages weight loss and improves insulin sympathy. However, the molecular mechanisms mediating its beneficial effects are not fully understood. Obesity associates with increased production of inflammatory cytokines, which in turn, subsidizes to systemic insulin resistance. LCN2 has been shown to have a significant association with body mass index (BMI). However, only few of the LCN2-related studies have investigated whether LCN2 constitutes a causal factor of the metabolic conditions in animals. One of the best strategies to prevent obesity and its associated inflammation is participation in regular physical activity. Objective: This study was designed to test the hypothesis that exercise mitigates this inflammatory response, thereby improving insulin sensitivity, we tested whether there is an insulin-sensitizing effect of exercise is associated with related changes in circulating LCN2 levels in rats. Design: A total number of 24 adult healthy male albino rats were used. Rats were divided into three groups: group I (control, C), group II (model of pre-diabetic obese rats without exercise, PD) and group III (model of pre-diabetic obese rats with acute voluntary exercise, PDE). Results: This study revealed that after a 2 days acute exercise program, insulin sensitivity was improved, as indicated by a significant decrease in serum insulin (1.98±0.04), serum glucose (121.75±2.85) and Homeostasis Model Assessment for Insulin Resistance Index (HOMA-IR) (0.59±0.02) in PDE in comparison to corresponding values in PD group (3.94±0.08), (159±1.49) and (1.44±0.11) respectively. Also, Serum LCN2 concentrations were significantly decreased (62.88±1.79) in PDE group in comparison to PD group (94.75±3.36). Conclusion: We concluded that exercise has an insulin sensitizing effect in the pre-diabetic stage and its mechanism could involve a reduction in LCN2 levels in exercise-trained group.},
year = {2015}
}
TY - JOUR T1 - Serum Lipocalin 2 Levels in Acute Exercised Prediabetic Rat Model in Comparison to Normal Healthy Control AU - Rania Reafaat Abdelkader Atia AU - Khaled Abdelfattah Abdelhamid Abulfadle Y1 - 2015/05/13 PY - 2015 N1 - https://doi.org/10.11648/j.ajcem.20150303.16 DO - 10.11648/j.ajcem.20150303.16 T2 - American Journal of Clinical and Experimental Medicine JF - American Journal of Clinical and Experimental Medicine JO - American Journal of Clinical and Experimental Medicine SP - 105 EP - 109 PB - Science Publishing Group SN - 2330-8133 UR - https://doi.org/10.11648/j.ajcem.20150303.16 AB - Background: Excess caloric intake expands adipose tissue resulting in a higher risk of metabolic disease. Lipocalin 2 (LCN2) is an adipokine having a role in innate immunity and energy metabolism. It is an acute phase protein that was recently correlated with potential effects on obesity and inflammation. The reaction of this protein to progressive exercise in animals has limited studies. Exercise encourages weight loss and improves insulin sympathy. However, the molecular mechanisms mediating its beneficial effects are not fully understood. Obesity associates with increased production of inflammatory cytokines, which in turn, subsidizes to systemic insulin resistance. LCN2 has been shown to have a significant association with body mass index (BMI). However, only few of the LCN2-related studies have investigated whether LCN2 constitutes a causal factor of the metabolic conditions in animals. One of the best strategies to prevent obesity and its associated inflammation is participation in regular physical activity. Objective: This study was designed to test the hypothesis that exercise mitigates this inflammatory response, thereby improving insulin sensitivity, we tested whether there is an insulin-sensitizing effect of exercise is associated with related changes in circulating LCN2 levels in rats. Design: A total number of 24 adult healthy male albino rats were used. Rats were divided into three groups: group I (control, C), group II (model of pre-diabetic obese rats without exercise, PD) and group III (model of pre-diabetic obese rats with acute voluntary exercise, PDE). Results: This study revealed that after a 2 days acute exercise program, insulin sensitivity was improved, as indicated by a significant decrease in serum insulin (1.98±0.04), serum glucose (121.75±2.85) and Homeostasis Model Assessment for Insulin Resistance Index (HOMA-IR) (0.59±0.02) in PDE in comparison to corresponding values in PD group (3.94±0.08), (159±1.49) and (1.44±0.11) respectively. Also, Serum LCN2 concentrations were significantly decreased (62.88±1.79) in PDE group in comparison to PD group (94.75±3.36). Conclusion: We concluded that exercise has an insulin sensitizing effect in the pre-diabetic stage and its mechanism could involve a reduction in LCN2 levels in exercise-trained group. VL - 3 IS - 3 ER -
Information
Email: