Exercise decrease the expression of MCP-1 in perivascular adipose tissue (PVAT) in obese mice

Hotimah Masdan  Salim; Aisyah Aisyah; Michio Shimabukuro

doi:10.15562/bmj.v11i3.3496

Exercise decrease the expression of MCP-1 in perivascular adipose tissue (PVAT) in obese mice

Hotimah Masdan Salim ,

Aisyah Aisyah ,

Michio Shimabukuro ,

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DOI: https://doi.org/10.15562/bmj.v11i3.3496 |
Published: 2022-09-11

Abstract

Introduction: Exercise has been believed to prevent metabolic syndrome (Mets) from occurring. Accumulation of inflammation factors such as monocytes chemoattractant protein-1 (MCP1) in adipose tissue is a factor in the development of MetS. However, the inflammatory mediators that play a role in the accumulation of macrophages are still unclear, so this study aims to determine the expression of MCP-1 in perivascular adipose tissue (PVAT).

Methods: Eight-week-old male wild-type mice, were divided into five groups. One control group was given a standard diet and four groups were given a high-fat diet (HFD) for 2 weeks. Exercise treatment was given to the HFD group by dividing HFD with exercise once a week, HFD with exercise three times a week, and HFD with exercise five times a week. As for the exercise, speed is given 10-18m/minute for 30 minutes. and this exercise is carried out for two weeks. Gene expression of MCP-1 in PVAT tissues was analyzed using quantitative chain reaction (PCR).

Results: The HFD group experienced an increase in body weight (P <0.01) and adipose tissue mass (P <0.01) compared to the control group. Furthermore, exercise decreased body weight (P <0.05) and adipose tissue in the HFD-Exc1 group (P <0.01). Furthermore, exercise tends to decrease the inflammatory mediator in macrophages MCP-1 in PVAT compared to the HFD group.

Conclusion: These results suggested that exercise partially reduces adiposity, tended to decreases MCP-1 in HFD-induced obesity.

References

Wynn TA, Chawla A, Pollard JW. Macrophage biology in development, homeostasis and disease. Nature. 2013;496(7446):445–55.
Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol. 2011;29:415–45.
Cancello R, Henegar C, Viguerie N, Taleb S, Poitou C, Rouault C, et al. Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss. Diabetes. 2005;54(8):2277–86.
McNelis JC, Olefsky JM. Macrophages, immunity, and metabolic disease. Immunity. 2014;41(1):36–48.
Hardy OT, Perugini RA, Nicoloro SM, Gallagher-Dorval K, Puri V, Straubhaar J, et al. Body mass index-independent inflammation in omental adipose tissue associated with insulin resistance in morbid obesity. Surg Obes Relat Dis Off J Am Soc Bariatr Surg. 2011;7(1):60–7.
Dallaire P, Bellmann K, Laplante M, Gélinas S, Centeno-Baez C, Penfornis P, et al. Obese mice lacking inducible nitric oxide synthase are sensitized to the metabolic actions of peroxisome proliferator-activated receptor-γ agonism. Diabetes. 2008;57(8):1999–2011.
Yang ZP, Xie YH, Ling DY, Li JR, Jiang J, Fan YH, et al. SCYL1BP1 has tumor-suppressive functions in human lung squamous carcinoma cells by regulating degradation of MDM2. Asian Pacific J Cancer Prev. 2014;15(17):7467–71.
Kamei N, Tobe K, Suzuki R, Ohsugi M, Watanabe T, Kubota N, et al. Overexpression of monocyte chemoattractant protein-1 in adipose tissues causes macrophage recruitment and insulin resistance. J Biol Chem. 2006;281(36):26602–14.
Duncan GE, Perri MG, Theriaque DW, Hutson AD, Eckel RH, Stacpoole PW. Exercise training, without weight loss, increases insulin sensitivity and postheparin plasma lipase activity in previously sedentary adults. Diabetes Care. 2003;26(3):557–62.
Henriksen EJ. Invited review: Effects of acute exercise and exercise training on insulin resistance. J Appl Physiol. 2002;93(2):788–96.
Bruun JM, Helge JW, Richelsen B, Stallknecht B. Diet and exercise reduce low-grade inflammation and macrophage infiltration in adipose tissue but not in skeletal muscle in severely obese subjects. Am J Physiol Endocrinol Metab. 2006;290(5):E961-7.
Ji LL. Modulation of skeletal muscle antioxidant defense by exercise: Role of redox signaling. Free Radic Biol Med. 2008;44(2):142–52.
Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003;112(12):1821–30.
Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante AWJ. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003;112(12):1796–808.
Schäffler A, Müller-Ladner U, Schölmerich J, Büchler C. Role of adipose tissue as an inflammatory organ in human diseases. Endocr Rev. 2006;27(5):449–67.
Wueest S, Rapold RA, Schumann DM, Rytka JM, Schildknecht A, Nov O, et al. Deletion of Fas in adipocytes relieves adipose tissue inflammation and hepatic manifestations of obesity in mice. J Clin Invest. 2010;120(1):191–202.
Kawanishi N, Yano H, Yokogawa Y, Suzuki K. Exercise training inhibits inflammation in adipose tissue via both suppression of macrophage infiltration and acceleration of phenotypic switching from M1 to M2 macrophages in high-fat-diet-induced obese mice. Exerc Immunol Rev. 2010;16:105–18.
Samaan MC, Marcinko K, Sikkema S, Fullerton MD, Ziafazeli T, Khan MI, et al. Endurance interval training in obese mice reduces muscle inflammation and macrophage content independently of weight loss. Physiol Rep. 2014;2(5).
Bradley RL, Jeon JY, Liu F-F, Maratos-Flier E. Voluntary exercise improves insulin sensitivity and adipose tissue inflammation in diet-induced obese mice. Am J Physiol Endocrinol Metab. 2008;295(3):E586-94.
Boardman NT, Hafstad AD, Lund J, Rossvoll L, Aasum E. Exercise of obese mice induces cardioprotection and oxygen sparing in hearts exposed to high-fat load. Am J Physiol Heart Circ Physiol. 2017;313(5):H1054–62.

[1] Wynn TA, Chawla A, Pollard JW. Macrophage biology in development, homeostasis and disease. Nature. 2013;496(7446):445–55.

[2] Gregor MF, Hotamisligil GS. Inflammatory mechanisms in obesity. Annu Rev Immunol. 2011;29:415–45.

[3] Cancello R, Henegar C, Viguerie N, Taleb S, Poitou C, Rouault C, et al. Reduction of macrophage infiltration and chemoattractant gene expression changes in white adipose tissue of morbidly obese subjects after surgery-induced weight loss. Diabetes. 2005;54(8):2277–86.

[4] McNelis JC, Olefsky JM. Macrophages, immunity, and metabolic disease. Immunity. 2014;41(1):36–48.

[5] Hardy OT, Perugini RA, Nicoloro SM, Gallagher-Dorval K, Puri V, Straubhaar J, et al. Body mass index-independent inflammation in omental adipose tissue associated with insulin resistance in morbid obesity. Surg Obes Relat Dis Off J Am Soc Bariatr Surg. 2011;7(1):60–7.

[6] Dallaire P, Bellmann K, Laplante M, Gélinas S, Centeno-Baez C, Penfornis P, et al. Obese mice lacking inducible nitric oxide synthase are sensitized to the metabolic actions of peroxisome proliferator-activated receptor-γ agonism. Diabetes. 2008;57(8):1999–2011.

[7] Yang ZP, Xie YH, Ling DY, Li JR, Jiang J, Fan YH, et al. SCYL1BP1 has tumor-suppressive functions in human lung squamous carcinoma cells by regulating degradation of MDM2. Asian Pacific J Cancer Prev. 2014;15(17):7467–71.

[8] Kamei N, Tobe K, Suzuki R, Ohsugi M, Watanabe T, Kubota N, et al. Overexpression of monocyte chemoattractant protein-1 in adipose tissues causes macrophage recruitment and insulin resistance. J Biol Chem. 2006;281(36):26602–14.

[9] Duncan GE, Perri MG, Theriaque DW, Hutson AD, Eckel RH, Stacpoole PW. Exercise training, without weight loss, increases insulin sensitivity and postheparin plasma lipase activity in previously sedentary adults. Diabetes Care. 2003;26(3):557–62.

[10] Henriksen EJ. Invited review: Effects of acute exercise and exercise training on insulin resistance. J Appl Physiol. 2002;93(2):788–96.

[11] Bruun JM, Helge JW, Richelsen B, Stallknecht B. Diet and exercise reduce low-grade inflammation and macrophage infiltration in adipose tissue but not in skeletal muscle in severely obese subjects. Am J Physiol Endocrinol Metab. 2006;290(5):E961-7.

[12] Ji LL. Modulation of skeletal muscle antioxidant defense by exercise: Role of redox signaling. Free Radic Biol Med. 2008;44(2):142–52.

[13] Xu H, Barnes GT, Yang Q, Tan G, Yang D, Chou CJ, et al. Chronic inflammation in fat plays a crucial role in the development of obesity-related insulin resistance. J Clin Invest. 2003;112(12):1821–30.

[14] Weisberg SP, McCann D, Desai M, Rosenbaum M, Leibel RL, Ferrante AWJ. Obesity is associated with macrophage accumulation in adipose tissue. J Clin Invest. 2003;112(12):1796–808.

[15] Schäffler A, Müller-Ladner U, Schölmerich J, Büchler C. Role of adipose tissue as an inflammatory organ in human diseases. Endocr Rev. 2006;27(5):449–67.

[16] Wueest S, Rapold RA, Schumann DM, Rytka JM, Schildknecht A, Nov O, et al. Deletion of Fas in adipocytes relieves adipose tissue inflammation and hepatic manifestations of obesity in mice. J Clin Invest. 2010;120(1):191–202.

[17] Kawanishi N, Yano H, Yokogawa Y, Suzuki K. Exercise training inhibits inflammation in adipose tissue via both suppression of macrophage infiltration and acceleration of phenotypic switching from M1 to M2 macrophages in high-fat-diet-induced obese mice. Exerc Immunol Rev. 2010;16:105–18.

[18] Samaan MC, Marcinko K, Sikkema S, Fullerton MD, Ziafazeli T, Khan MI, et al. Endurance interval training in obese mice reduces muscle inflammation and macrophage content independently of weight loss. Physiol Rep. 2014;2(5).

[19] Bradley RL, Jeon JY, Liu F-F, Maratos-Flier E. Voluntary exercise improves insulin sensitivity and adipose tissue inflammation in diet-induced obese mice. Am J Physiol Endocrinol Metab. 2008;295(3):E586-94.

[20] Boardman NT, Hafstad AD, Lund J, Rossvoll L, Aasum E. Exercise of obese mice induces cardioprotection and oxygen sparing in hearts exposed to high-fat load. Am J Physiol Heart Circ Physiol. 2017;313(5):H1054–62.

Exercise decrease the expression of MCP-1 in perivascular adipose tissue (PVAT) in obese mice

Abstract

References

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