ORIGINAL PAPER
Continuous and intermittent exercise training responses in liver and white adipose tissue aquaglyceroporins
More details
Hide details
1
Department of Exercise Physiology, Faculty of Physical Education and Sports Sciences, University of Mazandaran, Babolsar, Iran
2
Escola Superior de Desporto e Lazer, Instituto Politécnico de Viana do Castelo, Viana do Castelo, Portugal
3
Research Centre in Sports Sciences, Health Sciences and Human Development, Vila Real, Portugal
4
Tumour and Microenvironment Interactions Group, Institute of Biomedical Engineering, i3S – Instituto de Investigação e Inovação em Saúde, University of Porto, Porto, Portugal
Submission date: 2020-01-28
Acceptance date: 2021-05-17
Publication date: 2021-08-17
Hum Mov. 2022;23(1):105-112
KEYWORDS
TOPICS
ABSTRACT
Purpose:
We analysed the effects of moderate-intensity continuous training (MICT) and high-intensity interval training (HIIT) on hepatic and adipose tissue aquaglyceroporins (AQPs) in rats fed with high-fat diet (HFD).
Methods:
Overall, 48 male Wistar rats were fed with a normal diet (ND, 10.4 kcal% fat) or HFD (62.1 kcal% fat) over 10 weeks. Then, the animals were divided into 6 groups: ND sedentary (NS), N + MICT, N + HIIT, HS, H + MICT, and H + HIIT. The trained animals performed 10-week matched distances of MICT and HIIT on a motorized treadmill (5 times/week) while maintaining dietary treatments. The liver and epididymal white adipose tissue (eWAT) were investigated to determine triglycerides (TG) and AQP7 and AQP9 levels.
Results:
HFD increased body weight, liver and eWAT weight, plasma insulin and glucose levels, and insulin resistance. Both MICT and HIIT were able to decrease body weight and liver and eWAT weight in the HFD-fed group. HFD increased plasma TG, glucose, and insulin levels, attenuated by MICT and HIIT programs. HFD increased TG content and AQP7 and did not alter AQP9. MICT and HIIT programs decreased hepatic TG content and AQP7 and AQP9 levels in ND-fed animals. In HFD-fed animals, only MICT decreased AQP9, and both MICT and HIIT decreased TG content and AQP7 levels in eWAT.
Conclusions:
Our findings suggest that the regulation of adipose tissue AQP7 and hepatic AQP9 by both MICT and HIIT interventions can have a significant effect on fat metabolism and glucose homeostasis.
REFERENCES (29)
1.
Rodríguez A, Catalán V, Gómez-Ambrosi J, Frühbeck G. Aquaglyceroporins serve as metabolic gateways in adiposity and insulin resistance control. Cell Cycle. 2011;10(10):1548–1556; doi: 10.4161/cc.10.10.15672.
2.
Costa R, Rodrigues I, Guardão L, Rocha-Rodrigues S, Silva C, Magalhães J, et al. Xanthohumol and 8-prenylnaringenin ameliorate diabetic-related metabolic dysfunctions in mice. J Nutr Biochem. 2017;45:39–47; doi: 10.1016/j.jnutbio.2017.03.006.
3.
Frühbeck G, Méndez-Giménez L, Fernández-Formoso J-A, Fernández S, Rodríguez A. Regulation of adipocyte lipolysis. Nutr Res Rev. 2014;27(1):63–93; doi: 10.1017/S095442241400002X.
4.
Rodríguez A, Catalán V, Gómez-Ambrosi J, García-Navarro S, Rotellar F, Valentí V, et al. Insulin- and leptin-mediated control of aquaglyceroporins in human adipocytes and hepatocytes is mediated via the PI3K/Akt/mTOR signaling cascade. J Clin Endocrinol Metab.
5.
2011;96(4):E586–E597; doi: 10.1210/jc.2010-1408.
6.
Kuriyama H, Shimomura I, Kishida K, Kondo H, Furuyama N, Nishizawa H, et al. Coordinated regulation of fat-specific and liver-specific glycerol channels, aquaporin adipose and aquaporin 9. Diabetes. 2002;51(10):2915–2921; doi: 10.2337/diabetes.51.10.2915.
7.
Gonçalves IO, Passos E, Rocha-Rodrigues S, Torrella JR, Rizo D, Santos-Alves E, et al. Physical exercise antagonizes clinical and anatomical features characterizing Lieber-DeCarli diet-induced obesity and related metabolic disorders. Clin Nutr. 2015;34(2):241–247; doi: 10.1016/j.clnu.2014.03.010.
8.
Rocha-Rodrigues S, Rodríguez A, Becerril S, Ramírez B, Gonçalves IO, Beleza J, et al. Physical exercise remodels visceral adipose tissue and mitochondrial lipid metabolism in rats fed a high-fat diet. Clin Exp Pharmacol Physiol. 2017;44(3):386–394; doi: 10.1111/1440-1681.12706.
9.
Lebeck J, Østergård T, Rojek A, Füchtbauer E-M, Lund S, Nielsen S, et al. Gender-specific effect of physical training on AQP7 protein expression in human adipose tissue. Acta Diabetol. 2012;49(Suppl. 1):S215–S226; doi: 10.1007/s00592-012-0430-1.
10.
Trachta P, Drápalová J, Kaválková P, Toušková V, Cinkajzlová A, Lacinová Z, et al. Three months of regular aerobic exercise in patients with obesity improve systemic subclinical inflammation without major influence on blood pressure and endocrine production of subcutaneous fat. Physiol Res. 2014;63(Suppl. 2):299–308; doi: 10.33549/physiolres.932792.
11.
Ahmadi-Kani Golzar F, Fathi R, Mahjoub S. High-fat diet leads to adiposity and adipose tissue inflammation: the effect of whey protein supplementation and aerobic exercise training. Appl Physiol Nutr Metab. 2019;44(3):255–262; doi: 10.1139/apnm-2018-0307.
12.
Maillard F, Vazeille E, Sauvanet P, Sirvent P, Combaret L, Sourdrille A, et al. High intensity interval training promotes total and visceral fat mass loss in obese Zucker rats without modulating gut microbiota. PLoS One. 2019;14(4):e0214660; doi: 10.1371/journal.pone.0214660.
13.
Antunes LC, Elkfury JL, Jornada MN, Foletto KC, Bertoluci MC. Validation of HOMA-IR in a model of insulin- resistance induced by a high-fat diet in Wistar rats. Arch Endocrinol Metab. 2016;60(2):138–142; doi: 10.1590/2359-3997000000169.
14.
Lebeck J. Metabolic impact of the glycerol channels AQP7 and AQP9 in adipose tissue and liver. J Mol Endocrinol. 2014;52(2):R165–R178; doi: 10.1530/JME-13-0268.
15.
Rotondo F, Ho-Palma AC, Remesar X, Fernández-López JA, del Mar Romero M, Alemany M. Glycerol is synthesized and secreted by adipocytes to dispose of excess glucose, via glycerogenesis and increased acyl-glycerol turnover. Sci Rep. 2017;7(1):8983; doi: 10.1038/s41598-017-09450-4.
16.
Catalán V, Gómez-Ambrosi J, Pastor C, Rotellar F, Silva C, Rodríguez A, et al. Influence of morbid obesity and insulin resistance on gene expression levels of AQP7 in visceral adipose tissue and AQP9 in liver. Obes Surg. 2008;18(6):695–701; doi: 10.1007/s11695-008-9453-7.
17.
Kishida K, Kuriyama H, Funahashi T, Shimomura I, Kihara S, Ouchi N, et al. Aquaporin adipose, a putative glycerol channel in adipocytes. J Biol Chem. 2000;275(27):20896–20902; doi: 10.1074/jbc.M001119200.
18.
Lee D-H, Park D-B, Lee Y-K, An C-S, Oh Y-S, Kang J-S, et al. The effects of thiazolidinedione treatment on the regulations of aquaglyceroporins and glycerol kinase in OLETF rats. Metabolism. 2005;54(10):1282–1289; doi: 10.1016/j.metabol.2005.04.015.
19.
Prudente S, Flex E, Morini E, Turchi F, Capponi D, De Cosmo S, et al. A functional variant of the adipocyte glycerol channel aquaporin 7 gene is associated with obesity and related metabolic abnormalities. Diabetes. 2007;56(5):1468–1474; doi: 10.2337/db06-1389.
20.
Ceperuelo-Mallafré V, Miranda M, Chacón MR, Vilarrasa N, Megia A, Gutiérrez C, et al. Adipose tissue expression of the glycerol channel aquaporin-7 gene is altered in severe obesity but not in type 2 diabetes. J Clin Endocrinol Metab. 2007;92(9):3640–3645; doi: 10.1210/jc.2007-0531.
21.
Rodríguez A, Catalán V, Gómez-Ambrosi J, Frühbeck G. Role of aquaporin-7 in the pathophysiological control of fat accumulation in mice. FEBS Lett. 2006;580(20):4771–4776; doi: 10.1016/j.febslet.2006.07.080.
22.
Arner P. Human fat cell lipolysis: biochemistry, regulation and clinical role. Best Pract Res Clin Endocrinol Metab. 2005;19(4):471–482; doi: 10.1016/j.beem.2005.07.004.
23.
Rodríguez A, Catalán V, Gómez-Ambrosi J, Frühbeck G. Visceral and subcutaneous adiposity: are both potential therapeutic targets for tackling the metabolic syndrome? Curr Pharm Des. 2007;13(21):2169–2175; doi: 10.2174/138161207781039599.
24.
Gena P, Mastrodonato M, Portincasa P, Fanelli E, Mentino D, Rodríguez A, et al. Liver glycerol permeability and aquaporin-9 are dysregulated in a murine model of non-alcoholic fatty liver disease. PLoS One. 2013; 8(10):e78139; doi: 10.1371/journal.pone.0078139.
25.
Gena P, Del Buono N, D’Abbicco M, Mastrodonato M, Berardi M, Svelto M, et al. Dynamical modeling of liver aquaporin-9 expression and glycerol permeability in hepatic glucose metabolism. Eur J Cell Biol. 2017;96(1):61–69; doi: 10.1016/j.ejcb.2016.12.003.
26.
Cai C, Wang C, Ji W, Liu B, Kang Y, Hu Z, et al. Knockdown of hepatic aquaglyceroporin-9 alleviates high fat diet-induced non-alcoholic fatty liver disease in rats. Int Immunopharmacol. 2013;15(3):550–556; doi: 10.1016/j.intimp.2013.01.020.
27.
Londos C, Brasaemle DL, Schultz CJ, Adler-Wailes DC, Levin DM, Kimmel AR, et al. On the control of lipolysis in adipocytes. Ann N Y Acad Sci. 1999;892:155–168; doi: 10.1111/j.1749-6632.1999.tb07794.x.
28.
Wewege M, van den Berg R, Ward RE, Keech A. The effects of high-intensity interval training vs. moderate-intensity continuous training on body composition in overweight and obese adults: a systematic review and meta-analysis. Obes Rev. 2017;18(6):635–646; doi: 10.1111/obr.12532.
29.
Kawano Y, Cohen DE. Mechanisms of hepatic triglyceride accumulation in non-alcoholic fatty liver disease. J Gastroenterol. 2013;48(4):434–441; doi: 10.1007/s00535-013-0758-5.