Next Article in Journal
Association and Risk Factors for Obstructive Sleep Apnea and Cardiovascular Diseases: A Systematic Review
Next Article in Special Issue
Structural Analysis of SMYD3 Lysine Methyltransferase for the Development of Competitive and Specific Enzyme Inhibitors
Previous Article in Journal
Colorectal Dysplasia and Cancer Surveillance in Ulcerative Colitis
Previous Article in Special Issue
Anticancer Impact of Nitric Oxide (NO) and NO Combination with SMYD-3 Inhibitor on Breast Carcinomas
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:

Ageing and Obesity Shared Patterns: From Molecular Pathogenesis to Epigenetics

Abdelaziz Ghanemi
Mayumi Yoshioka
1,2 and
Jonny St-Amand
Functional Genomics Laboratory, Endocrinology and Nephrology Axis, CHU de Québec-Université Laval Research Center, Québec City, QC G1V 4G2, Canada
Department of Molecular Medicine, Faculty of Medicine, Laval University, Québec City, QC G1V 0A6, Canada
Author to whom correspondence should be addressed.
Diseases 2021, 9(4), 87;
Submission received: 29 October 2021 / Revised: 23 November 2021 / Accepted: 28 November 2021 / Published: 29 November 2021
(This article belongs to the Special Issue Epigenetics and Disease II)


In modern societies, ageing and obesity represent medical challenges for healthcare professionals and caregivers. Obesity and ageing share common features including the related cellular and molecular pathways as well as the impacts they have as risk factors for a variety of diseases and health problems. Both of these health problems also share exercise and a healthy lifestyle as the best therapeutic options. Importantly, ageing and obesity also have common epigenetic changes (histone modification, DNA methylation, noncoding RNAs, and chromatin remodeling) that are also impacted by exercise. This suggests that epigenetic pathways are among the mechanisms via which exercise induces its benefits, including ageing and obesity improvements. Exploring these interrelations and based on the fact that both ageing and obesity represent risk factors for each other, would lead to optimizing the available therapeutic approaches towards improved obesity management and healthy ageing.

1. Biological Similarities between Ageing and Obesity

Ageing and obesity are major topics in biomedical studies, mainly because both represent risk factors for numerous diseases and health conditions [1]. The modern lifestyle and industrial development have increased obesity rates as well as the aged population percentage worldwide. Obesity is specifically increasing among the elderly [2,3], which contributes to sarcopenic obesity, a chronic, age-related class of obesity [4,5]. These interactions between two important risk factors strengthen the need to further deepen our biological and clinical understanding of the interrelation and correlations between ageing and obesity. Such mechanistic elucidation would allow to develop the medical care including geriatrics and obesity management, among other chronic diseases. Within this piece of writing, we aim to elucidate selected links between ageing and obesity through different illustrations starting from pathogenesis and molecular pathways towards epigenetics, supported by evidences from exercise being a therapeutic tool for both.
Obesity is defined as an abnormal accumulation of adiposity resulting from a disturbed energy balance in which energy intake is higher than energy expenditure [6] with a modified metabolic phenotype [7], complex neuroendocrine changes [8], and pathogenic implications [9]. Obesity has even been classified as a disease [10] and associated with health problems including impaired fertility [11,12], neurodegenerative disease [13], cognitive decline (in mid-life) [14], coronavirus disease 2019 (COVID-19) severity and resulting health problems [15,16,17,18], type 2 diabetes [19], cancer [20], cardiovascular diseases [21], pulmonary diseases [22], insulin resistance [23], atherosclerosis [24], mitochondrial dysfunction [25], dyslipidemia [26], liver disease [27], impaired immunity [28,29], and impaired regeneration [30]. Ageing, on the other hand, represents the progressive decline of the biological functions with time [31]. It also represents a risk factor for numerous diseases and health conditions, many of which are similar to those associated with obesity. These include neurodegenerative disease [32], cognitive decline [33], COVID-19 severity [34], type 2 diabetes [35], skeletal muscle loss [36], cancer [37], cardiovascular disease [38], pulmonary disease [39], insulin resistance [40], atherosclerosis [41], mitochondrial dysfunction [42], dyslipidemia [43], liver disease [44], fertility alteration [45,46] immunity alteration [47], and declined regeneration [48].
Although the risks related to obesity are independent from ageing and those related to ageing are independent from obesity, such similarities between ageing and obesity as risk factors suggest common patterns and share underlying mechanisms of both ageing and obesity. Early epidemiologic data approved the prevalence of obesity increases by ageing, especially in women. Therefore, the ongoing step is to know more about how ageing and obesity could be related at the molecular level. Within this context, obesity and ageing have been described as sharing common pathways at the molecular and cellular levels. For instance, in both, we have increased inflammation [49,50], free radicals, and oxidative stress [51,52] as well as microbiota changes [53,54]. In addition, healthy diet and physical activity are prescribed to manage obesity [55,56] and also optimize healthy ageing [57,58]. While the main goal of prescribing the physical activity in obesity is to increase the energy expenditure and, thus, reduce the adiposity and lose weight [59,60], in ageing, the physical activity aims mostly to improve muscular and metabolic performance [57,61,62]. Importantly, physical activity as a common therapy for both ageing and obesity has significant impacts on reducing the risk factors mediated by ageing and obesity and also improves numerous biomolecular markers and pathological profiles. As illustrations, physical activity improves and optimizes treatment/prevention or reduces the risk of metabolic disorders [63], cancer [64], cardiovascular disease [65,66,67], immune functions [68], insulin resistance [69], oxidative stress [70], liver disease [71], regeneration [72,73], pulmonary disease [74,75], atherosclerosis [76], and mitochondrial remodeling [77]. These evidences add up on those of functional genomics [78,79,80,81] as illustrated by the secreted protein acidic and rich in cysteine (SPARC). Indeed, SPARC expression changes during obesity [82] and with ageing [83] and Sparc/SPARC represents an exercise-induced gene upon which exercise-induced muscle phenotype changes would depend [84,85]. In addition, SPARC is involved in diverse biological activities [86] related to those described above in the context of obesity, ageing, and exercise. These include metabolic and homeostatic properties [87], inflammation [88], cancer [89], regeneration [90], and metabolism [91]. This exercise-induced key myokine with obesity and age-related expression patterns further points to molecular links between obesity and ageing.

2. Epigenetics: An Additional Link between Ageing and Obesity

Furthermore, epigenetics studies provide additional evidences of similar patterns shared by obesity and ageing. Therefore, epigenetics represents a field worth exploring to reveal further links between obesity and ageing. This is reflected by the changes such as histone modification, DNA methylation, noncoding RNAs, and chromatin remodeling that have been associated with both ageing [31,92,93,94,95,96,97] and obesity [98,99,100,101,102,103]. These changes can follow diverse patterns. For instance, region-specific DNA hypermethylation [104] and proliferation-dependent alterations of the DNA methylation [105] have been reported in ageing during which we talk about epigenetic clocks [106]. The possible use of DNA-methylation-based measures as a tool to evaluate the accelerated biological ageing [107,108,109,110] represents a potential application of the DNA methylation age (DNAmAge), which would contribute to several diseases such as obesity. Similarly, obesity-related DNA methylation can be site-specific [111] and with specific methylation signatures [112]. Other related features such as telomere attrition are also shared between ageing [31] and obesity [113,114].
Importantly, exercise—prescribed for both elderly and obese patients—has impacts on the epigenetics patterns related to both ageing and obesity including DNA methylation [115], histone modification [116], chromatin modifications [117], and noncoding RNAs [118]. These exercise-related properties suggest that epigenetics pathways are among the mechanisms via which exercise induces its benefits—as it has been shown, for instance, for exercise-mediated heart protection [119]. They further support targeting epigenetic pathways as a therapy [120,121] as well; potentially, to treat obesity and improve ageing. These observations also suggest correlations between epigenetics changes and obesity/ageing-related pathologic phenotypes. In addition, these molecular and clinical evidences, from genetics to epigenetics and pathogenesis, further present obesity as a risk factor for ageing and, at the same time, highlight ageing as a risk factor for obesity [1]. This would explain why losing weight “rejuvenates”. Moreover, dietary restriction (that has both antiageing and antiobesity effects) also impacts epigenetics towards significant health benefits [122,123] bringing an additional correlation between ageing and obesity.

3. Perspectives

These introduced concepts would have important applications in the medical fields, especially that both ageing and obesity are among what medically characterize the epidemiological and pathological profiles of most modern societies. Although a healthy ageing is the optimum target of geriatrics, we have limited options to manage ageing (irreversible time effects). However, obesity, on the other hand, has realistically more management options since it remains relatively reversible. Therefore, managing obesity toward healthy ageing remains more practical than targeting healthy ageing to manage obesity. It is worth noting, however, that treating obesity would optimize ageing and healthy ageing would decrease obesity risk. Nevertheless, the key approach remains to target a healthy lifestyle including exercise, diet, sleeping, and psychological well-being to manage obesity, optimize healthy ageing, and control most diseases’ risk factors.
We would like to introduce a new concept via which there is a potential to combine the age-related and the obesity-related epegentics measures to obtain a full evaluation of how deep both the age and obesity worsen the other as well as the various diseases and risk factos for which either ageing or obesity represent a risk factor. The need to actualize this idea nowadays comes from the urgent epedemiological situations related to ageing and obesity in the modern societies both in developed and in developing countries. To expand this vision, the advances and added value of this work is that it puts epigenetics along with pathological phenotype, molecular patterns, and lifestyle impacts as a set that regroups the elements shared between obesity and ageing (Figure 1). Such approches would allow for optimizing therapies and lifestyle management choices.

Author Contributions

A.G. designed the manuscript structure and wrote it. A.G., M.Y., and J.S.-A. discussed the content and exchanged ideas and suggestions (concepts to add, the figure, references selection, etc.) throughout the writing process, edited, and critically revised the paper. J.S.-A. gave the final approval for the version to be published. All authors have read and agreed to the published version of the manuscript.


This work received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.


Abdelaziz Ghanemi received a scholarship under the Merit Scholarship Program for foreign students from the Ministry of Education and Higher Education of Quebec, Canada. The Fonds de recherche du Québec—Nature et technologies (FRQNT) is responsible for managing the program (Bourses d’excellence pour étudiants étrangers du Ministère de l’Éducation et de l’Enseignement supérieur du Québec, Le Fonds de recherche du Québec—Nature et technologies (FRQNT) est responsable de la gestion du programme). Abdelaziz Ghanemi is the received the scholarship « Bourse Tremplin -Stage en milieu de pratique» (Internship scholarship) from the Fonds de recherche du Québec-Sante (FRQS), Quebec, Canada. Figure 1 was created using images from and Servier Medical Art by Servier is licensed under a Creative Commons Attribution 3.0 Unported License (accessed on 26 October 2021).

Conflicts of Interest

The authors declare no conflict of interest.


  1. Jura, M.; Kozak, L.P. Obesity and related consequences to ageing. Age 2016, 38, 23. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  2. Han, T.S.; Tajar, A.; Lean, M.E. Obesity and weight management in the elderly. Br. Med. Bull. 2011, 97, 169–196. [Google Scholar] [CrossRef]
  3. Han, T.S.; Wu, F.C.; Lean, M.E. Obesity and weight management in the elderly: A focus on men. Best Pract. Res. Clin. Endocrinol. Metab. 2013, 27, 509–525. [Google Scholar] [CrossRef] [PubMed]
  4. Batsis, J.A.; Villareal, D.T. Sarcopenic obesity in older adults: Aetiology, epidemiology and treatment strategies. Nat. Rev. Endocrinol. 2018, 14, 513–537. [Google Scholar] [CrossRef]
  5. Polyzos, S.A.; Margioris, A.N. Sarcopenic obesity. Hormones 2018, 17, 321–331. [Google Scholar] [CrossRef] [PubMed]
  6. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Broken Energy Homeostasis and Obesity Pathogenesis: The Surrounding Concepts. J. Clin. Med. 2018, 7, 453. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  7. Goossens, G.H. The Metabolic Phenotype in Obesity: Fat Mass, Body Fat Distribution, and Adipose Tissue Function. Obes. Facts 2017, 10, 207–215. [Google Scholar] [CrossRef] [PubMed]
  8. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Obesity as a Neuroendocrine Reprogramming. Medicina 2021, 57, 66. [Google Scholar] [CrossRef]
  9. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Obese Animals as Models for Numerous Diseases: Advantages and Applications. Medicina 2021, 57, 999. [Google Scholar] [CrossRef] [PubMed]
  10. Ghanemi, A.; St-Amand, J. Redefining obesity toward classifying as a disease. Eur. J. Intern. Med. 2018, 55, 20–22. [Google Scholar] [CrossRef] [PubMed]
  11. Škurla, M.; Rybář, R. Obesity and reduced fertility of men. Ceska Gynekol. 2018, 83, 212–217. [Google Scholar] [PubMed]
  12. Best, D.; Bhattacharya, S. Obesity and fertility. Horm. Mol. Biol. Clin. Investig. 2015, 24, 5–10. [Google Scholar] [CrossRef]
  13. Saad, M.J.; Santos, A.; Prada, P.O. Linking Gut Microbiota and Inflammation to Obesity and Insulin Resistance. Physiology 2016, 31, 283–293. [Google Scholar] [CrossRef] [PubMed]
  14. Dye, L.; Boyle, N.B.; Champ, C.; Lawton, C. The relationship between obesity and cognitive health and decline. Proc. Nutr. Soc. 2017, 76, 443–454. [Google Scholar] [CrossRef] [Green Version]
  15. Petrakis, D.; Margină, D.; Tsarouhas, K.; Tekos, F.; Stan, M.; Nikitovic, D.; Kouretas, D.; Spandidos, D.A.; Tsatsakis, A. Obesity—A risk factor for increased COVID-19 prevalence, severity and lethality (Review). Mol. Med. Rep. 2020, 22, 9–19. [Google Scholar] [CrossRef] [PubMed]
  16. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Will an obesity pandemic replace the coronavirus disease-2019 (COVID-19) pandemic? Med. Hypotheses 2020, 144, 110042. [Google Scholar] [CrossRef]
  17. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Coronavirus Disease 2019 (COVID-19) Crisis: Losing Our Immunity When We Need It the Most. Biology 2021, 10, 545. [Google Scholar] [CrossRef] [PubMed]
  18. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Post-Coronavirus Disease-2019 (COVID-19): Toward a Severe Multi-Level Health Crisis? Med. Sci. 2021, 9, 68. [Google Scholar] [CrossRef]
  19. Rubio-Almanza, M.; Cámara-Gómez, R.; Merino-Torres, J.F. Obesity and type 2 diabetes: Also linked in therapeutic options. Endocrinol. Diabetes Nutr. 2019, 66, 140–149. [Google Scholar] [CrossRef] [PubMed]
  20. Avgerinos, K.I.; Spyrou, N.; Mantzoros, C.S.; Dalamaga, M. Obesity and cancer risk: Emerging biological mechanisms and perspectives. Metabolism 2019, 92, 121–135. [Google Scholar] [CrossRef]
  21. Koliaki, C.; Liatis, S.; Kokkinos, A. Obesity and cardiovascular disease: Revisiting an old relationship. Metabolism 2019, 92, 98–107. [Google Scholar] [CrossRef] [PubMed]
  22. Dixon, A.E.; Peters, U. The effect of obesity on lung function. Expert Rev. Respir. Med. 2018, 12, 755–767. [Google Scholar] [CrossRef]
  23. Barazzoni, R.; Gortan Cappellari, G.; Ragni, M.; Nisoli, E. Insulin resistance in obesity: An overview of fundamental alterations. Eat Weight Disord. 2018, 23, 149–157. [Google Scholar] [CrossRef] [PubMed]
  24. Csige, I.; Ujvárosy, D.; Szabó, Z.; Lőrincz, I.; Paragh, G.; Harangi, M.; Somodi, S. The Impact of Obesity on the Cardiovascular System. J. Diabetes Res. 2018, 2018, 3407306. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  25. De Mello, A.H.; Costa, A.B.; Engel, J.D.G.; Rezin, G.T. Mitochondrial dysfunction in obesity. Life Sci. 2018, 192, 26–32. [Google Scholar] [CrossRef]
  26. Vekic, J.; Zeljkovic, A.; Stefanovic, A.; Jelic-Ivanovic, Z.; Spasojevic-Kalimanovska, V. Obesity and dyslipidemia. Metabolism 2019, 92, 71–81. [Google Scholar] [CrossRef]
  27. Polyzos, S.A.; Kountouras, J.; Mantzoros, C.S. Obesity and nonalcoholic fatty liver disease: From pathophysiology to therapeutics. Metabolism 2019, 92, 82–97. [Google Scholar] [CrossRef] [PubMed]
  28. Andersen, C.J.; Murphy, K.E.; Fernandez, M.L. Impact of Obesity and Metabolic Syndrome on Immunity. Adv. Nutr. 2016, 7, 66–75. [Google Scholar] [CrossRef] [Green Version]
  29. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Impact of Adiposity and Fat Distribution, Rather Than Obesity, on Antibodies as an Illustration of Weight-Loss-Independent Exercise Benefits. Medicines 2021, 8, 57. [Google Scholar] [CrossRef] [PubMed]
  30. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Regeneration during Obesity: An Impaired Homeostasis. Animals 2020, 10, 2344. [Google Scholar] [CrossRef] [PubMed]
  31. López-Otín, C.; Blasco, M.A.; Partridge, L.; Serrano, M.; Kroemer, G. The hallmarks of aging. Cell 2013, 153, 1194–1217. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  32. Hou, Y.; Dan, X.; Babbar, M.; Wei, Y.; Hasselbalch, S.G.; Croteau, D.L.; Bohr, V.A. Ageing as a risk factor for neurodegenerative disease. Nat. Rev. Neurol. 2019, 15, 565–581. [Google Scholar] [CrossRef] [PubMed]
  33. Bramorska, A.; Zarzycka, W.; Podolecka, W.; Kuc, K.; Brzezicka, A. Age-Related Cognitive Decline May Be Moderated by Frequency of Specific Food Products Consumption. Nutrients 2021, 13, 2504. [Google Scholar] [CrossRef] [PubMed]
  34. Gallo Marin, B.; Aghagoli, G.; Lavine, K.; Yang, L.; Siff, E.J.; Chiang, S.S.; Salazar-Mather, T.P.; Dumenco, L.; Savaria, M.C.; Aung, S.N.; et al. Predictors of COVID-19 severity: A literature review. Rev. Med. Virol. 2021, 31, 1–10. [Google Scholar] [CrossRef]
  35. Al-Sofiani, M.E.; Ganji, S.S.; Kalyani, R.R. Body composition changes in diabetes and aging. J. Diabetes Complicat. 2019, 33, 451–459. [Google Scholar] [CrossRef] [PubMed]
  36. Park, S.W.; Goodpaster, B.H.; Lee, J.S.; Kuller, L.H.; Boudreau, R.; de Rekeneire, N.; Harris, T.B.; Kritchevsky, S.; Tylavsky, F.A.; Nevitt, M.; et al. Excessive loss of skeletal muscle mass in older adults with type 2 diabetes. Diabetes Care 2009, 32, 1993–1997. [Google Scholar] [CrossRef] [Green Version]
  37. Fane, M.; Weeraratna, A.T. How the ageing microenvironment influences tumour progression. Nat. Rev. Cancer 2020, 20, 89–106. [Google Scholar] [CrossRef]
  38. Costantino, S.; Paneni, F.; Cosentino, F. Ageing, metabolism and cardiovascular disease. J. Physiol. 2016, 594, 2061–2073. [Google Scholar] [CrossRef] [PubMed]
  39. Barnes, P.J. Pulmonary Diseases and Ageing. Subcell. Biochem. 2019, 91, 45–74. [Google Scholar] [PubMed]
  40. Consitt, L.A.; Dudley, C.; Saxena, G. Impact of Endurance and Resistance Training on Skeletal Muscle Glucose Metabolism in Older Adults. Nutrients 2019, 11, 2636. [Google Scholar] [CrossRef] [Green Version]
  41. Tyrrell, D.J.; Goldstein, D.R. Ageing and atherosclerosis: Vascular intrinsic and extrinsic factors and potential role of IL-6. Nat. Rev. Cardiol. 2021, 18, 58–68. [Google Scholar] [CrossRef] [PubMed]
  42. Tyrrell, D.J.; Blin, M.G.; Song, J.; Wood, S.C.; Zhang, M.; Beard, D.A.; Goldstein, D.R. Age-Associated Mitochondrial Dysfunction Accelerates Atherogenesis. Circ. Res. 2020, 126, 298–314. [Google Scholar] [CrossRef]
  43. Liu, H.H.; Li, J.J. Aging and dyslipidemia: A review of potential mechanisms. Ageing Res. Rev. 2015, 19, 43–52. [Google Scholar] [CrossRef] [PubMed]
  44. Stahl, E.C.; Haschak, M.J.; Popovic, B.; Brown, B.N. Macrophages in the Aging Liver and Age-Related Liver Disease. Front. Immunol. 2018, 9, 2795. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  45. Almeida, S.; Rato, L.; Sousa, M.; Alves, M.G.; Oliveira, P.F. Fertility and Sperm Quality in the Aging Male. Curr. Pharm. Des. 2017, 23, 4429–4437. [Google Scholar] [CrossRef]
  46. American College of Obstetricians and Gynecologists Committee on Gynecologic Practice and Practice Committee. Female age-related fertility decline. Committee Opinion No. 589. Fertil. Steril. 2014, 101, 633–634. [Google Scholar] [CrossRef]
  47. Sadighi Akha, A.A. Aging and the immune system: An overview. J. Immunol. Methods 2018, 463, 21–26. [Google Scholar] [CrossRef]
  48. Sousounis, K.; Baddour, J.A.; Tsonis, P.A. Aging and regeneration in vertebrates. Curr. Top Dev. Biol. 2014, 108, 217–246. [Google Scholar]
  49. Cox, A.J.; West, N.P.; Cripps, A.W. Obesity, inflammation, and the gut microbiota. Lancet Diabetes Endocrinol. 2015, 3, 207–215. [Google Scholar] [CrossRef]
  50. Sendama, W. The effect of ageing on the resolution of inflammation. Ageing Res. Rev. 2020, 57, 101000. [Google Scholar] [CrossRef]
  51. Pomatto, L.C.D.; Davies, K.J.A. Adaptive homeostasis and the free radical theory of ageing. Free Radic. Biol Med. 2018, 124, 420–430. [Google Scholar] [CrossRef] [PubMed]
  52. Rani, V.; Deep, G.; Singh, R.K.; Palle, K.; Yadav, U.C. Oxidative stress and metabolic disorders: Pathogenesis and therapeutic strategies. Life Sci. 2016, 148, 183–193. [Google Scholar] [CrossRef] [PubMed]
  53. Torres-Fuentes, C.; Schellekens, H.; Dinan, T.G.; Cryan, J.F. The microbiota-gut-brain axis in obesity. Lancet Gastroenterol. Hepatol. 2017, 2, 747–756. [Google Scholar] [CrossRef]
  54. Dinan, T.G.; Cryan, J.F. Gut instincts: Microbiota as a key regulator of brain development, ageing and neurodegeneration. J. Physiol. 2017, 595, 489–503. [Google Scholar] [CrossRef] [PubMed]
  55. Fock, K.M.; Khoo, J. Diet and exercise in management of obesity and overweight. J. Gastroenterol. Hepatol. 2013, 28 (Suppl. S4), 59–63. [Google Scholar] [CrossRef]
  56. Swift, D.L.; McGee, J.E.; Earnest, C.P.; Carlisle, E.; Nygard, M.; Johannsen, N.M. The Effects of Exercise and Physical Activity on Weight Loss and Maintenance. Prog. Cardiovasc. Dis. 2018, 61, 206–213. [Google Scholar] [CrossRef]
  57. Papaioannou, K.G.; Nilsson, A.; Nilsson, L.M.; Kadi, F. Healthy Eating Is Associated with Sarcopenia Risk in Physically Active Older Adults. Nutrients 2021, 13, 2813. [Google Scholar] [CrossRef]
  58. Mora, J.C.; Valencia, W.M. Exercise and Older Adults. Clin. Geriatr. Med. 2018, 34, 145–162. [Google Scholar] [CrossRef] [PubMed]
  59. Stoner, L.; Beets, M.W.; Brazendale, K.; Moore, J.B.; Weaver, R.G. Exercise Dose and Weight Loss in Adolescents with Overweight-Obesity: A Meta-Regression. Sports Med. 2019, 49, 83–94. [Google Scholar] [CrossRef] [PubMed]
  60. Swift, D.L.; Johannsen, N.M.; Lavie, C.J.; Earnest, C.P.; Church, T.S. The role of exercise and physical activity in weight loss and maintenance. Prog. Cardiovasc. Dis. 2014, 56, 441–447. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  61. Elia, M. Obesity in the elderly. Obes. Res. 2001, 9 (Suppl. S4), 244s–248s. [Google Scholar] [CrossRef]
  62. Fleg, J.L. Aerobic exercise in the elderly: A key to successful aging. Discov. Med. 2012, 13, 223–228. [Google Scholar] [PubMed]
  63. Ghanemi, A.; St-Amand, J. Interleukin-6 as a “metabolic hormone”. Cytokine 2018, 112, 132–136. [Google Scholar] [CrossRef] [PubMed]
  64. Idorn, M.; Thor Straten, P. Exercise and cancer: From “healthy” to “therapeutic”? Cancer Immunol. Immunother. 2017, 66, 667–671. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  65. Cattadori, G.; Segurini, C.; Picozzi, A.; Padeletti, L.; Anzà, C. Exercise and heart failure: An update. ESC Heart Fail. 2018, 5, 222–232. [Google Scholar] [CrossRef]
  66. Fiuza-Luces, C.; Santos-Lozano, A.; Joyner, M.; Carrera-Bastos, P.; Picazo, O.; Zugaza, J.L.; Izquierdo, M.; Ruilope, L.M.; Lucia, A. Exercise benefits in cardiovascular disease: Beyond attenuation of traditional risk factors. Nat. Rev. Cardiol. 2018, 15, 731–743. [Google Scholar] [CrossRef]
  67. Hansen, D.; Niebauer, J.; Cornelissen, V.; Barna, O.; Neunhäuserer, D.; Stettler, C.; Tonoli, C.; Greco, E.; Fagard, R.; Coninx, K.; et al. Exercise Prescription in Patients with Different Combinations of Cardiovascular Disease Risk Factors: A Consensus Statement from the EXPERT Working Group. Sports Med. 2018, 48, 1781–1797. [Google Scholar] [CrossRef]
  68. Wang, J.; Liu, S.; Li, G.; Xiao, J. Exercise Regulates the Immune System. Adv. Exp. Med. Biol. 2020, 1228, 395–408. [Google Scholar] [PubMed]
  69. Whillier, S. Exercise and Insulin Resistance. Adv. Exp. Med. Biol. 2020, 1228, 137–150. [Google Scholar]
  70. De Sousa, C.V.; Sales, M.M.; Rosa, T.S.; Lewis, J.E.; de Andrade, R.V.; Simões, H.G. The Antioxidant Effect of Exercise: A Systematic Review and Meta-Analysis. Sports Med. 2017, 47, 277–293. [Google Scholar] [CrossRef]
  71. Van der Windt, D.J.; Sud, V.; Zhang, H.; Tsung, A.; Huang, H. The Effects of Physical Exercise on Fatty Liver Disease. Gene Expr. 2018, 18, 89–101. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  72. Saito, Y.; Chikenji, T.S.; Matsumura, T.; Nakano, M.; Fujimiya, M. Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors. Nat. Commun. 2020, 11, 889. [Google Scholar] [CrossRef] [PubMed]
  73. Schüttler, D.; Clauss, S.; Weckbach, L.T.; Brunner, S. Molecular Mechanisms of Cardiac Remodeling and Regeneration in Physical Exercise. Cells 2019, 8, 1128. [Google Scholar] [CrossRef] [Green Version]
  74. Paneroni, M.; Simonelli, C.; Vitacca, M.; Ambrosino, N. Aerobic Exercise Training in Very Severe Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis. Am. J. Phys. Med. Rehabil. 2017, 96, 541–548. [Google Scholar] [CrossRef]
  75. Nolan, C.M.; Rochester, C.L. Exercise Training Modalities for People with Chronic Obstructive Pulmonary Disease. COPD 2019, 16, 378–389. [Google Scholar] [CrossRef] [PubMed]
  76. Yang, J.; Cao, R.Y.; Gao, R.; Mi, Q.; Dai, Q.; Zhu, F. Physical Exercise Is a Potential “Medicine” for Atherosclerosis. Adv. Exp. Med. Biol. 2017, 999, 269–286. [Google Scholar]
  77. Gan, Z.; Fu, T.; Kelly, D.P.; Vega, R.B. Skeletal muscle mitochondrial remodeling in exercise and diseases. Cell Res. 2018, 28, 969–980. [Google Scholar] [CrossRef]
  78. Ghanemi, A.; Melouane, A.; Yoshioka, M.; St-Amand, J. Exercise and High-Fat Diet in Obesity: Functional Genomics Perspectives of Two Energy Homeostasis Pillars. Genes 2020, 11, 875. [Google Scholar] [CrossRef]
  79. Melouane, A.; Ghanemi, A.; Yoshioka, M.; St-Amand, J. Functional genomics applications and therapeutic implications in sarcopenia. Mutat. Res. Rev. Mutat. Res. 2019, 781, 175–185. [Google Scholar] [CrossRef]
  80. Melouane, A.; Ghanemi, A.; Aubé, S.; Yoshioka, M.; St-Amand, J. Differential gene expression analysis in ageing muscle and drug discovery perspectives. Ageing Res. Rev. 2018, 41, 53–63. [Google Scholar] [CrossRef]
  81. Mucunguzi, O.; Melouane, A.; Ghanemi, A.; Yoshioka, M.; Boivin, A.; Calvo, E.L.; St-Amand, J. Identification of the principal transcriptional regulators for low-fat and high-fat meal responsive genes in small intestine. Nutr. Metab. 2017, 14, 66. [Google Scholar] [CrossRef] [Green Version]
  82. Atorrasagasti, C.; Onorato, A.; Gimeno, M.L.; Andreone, L.; Garcia, M.; Malvicini, M.; Fiore, E.; Bayo, J.; Perone, M.J.; Mazzolini, G.D. SPARC is required for the maintenance of glucose homeostasis and insulin secretion in mice. Clin. Sci. 2019, 133, 351–365. [Google Scholar] [CrossRef]
  83. Kwon, J.H.; Moon, K.M.; Min, K.W. Exercise-Induced Myokines can Explain the Importance of Physical Activity in the Elderly: An Overview. Healthcare 2020, 8, 378. [Google Scholar] [CrossRef] [PubMed]
  84. Ghanemi, A.; Melouane, A.; Yoshioka, M.; St-Amand, J. Exercise Training of Secreted Protein Acidic and Rich in Cysteine (Sparc) KO Mice Suggests That Exercise-Induced Muscle Phenotype Changes Are SPARC-Dependent. Appl. Sci. 2020, 10, 9108. [Google Scholar] [CrossRef]
  85. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Measuring Exercise-Induced Secreted Protein Acidic and Rich in Cysteine Expression as a Molecular Tool to Optimize Personalized Medicine. Genes 2021, 12, 1832. [Google Scholar] [CrossRef] [PubMed]
  86. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Secreted Protein Acidic and Rich in Cysteine as a Molecular Physiological and Pathological Biomarker. Biomolecules 2021, 11, 1689. [Google Scholar] [CrossRef]
  87. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Secreted Protein Acidic and Rich in Cysteine: Metabolic and Homeostatic Properties beyond the Extracellular Matrix Structure. Appl. Sci. 2020, 10, 2388. [Google Scholar] [CrossRef] [Green Version]
  88. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Secreted protein acidic and rich in cysteine and inflammation: Another homeostatic property? Cytokine 2020, 133, 155179. [Google Scholar] [CrossRef] [PubMed]
  89. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Secreted protein acidic and rich in cysteine and cancer: A homeostatic hormone? Cytokine 2020, 127, 154996. [Google Scholar] [CrossRef]
  90. Ghanemi, A.; Yoshioka, M.; St-Amand, J. Secreted Protein Acidic and Rich in Cysteine as a Regeneration Factor: Beyond the Tissue Repair. Life 2021, 11, 38. [Google Scholar] [CrossRef]
  91. Ghanemi, A.; Melouane, A.; Yoshioka, M.; St-Amand, J. Secreted protein acidic and rich in cysteine and bioenergetics: Extracellular matrix, adipocytes remodeling and skeletal muscle metabolism. Int. J. Biochem. Cell Biol. 2019, 117, 105627. [Google Scholar] [CrossRef]
  92. Morgan, A.E.; Davies, T.J.; Mc Auley, M.T. The role of DNA methylation in ageing and cancer. Proc. Nutr. Soc. 2018, 77, 412–422. [Google Scholar] [CrossRef] [PubMed]
  93. Zhang, W.; Qu, J.; Liu, G.H.; Belmonte, J.C.I. The ageing epigenome and its rejuvenation. Nat. Rev. Mol. Cell Biol. 2020, 21, 137–150. [Google Scholar] [CrossRef] [PubMed]
  94. Covarrubias, A.J.; Perrone, R.; Grozio, A.; Verdin, E. NAD(+) metabolism and its roles in cellular processes during ageing. Nat. Rev. Mol. Cell Biol. 2021, 22, 119–141. [Google Scholar] [CrossRef] [PubMed]
  95. Booth, L.N.; Brunet, A. The Aging Epigenome. Mol. Cell. 2016, 62, 728–744. [Google Scholar] [CrossRef] [Green Version]
  96. Thum, T. Non-coding RNAs in ageing. Ageing Res. Rev. 2014, 17, 1–2. [Google Scholar] [CrossRef]
  97. Gupta, S.K.; Piccoli, M.T.; Thum, T. Non-coding RNAs in cardiovascular ageing. Ageing Res. Rev. 2014, 17, 79–85. [Google Scholar] [CrossRef]
  98. Samblas, M.; Milagro, F.I.; Martínez, A. DNA methylation markers in obesity, metabolic syndrome, and weight loss. Epigenetics 2019, 14, 421–444. [Google Scholar] [CrossRef]
  99. Ling, C.; Rönn, T. Epigenetics in Human Obesity and Type 2 Diabetes. Cell Metab. 2019, 29, 1028–1044. [Google Scholar] [CrossRef] [Green Version]
  100. Horikoshi, M.; Beaumont, R.N.; Day, F.R.; Warrington, N.M.; Kooijman, M.N.; Fernandez-Tajes, J.; Feenstra, B.; van Zuydam, N.R.; Gaulton, K.J.; Grarup, N.; et al. Genome-wide associations for birth weight and correlations with adult disease. Nature 2016, 538, 248–252. [Google Scholar] [CrossRef]
  101. Eeckhoute, J.; Oger, F.; Staels, B.; Lefebvre, P. Coordinated Regulation of PPARγ Expression and Activity through Control of Chromatin Structure in Adipogenesis and Obesity. PPAR Res. 2012, 2012, 164140. [Google Scholar] [CrossRef]
  102. Shi, Y.; Qu, J.; Gai, L.; Yuan, D.; Yuan, C. Long Non-coding RNAs in Metabolic and Inflammatory Pathways in Obesity. Curr. Pharm. Des. 2020, 26, 3317–3325. [Google Scholar] [CrossRef] [PubMed]
  103. Ouni, M.; Schürmann, A. Epigenetic contribution to obesity. Mamm. Genome. 2020, 31, 134–145. [Google Scholar] [CrossRef] [Green Version]
  104. Jung, M.; Pfeifer, G.P. Aging and DNA methylation. BMC Biol. 2015, 13, 7. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  105. Beerman, I.; Bock, C.; Garrison, B.S.; Smith, Z.D.; Gu, H.; Meissner, A.; Rossi, D.J. Proliferation-dependent alterations of the DNA methylation landscape underlie hematopoietic stem cell aging. Cell Stem. Cell 2013, 12, 413–425. [Google Scholar] [CrossRef] [Green Version]
  106. Unnikrishnan, A.; Freeman, W.M.; Jackson, J.; Wren, J.D.; Porter, H.; Richardson, A. The role of DNA methylation in epigenetics of aging. Pharmacol. Ther. 2019, 195, 172–185. [Google Scholar] [CrossRef] [PubMed]
  107. Sibbett, R.A.; Altschul, D.M.; Marioni, R.E.; Deary, I.J.; Starr, J.M.; Russ, T.C. DNA methylation-based measures of accelerated biological ageing and the risk of dementia in the oldest-old: A study of the Lothian Birth Cohort 1921. BMC Psychiatry 2020, 20, 91. [Google Scholar] [CrossRef] [Green Version]
  108. Matías-García, P.R.; Ward-Caviness, C.K.; Raffield, L.M.; Gao, X.; Zhang, Y.; Wilson, R.; Gào, X.; Nano, J.; Bostom, A.; Colicino, E.; et al. DNAm-based signatures of accelerated aging and mortality in blood are associated with low renal function. Clin. Epigenetics 2021, 13, 121. [Google Scholar] [CrossRef]
  109. Ambatipudi, S.; Horvath, S.; Perrier, F.; Cuenin, C.; Hernandez-Vargas, H.; Le Calvez-Kelm, F.; Durand, G.; Byrnes, G.; Ferrari, P.; Bouaoun, L.; et al. DNA methylome analysis identifies accelerated epigenetic ageing associated with postmenopausal breast cancer susceptibility. Eur. J. Cancer 2017, 75, 299–307. [Google Scholar] [CrossRef] [Green Version]
  110. Peng, C.; Cardenas, A.; Rifas-Shiman, S.L.; Hivert, M.F.; Gold, D.R.; Platts-Mills, T.A.; Lin, X.; Oken, E.; Avila, L.; Celedón, J.C.; et al. Epigenetic age acceleration is associated with allergy and asthma in children in Project Viva. J. Allergy Clin. Immunol. 2019, 143, 2263–2270.e2214. [Google Scholar] [CrossRef] [Green Version]
  111. Van Dijk, S.J.; Molloy, P.L.; Varinli, H.; Morrison, J.L.; Muhlhausler, B.S. Epigenetics and human obesity. Int. J. Obes. 2015, 39, 85–97. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  112. Ahrens, M.; Ammerpohl, O.; von Schönfels, W.; Kolarova, J.; Bens, S.; Itzel, T.; Teufel, A.; Herrmann, A.; Brosch, M.; Hinrichsen, H.; et al. DNA methylation analysis in nonalcoholic fatty liver disease suggests distinct disease-specific and remodeling signatures after bariatric surgery. Cell Metab. 2013, 18, 296–302. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  113. Zhou, Y.; Hambly, B.D.; McLachlan, C.S. FTO associations with obesity and telomere length. J. Biomed. Sci. 2017, 24, 65. [Google Scholar] [CrossRef] [PubMed] [Green Version]
  114. Gurung, R.L.; Liu, S.; Liu, J.J.; Chan, S.M.; Moh, M.C.; Ang, K.; Tang, W.E.; Sum, C.F.; Tavintharan, S.; Lim, S.C. Ethnic disparities in relationships of obesity indices with telomere length in Asians with type 2 diabetes. J. Diabetes 2019, 11, 386–393. [Google Scholar] [CrossRef] [PubMed]
  115. Voisin, S.; Eynon, N.; Yan, X.; Bishop, D.J. Exercise training and DNA methylation in humans. Acta Physiol. 2015, 213, 39–59. [Google Scholar] [CrossRef]
  116. Fernandes, J.; Arida, R.M.; Gomez-Pinilla, F. Physical exercise as an epigenetic modulator of brain plasticity and cognition. Neurosci. Biobehav. Rev. 2017, 80, 443–456. [Google Scholar] [CrossRef]
  117. Solagna, F.; Nogara, L.; Dyar, K.A.; Greulich, F.; Mir, A.A.; Türk, C.; Bock, T.; Geremia, A.; Baraldo, M.; Sartori, R.; et al. Exercise-dependent increases in protein synthesis are accompanied by chromatin modifications and increased MRTF-SRF signalling. Acta Physiol. 2020, 230, e13496. [Google Scholar] [CrossRef]
  118. Bonilauri, B.; Dallagiovanna, B. Long Non-coding RNAs Are Differentially Expressed after Different Exercise Training Programs. Front. Physiol. 2020, 11, 567614. [Google Scholar] [CrossRef] [PubMed]
  119. Zhang, Y.; He, N.; Feng, B.; Ye, H. Exercise Mediates Heart Protection via Non-coding RNAs. Front. Cell Dev. Biol. 2020, 8, 182. [Google Scholar] [CrossRef]
  120. Dawson, M.A.; Kouzarides, T. Cancer epigenetics: From mechanism to therapy. Cell 2012, 150, 12–27. [Google Scholar] [CrossRef] [Green Version]
  121. Miranda Furtado, C.L.; Dos Santos Luciano, M.C.; Silva Santos, R.D.; Furtado, G.P.; Moraes, M.O.; Pessoa, C. Epidrugs: Targeting epigenetic marks in cancer treatment. Epigenetics 2019, 14, 1164–1176. [Google Scholar] [CrossRef] [PubMed]
  122. Yong-Quan Ng, G.; Yang-Wei Fann, D.; Jo, D.G.; Sobey, C.G.; Arumugam, T.V. Dietary Restriction and Epigenetics: Part I. Cond. Med. 2019, 2, 284–299. [Google Scholar] [PubMed]
  123. Yong-Quan Ng, G.; Fann, D.Y.; Jo, D.G.; Sobey, C.G.; Arumugam, T.V. Epigenetic Regulation by Dietary Restriction: Part II. Cond. Med. 2019, 2, 300–310. [Google Scholar]
Figure 1. Examples of ageing and obesity shared patterns. Both ageing and obesity represent a risk factor foreach other. Elucidating the patterns shared between ageing and obesity, from epigenetics to molecular pathogenesis, would allow to both optimize healthy ageing and manage obesity.
Figure 1. Examples of ageing and obesity shared patterns. Both ageing and obesity represent a risk factor foreach other. Elucidating the patterns shared between ageing and obesity, from epigenetics to molecular pathogenesis, would allow to both optimize healthy ageing and manage obesity.
Diseases 09 00087 g001
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Share and Cite

MDPI and ACS Style

Ghanemi, A.; Yoshioka, M.; St-Amand, J. Ageing and Obesity Shared Patterns: From Molecular Pathogenesis to Epigenetics. Diseases 2021, 9, 87.

AMA Style

Ghanemi A, Yoshioka M, St-Amand J. Ageing and Obesity Shared Patterns: From Molecular Pathogenesis to Epigenetics. Diseases. 2021; 9(4):87.

Chicago/Turabian Style

Ghanemi, Abdelaziz, Mayumi Yoshioka, and Jonny St-Amand. 2021. "Ageing and Obesity Shared Patterns: From Molecular Pathogenesis to Epigenetics" Diseases 9, no. 4: 87.

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop