Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Gewählte Publikation:

Semeraro, M.
The impact of Physical Activity and Nutrition on Telomere Biology
Doktoratsstudium der Medizinischen Wissenschaft; Humanmedizin; [ Dissertation ] Medizinische Universität Graz; 2022. pp. 154 [OPEN ACCESS]


Autor*innen der Med Uni Graz:
Semeraro Maria Donatella
Gruber Hans-Jürgen
Herrmann Markus
Sedej Simon

(1) Telomeres are protective nucleoprotein structures at the end of chromosomes that shorten with age. Obesity and exercise are believed to modify age-related telomere shortening by regulating telomerase and shelterin expression. Previous studies that have addressed this topic are inconsistent and limited to the analysis of telomere length (TL) in blood and selected solid tissues. The present in-vivo study aimed to analyze systematically the effects of age, diet, and exercise in peripheral blood mononuclear cells (PBMCs) and a broad range of solid tissues. (2) For a period of 10 months, ninety-six female Sprague Dawley rats received either standard (ND) or high-fat diet (HFD). Half of the animals from both diet groups performed 30 min running sessions at 30 cm/s on five consecutive days per week for the entire duration of the study. The remaining animals served as sedentary controls. For the investigation of age effects, an additional group of 24 young animals (four months of age) was sacrificed after one week of acclimatization. Relative telomere length (RTL) and mRNA expression of telomerase (TERT), TERF-1, and TERF-2 were mapped in PBMCs and the following nine solid tissues: liver, skeletal muscle, thoracic aorta, large intestine, spleen, kidneys, brain, lungs, and visceral fat. (3) There was no systematic correlation between RTL in PBMCs and solid tissues. RTL in kidney, skeletal muscle, and liver was positively correlated with that in PBMCs, whereas large intestine and aorta showed an inverse correlation. Ten months of aging did not result in a systematic shortening of telomeres in PBMCs and solid tissues. In lung and visceral fat of aged animals RTL was higher than in young animals, the opposite was found in aorta. HFD induced obesity (coND = 413.41± 6.17 vs. coHFD = 523.75± 14.33, p < 0.0001), but RTL was not systematically altered in obese animals when compared to their lean counterparts. In addition, the mRNA expression of the telomere-associated genes TERT, TERF-1, and TERF-2 was comparable in obese and lean animals. Only in kidney and visceral fat of obese animals, RTL, and mRNA expression of TERT, TERF-1, and TERF-2 were significantly different from lean animals. Exercise had heterogeneous effects on RTL and the expression of telomere-associated genes. Again, only in selected tissues, such as aorta and large intestine, an increase of one or more telomere-regulating genes was associated with an increase in RTL of exercising animals compared to lean sedentary controls. An interaction between HFD and exercise was only observed in kidneys, where exercising obese rats exhibited a similar RTL to sedentary lean controls. Regardless of the diet, long-term exercise-induced a state of oxidative-nitrosative stress that explained part of RTL variation in blood. Conversely, exercise significantly reduced inflammatory cytokines in obese rats. (4) The present results suggest that RTL and the expression of telomere-regulating genes, such as telomerase and shelterins, is tissue-specific. Furthermore, ten months of aging do not systematically shorten telomeres in PBMCs and solid tissues. Modifiable lifestyle factors, such as exercise and diet have no systematic effects on RTL and the expression of telomere-regulating genes. Therefore, the present results challenge the role of RTL in PBMCs as a surrogate marker of RTL in solid tissues. Furthermore, average RTL, as assessed with the PCR-based method used in this study, is not systematically affected by regular exercise and the consumption of HFD. (1) Background; (2) Materials and methods; (3) Results; (4) Conclusions

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