Strength training and aerobic exercise alter mitochondrial parameters in brown adipose tissue and equally reduce body adiposity in aged rats

Thirupathi, Anand; Pieri, Bruno Luiz da Silva; Queiroz, João Annibal Milano Peixoto; Rodrigues, Matheus Scarpatto; Silveira, Gustavo de Bem; Souza, Daniela R.; Luciano, Thais F.; Silveira, Paulo César Lock; Souza, Cláudio Teodoro de

doi:10.1007/s13105-019-00663-x

Cited by 28 publications

(9 citation statements)

References 39 publications

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“…Studies evaluating the effect of exercise on BAT in old rodents and humans have been published with conflicting results. In a recent study conducted in old rats, both strength and aerobic training determined an increase in BAT, in mitochondrial activity, thus reducing total body fat (65). These results were also confirmed in other rodent models, where the physical exercise-associated browning of subcutaneous WAT has been demonstrated (66).…”

Section: Brown and Beige Aging: Potential Intervention Targetsmentioning

confidence: 99%

Brown and Beige Adipose Tissue and Aging

et al. 2019

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Across aging, adipose tissue (AT) changes its quantity and distribution: AT becomes dysfunctional with an increase in production of inflammatory peptides, a decline of those with anti-inflammatory activity and infiltration of macrophages. Adipose organ dysfunction may lead to age-related metabolic alterations. Aging is characterized by an increase in adiposity and a decline in brown adipose tissue (BAT) depots and activity, and UCP1 expression. There are many possible links to age-associated involution of BAT, including the loss of mitochondrial function, impairment of the sympathetic nervous system, age-induced alteration of brown adipogenic stem/progenitor cell function and changes in endocrine signals. Aging is also associated with a reduction in beige adipocyte formation. Beige adipocytes are known to differentiate from a sub-population of progenitors resident in white adipose tissue (WAT); a defective ability of progenitor cells to proliferate and differentiate has been hypothesized with aging. The loss of beige adipocytes with age may be caused by changes in trophic factors in the adipose tissue microenvironment, which regulate progenitor cell proliferation and differentiation. This review focuses on possible mechanisms involved in the reduction of BAT and beige activity with aging, along with possible targets for age-related metabolic disease therapy.

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Section: Brown and Beige Aging: Potential Intervention Targetsmentioning

confidence: 99%

Brown and Beige Adipose Tissue and Aging

et al. 2019

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“…Han et al 31 suggested that AMPK induces FOXO1 activation and deacetylation of PGC-1α, which results in maintaining cell homeostasis and preventing aging. In addition, according to previous studies, 23,[32][33][34][35] while aging reduced NAD + and PGC-1α levels, exercise intervention increased SIRT1 levels and regulated the proteins of PGC-1α and FOXO1, which had a positive impact on delayed mitochondrial metabolism and aging. Exercise also increased NAD + protein levels, thereby regulating aging-related mechanisms.…”

Section: Changes In Ampk Levelsmentioning

confidence: 55%

Effects of Exercise Training on Aging-Related Nad+/Sirt1 Pathway in Middle-Aged and Aged Mice

2020

jomh

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Background and objective The purpose of this study was to investigate the effects of regular exercise training on nicotinamide adenine dinucleotide/sirtuin 1 (NAD + /SIRT1) signaling protein levels in skeletal muscles of middle-aged and old-aged mice. Material and methods Experimental animals were 40 male C57BL/6 mice out of which 20 were 38-week-old (middle-aged) and the other 20 were 58-week-old (aged). They were divided into four groups: middle-aged control (MC), middle-aged exercise (ME), aged control (AC), and aged exercise (AE) groups (n = 10, each group). ME and AE groups performed exercise training five times weekly for 8 weeks using animal treadmill, after which gastrocnemius muscles were excised and analyzed. Results After 8 weeks of intervention, protein levels of AMP-activated protein kinase (AMPK), SIRT1, forkhead box protein 1 (FOXO1), and NAD + levels were significantly lower in AC group than in MC group (p < 0.05). In addition, AMPK, SIRT1, FOXO1, NAD + , and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) levels were significantly higher in ME and AE groups that exercised for 8 weeks than in MC and AC groups that did not exercise (p < 0.05).

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“…The previous results had suggested that Sirt1 could be restored by the mechanical stimuli. Thirupathi A et al found that strength training and aerobic exercise could significantly increase the Sirt1 to cause a decrease of body fat percentage and adiposity index [ 38 ]. Another study reported exercise training could enhance the Sirt1 expression to improve cardiomyocyte survival [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Low magnitude vibration alleviates age-related bone loss by inhibiting cell senescence of osteogenic cells in naturally senescent rats

Wen

Bao

Tang

et al. 2021

Aging

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Dysfunction of bone marrow mesenchymal stem cells (BMSCs), osteoblasts and osteocytes may be one of the main causes of bone loss in the elderly. In the present study, we found osteogenic cells from aged rats all exhibited senescence changes, with the most pronounced senescence changes in osteocytes. Meanwhile, the proliferative capacity and functional activity of osteogenic cells from aged rats were suppressed. Osteogenic differentiation capacity of BMSCs from aged rats decreased while adipogenic capacity increased. The mineralization capacity, ALP activity and osteogenic proteins expression of osteoblasts from aged rats decreased. Additionally, osteocytes from aged rats up-expressed sclerosteosis protein, a negative regulator of bone formation. To inhibit osteogenic cell senescence, we use low magnitude vibration (LMV) to eliminate the senescent osteogenic cells. After LMV treatment, the number of osteogenic cells staining positively for senescence-associated-β-galactosidase (SA-β-Gal) decreased significantly. Besides, the expression of anti-aging protein SIRT1 was upregulated significantly, while p53 and p21 were downregulated significantly after LMV treatment. Thus, the LMV can inhibit the senescence of osteogenic cells partly through the Sirt1/p53/p21 axis. Furthermore, LMV was found to promote bone formation of aged rats. These results suggest that the inhibition of osteogenic cell senescence by LMV is a valuable treatment to prevent or delay osteoporosis.

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Strength training and aerobic exercise alter mitochondrial parameters in brown adipose tissue and equally reduce body adiposity in aged rats

Cited by 28 publications

References 39 publications

Brown and Beige Adipose Tissue and Aging

Brown and Beige Adipose Tissue and Aging

Effects of Exercise Training on Aging-Related Nad+/Sirt1 Pathway in Middle-Aged and Aged Mice

Low magnitude vibration alleviates age-related bone loss by inhibiting cell senescence of osteogenic cells in naturally senescent rats

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