Adipose tissue inflammation in aging

Mau, Theresa; Yung, Raymond

doi:10.1016/j.exger.2017.10.014

Cited by 84 publications

(88 citation statements)

References 81 publications

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“…(Salminen et al, ; Zhang et al, )). It is also notable that the adipose dataset, a tissue with a known role in inflammaging (Mau & Yung, ), also shows an ADICT trend. Meanwhile, apoptosis is crucial for eliminating senescent cells during healthy aging and disruptions in apoptosis could lead to accumulation of dysfunctional cells over time.…”

Section: Discussionmentioning

confidence: 97%

Molecular footprint of Medawar’s mutation accumulation process in mammalian aging

et al. 2019

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Medawar's mutation accumulation hypothesis explains aging by the declining force of natural selection with age: Slightly deleterious germline mutations expressed in old age can drift to fixation and thereby lead to aging‐related phenotypes. Although widely cited, empirical evidence for this hypothesis has remained limited. Here, we test one of its predictions that genes relatively highly expressed in old adults should be under weaker purifying selection than genes relatively highly expressed in young adults. Combining 66 transcriptome datasets (including 16 tissues from five mammalian species) with sequence conservation estimates across mammals, here we report that the overall conservation level of expressed genes is lower at old age compared to young adulthood. This age‐related decrease in transcriptome conservation (ADICT) is systematically observed in diverse mammalian tissues, including the brain, liver, lung, and artery, but not in others, most notably in the muscle and heart. Where observed, ADICT is driven partly by poorly conserved genes being up‐regulated during aging. In general, the more often a gene is found up‐regulated with age among tissues and species, the lower its evolutionary conservation. Poorly conserved and up‐regulated genes have overlapping functional properties that include responses to age‐associated tissue damage, such as apoptosis and inflammation. Meanwhile, these genes do not appear to be under positive selection. Hence, genes contributing to old age phenotypes are found to harbor an excess of slightly deleterious alleles, at least in certain tissues. This supports the notion that genetic drift shapes aging in multicellular organisms, consistent with Medawar's mutation accumulation hypothesis.

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Section: Discussionmentioning

confidence: 97%

Molecular footprint of Medawar’s mutation accumulation process in mammalian aging

et al. 2019

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“…Although there is less research specifically examining adipose tissue in the context ageing compared to obesity, a role for adipose tissue in late-onset disease development has been established. Ageing is associated with increased abdominal and ectopic adipose tissue accumulation, which is linked with the onset of frailty and cardiometabolic disease ( 167 ). Moreover, organelle stress and the accumulation of senescent cells (p16INK4a+) within adipose tissue that secrete IL-6, IL-8, and TNF-α further contribute to a pro-inflammatory, dysfunctional adipose tissue with age ( 168 , 169 ).…”

Section: Immunological Ageing and Adipose Tissuementioning

confidence: 99%

Parallels in Immunometabolic Adipose Tissue Dysfunction with Ageing and Obesity

2018

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Ageing, like obesity, is often associated with alterations in metabolic and inflammatory processes resulting in morbidity from diseases characterised by poor metabolic control, insulin insensitivity, and inflammation. Ageing populations also exhibit a decline in immune competence referred to as immunosenescence, which contributes to, or might be driven by chronic, low-grade inflammation termed “inflammageing”. In recent years, animal and human studies have started to uncover a role for immune cells within the stromal fraction of adipose tissue in driving the health complications that come with obesity, but relatively little work has been conducted in the context of immunometabolic adipose function in ageing. It is now clear that aberrant immune function within adipose tissue in obesity—including an accumulation of pro-inflammatory immune cell populations—plays a major role in the development of systemic chronic, low-grade inflammation, and limiting the function of adipocytes leading to an impaired fat handling capacity. As a consequence, these changes increase the chance of multiorgan dysfunction and disease onset. Considering the important role of the immune system in obesity-associated metabolic and inflammatory diseases, it is critically important to further understand the interplay between immunological processes and adipose tissue function, establishing whether this interaction contributes to age-associated immunometabolic dysfunction and inflammation. Therefore, the aim of this article is to summarise how the interaction between adipose tissue and the immune system changes with ageing, likely contributing to the age-associated increase in inflammatory activity and loss of metabolic control. To understand the potential mechanisms involved, parallels will be drawn to the current knowledge derived from investigations in obesity. We also highlight gaps in research and propose potential future directions based on the current evidence.

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“…But the findings in this study showed a marked difference in insulin resistance between young rats and old-aged rats, both groups displaying aggravation of insulin resistance during diet-induced obesity. Thus, increase in adipose tissue due to aging and obesity was clearly verified as a key factor promoting insulin resistance [26,27]. Also to cause insulin resistance [33], and active release of IL-10 and IL-4 when obesity and pro-inflammation are relatively ameliorated [6].…”

Section: Resultsmentioning

confidence: 97%

Effects of Endurance Exercise Training on Adipose Tissue Inflammatory Gene Expression in Elderly Rats with Diet-Induced Obesity

Kim

2019

Asian J Kinesiol

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OBJECTIVES The study aimed to investigate the effects of the exercise training on inflammatory gene expression in adipose tissue via aging and obesity. METHODS The study subjects were forty 10-week old and 70-week old male Wistar rats. The young and oldaged rats were divided into four groups of ten: control (non-exercise) group (Y-Non; O-Non) and exercise group (Y-Ex; O-Ex). After the exercise training, intergroup differences in body composition, oral glucose tolerance test result, and protein expression levels of IL-6, TNFα, IL-10, and IL-4 in adipose tissue, were compared. RESULTS Both body weight and body fat-free mass were lower in old-aged rats than young rats; O-Non group, in particular, displayed the highest body fat mass and lowest fat-free mass. In oral glucose tolerance test result, old-aged rats exhibited higher blood glucose and insulin concentrations than young rats. TNF-α protein expression was higher in old-aged rats than young rats with the Y-Ex group displaying the lowest expression. IL-6 protein expression was significantly lower in the exercise group than in the control group for both old-aged and young rats (p < 0.05). IL-10 protein expression was not significantly different between the exercise group and the control group for either old-aged or young rats. IL-4 protein expression was significantly lower in the exercise group of young rats (p < 0.05). CONCLUSIONS Based on these findings, the analysis of the effects of exercise training on inflammatory gene expression in the adipose tissue of obese old-aged rats showed that the exercise training has effectively promoted the shift to M2 of cytokines secretion pattern related to obesity-induced pro-inflammation in old-aged rats and helped to improve insulin sensitivity.

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Adipose tissue inflammation in aging

Cited by 84 publications

References 81 publications

Molecular footprint of Medawar’s mutation accumulation process in mammalian aging

Molecular footprint of Medawar’s mutation accumulation process in mammalian aging

Parallels in Immunometabolic Adipose Tissue Dysfunction with Ageing and Obesity

Effects of Endurance Exercise Training on Adipose Tissue Inflammatory Gene Expression in Elderly Rats with Diet-Induced Obesity

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