IL‐10 prevents aging‐associated inflammation and insulin resistance in skeletal muscle

Dagdeviren, Sezin; Jung, Dae Young; Friedline, Randall H.; Noh, Hye Lim; Kim, Jong Hun; Patel, Payal R.; Tsitsilianos, Nicholas; Inashima, Kunikazu; Tran, Duy A.; Hu, Xiaodi; Loubato, Marilia M.; Craige, Siobhan M.; Kwon, Jung Yeon; Lee, Ki W.-O.-N.; Kim, Jason K.

doi:10.1096/fj.201600832r

Cited by 115 publications

(80 citation statements)

References 46 publications

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“…Older people also exhibit lower skeletal muscle insulin-stimulated Akt activity [59], impaired insulin signaling, and decreased skeletal muscle insulin sensitivity. In addition, skeletal muscle insulin sensitivity in aged mice is reduced, and insulin resistance occurs [24,84]. These data indicate that the glucose metabolism capacity of the skeletal muscle decreased and the risk of insulin resistance increased.…”

Section: Introductionmentioning

confidence: 93%

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Shou

Chen

Xiao

2020

Diabetol Metab Syndr

179

112

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As age increases, the risk of developing type 2 diabetes increases, which is associated with senile skeletal muscle dysfunction. During skeletal muscle aging, mitochondrial dysfunction, intramyocellular lipid accumulation, increased inflammation, oxidative stress, modified activity of insulin sensitivity regulatory enzymes, endoplasmic reticulum stress, decreased autophagy, sarcopenia and over-activated renin-angiotensin system may occur. These changes can impair skeletal muscle insulin sensitivity and increase the risk of insulin resistance and type 2 diabetes during skeletal muscle aging. This review of the mechanism of the increased risk of insulin resistance during skeletal muscle aging will provide a more comprehensive explanation for the increased incidence of type 2 diabetes in elderly individuals, and will also provide a more comprehensive perspective for the prevention and treatment of type 2 diabetes in elderly populations.

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Section: Introductionmentioning

confidence: 93%

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Shou

Chen

Xiao

2020

Diabetol Metab Syndr

179

112

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“…McAulty et al (61) found that the daily consumption of blueberries for 6 weeks elevated innate immune indices, including plasma IL-10. Furthermore, consumption of foods rich in anthocyanins has also been shown to increase the IL-10: TNFα ratio, promoting a shift toward an anti-inflammatory/antioxidant status (62)(63)(64)(65). Nutritional intervention studies targeting the amelioration of chronic inflammation found that administration of other polyphenolic compounds suppressed inflammation by creating an anti-inflammatory/antioxidant environment.…”

Section: Discussionmentioning

confidence: 99%

Daily Consumption of an Anthocyanin-Rich Extract Made From New Zealand Blackcurrants for 5 Weeks Supports Exercise Recovery Through the Management of Oxidative Stress and Inflammation: A Randomized Placebo Controlled Pilot Study

et al. 2020

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“…Curiously at 3 days post injury IL-10 was upregulated in old but not young muscle and this trend was similar in LPS stimulated macrophages. This was initially surprising one may expect upregulation of an anti-inflammatory cytokine to be beneficial, and IL-10 is required for myogenesis post injury 21 and muscle-specific expression of IL-10 in aged muscle reduces inflammation and insulin resistance 28 . However, IL-10 does not directly act on myoblasts but instead induces polarization of muscle-macrophages to M2, which then induce myogenesis via changes to the microenvironment 21 .…”

Section: Discussionmentioning

confidence: 99%

Delineating the relationship between immune system aging and myogenesis in muscle repair

Tobin

Alibhai

Wlodarek

et al. 2020

Preprint

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12How aging affects the communication between immune cells and myoblasts during myogenesis 13 is unclear. We therefore investigated how aging impacts the cellular synchronization of these two 14 processes after muscle injury. Muscles of old mice (20 months) had chronic inflammation and 15 fewer satellite cells compared to young mice (3 months). After injury, young mice developed a 16 robust, but transient inflammatory response and a stepwise myogenic gene expression program. 17 These responses were impaired with age. Replacement of old bone marrow (BM) via 18 heterochronic bone marrow transplantation (BMT) increased muscle mass and performance on 19 locomotive and behavioural tests. After injury, Y-O BMT restored the immune cell and cytokine 20 profiles to a young phenotype and enhanced satellite cell activity while O-O BMT amplified a 21late-onset proinflammatory response. In vitro, conditioned media from young or old 22 macrophages had no effect or impaired myoblast proliferation, respectively. Thus, BM age 23 negatively affects myogenesis by inhibiting myoblast proliferation. 24 25 26 29proliferate and differentiate into mature muscle. The satellite cell population is limited, however, 30 as extensive activation caused by chronic injury may exhaust the stem cell pool 1 . Aging also 31 results in homeostatic and regenerative defects that leads to muscle loss via signals that are both 32 intrinsic and extrinsic to the satellite cell 2 . These signals ultimately impact absolute progenitor 33 cell number and function. 34Satellite cells become inherently defective with age, as transplantation of old satellite 35 cells to young muscle fail to repair muscle effectively 3,4 . Intrinsic factors that may account for 36 satellite cell aging include increased DNA damage, increased expression of cell cycle checkpoint 37 regulators such as p16 and p53, and loss of H3K27me3 histone methylation via reduced Ezh2 38 activity 5-7 . Aged muscle is subject to higher levels of muscle turnover by changes in the satellite 39 cell niche which may exhaust the stem cell pool 8 . With age, satellite cells also become prone to 40 higher levels of symmetric division, leading to fewer Pax7 + progenitor cells 4 , and geriatric 41 satellite cells may also enter an irreversible state of quiescence 7 . Myogenesis may also be 42 influenced by extrinsic factors in the blood that differ with age. This has been documented using 43 heterochronic parabiosis and blood transfusion 9-11 . Circulating factors, particularly members of 44 the TGF-β superfamily, increase with age and contribute to muscle wasting via upregulation of 45 cyclin dependent kinase inhibitors 12 . Despite moderate improvements in aged mice that receive 46 young blood 11 , the aged muscle microenvironment limits regenerative capacity. 47In addition to satellite cells, there are muscle-resident cells such as macrophages, 48 endothelial cells, Hoechst dye-excluding Side Population cells, and mesenchymal stem cells. 49Some of these cells arise from circulating cells which originate f...

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IL‐10 prevents aging‐associated inflammation and insulin resistance in skeletal muscle

Cited by 115 publications

References 46 publications

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Mechanism of increased risk of insulin resistance in aging skeletal muscle

Daily Consumption of an Anthocyanin-Rich Extract Made From New Zealand Blackcurrants for 5 Weeks Supports Exercise Recovery Through the Management of Oxidative Stress and Inflammation: A Randomized Placebo Controlled Pilot Study

Delineating the relationship between immune system aging and myogenesis in muscle repair

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