Irisin is a predictor of sarcopenic obesity in type 2 diabetes mellitus

Oğuz, Ayten; Şahin, Murat; Tüzün, Dilek; Kurutas, Ergul; Ulgen, Cansu; Bozkus, Ozlem; Gül, Kamile

doi:10.1097/md.0000000000026529

Cited by 31 publications

(13 citation statements)

References 46 publications

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“…In older rats, irisin expression was lower than in young rats [ 296 ]. Research in recent years suggests that irisin may be used as a biomarker of sarcopenia and SO and be used in early screening for age-related muscle changes [ 295 , 297 , 298 , 299 , 300 ].…”

Section: A Role For Myokines In Sarcopenia: Cross-talk Between Muscle and Adipose Tissuementioning

confidence: 99%

Multifactorial Mechanism of Sarcopenia and Sarcopenic Obesity. Role of Physical Exercise, Microbiota and Myokines

Bilski

Pierzchalski

Szczepanik

et al. 2022

Cells

100

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Obesity and ageing place a tremendous strain on the global healthcare system. Age-related sarcopenia is characterized by decreased muscular strength, decreased muscle quantity, quality, and decreased functional performance. Sarcopenic obesity (SO) is a condition that combines sarcopenia and obesity and has a substantial influence on the older adults’ health. Because of the complicated pathophysiology, there are disagreements and challenges in identifying and diagnosing SO. Recently, it has become clear that dysbiosis may play a role in the onset and progression of sarcopenia and SO. Skeletal muscle secretes myokines during contraction, which play an important role in controlling muscle growth, function, and metabolic balance. Myokine dysfunction can cause and aggravate obesity, sarcopenia, and SO. The only ways to prevent and slow the progression of sarcopenia, particularly sarcopenic obesity, are physical activity and correct nutritional support. While exercise cannot completely prevent sarcopenia and age-related loss in muscular function, it can certainly delay development and slow down the rate of sarcopenia. The purpose of this review was to discuss potential pathways to muscle deterioration in obese individuals. We also want to present the current understanding of the role of various factors, including microbiota and myokines, in the process of sarcopenia and SO.

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Section: A Role For Myokines In Sarcopenia: Cross-talk Between Muscle and Adipose Tissuementioning

confidence: 99%

Multifactorial Mechanism of Sarcopenia and Sarcopenic Obesity. Role of Physical Exercise, Microbiota and Myokines

Bilski

Pierzchalski

Szczepanik

et al. 2022

Cells

100

View full text Add to dashboard Cite

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“…In addition, circulating irisin levels are lower in the sarcopenia group than in the normal group ( 55 ). Therefore, serum levels of irisin could be used as a biological marker of muscle dysfunction to independently predict the onset of sarcopenia obesity ( 13 , 56 , 57 ). Elderly studies have reported lower levels of irisin in the bloodstream of older people than younger people.…”

Section: Irisinmentioning

confidence: 99%

Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Pahlavani

2022

Front. Endocrinol.

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Sarcopenic obesity is defined as a multifactorial disease in aging with decreased body muscle, decreased muscle strength, decreased independence, increased fat mass, due to decreased physical activity, changes in adipokines and myokines, and decreased satellite cells. People with sarcopenic obesity cause harmful changes in myokines and adipokines. These changes are due to a decrease interleukin-10 (IL-10), interleukin-15 (IL-15), insulin-like growth factor hormone (IGF-1), irisin, leukemia inhibitory factor (LIF), fibroblast growth factor-21 (FGF-21), adiponectin, and apelin. While factors such as myostatin, leptin, interleukin-6 (IL-6), interleukin-8 (IL-8), and resistin increase. The consequences of these changes are an increase in inflammatory factors, increased degradation of muscle proteins, increased fat mass, and decreased muscle tissue, which exacerbates sarcopenia obesity. In contrast, exercise, especially strength training, reverses this process, which includes increasing muscle protein synthesis, increasing myogenesis, increasing mitochondrial biogenesis, increasing brown fat, reducing white fat, reducing inflammatory factors, and reducing muscle atrophy. Since some people with chronic diseases are not able to do high-intensity strength training, exercises with blood flow restriction (BFR) are newly recommended. Numerous studies have shown that low-intensity BFR training produces the same increase in hypertrophy and muscle strength such as high-intensity strength training. Therefore, it seems that exercise interventions with BFR can be an effective way to prevent the exacerbation of sarcopenia obesity. However, due to limited studies on adipokines and exercises with BFR in people with sarcopenic obesity, more research is needed.

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“…49 This imbalance in the myokines can also have an effect on fat metabolism, provoking fat gain and insulin resistance. 50 Correspondingly, crosssectional studies show that irisin is downregulated while myostatin is upregulated in both sarcopenia and T2D. 51…”

Section: Changes In Hormonal Balancementioning

confidence: 99%

“…On the contrary, myostatin suppresses muscle cell growth by inducing the production of reactive oxygen species (ROS), leading to cell damage 49 . This imbalance in the myokines can also have an effect on fat metabolism, provoking fat gain and insulin resistance 50 . Correspondingly, cross‐sectional studies show that irisin is downregulated while myostatin is upregulated in both sarcopenia and T2D 51 …”

Section: Changes In Hormonal Balancementioning

confidence: 99%

Pathophysiological interactions between sarcopenia and type 2 diabetes: A two‐way street influencing diagnosis and therapeutic options

Tack,

De Cock,

Dirinck

et al. 2023

Diabetes Obesity Metabolism

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This review will try to elucidate the interconnected pathophysiology of sarcopenia and type 2 diabetes (T2D) and will try to identify a common pathway to explain their development. To this end, the PubMed and Scopus databases were searched for articles published about the underlying pathophysiology, diagnosis and treatment of both sarcopenia and T2D. The medical subject heading (MeSH) terms ‘sarcopenia’ AND ‘diabetes mellitus’ AND (‘physiopathology’ OR ‘diagnosis’ OR ‘therapeutics’ OR ‘aetiology’ OR ‘causality’) were used. After screening, 32 papers were included. It was evident that sarcopenia and T2D share multiple pathophysiological mechanisms. Common changes in muscle architecture consist of a shift in myocyte composition, increased myosteatosis and a decreased capacity for muscle regeneration. Further, both diseases are linked to an imbalance in myokine and sex hormone production. Chronic low‐grade inflammation and increased levels of oxidative stress are also known pathophysiological contributors. In the future, research efforts should be directed towards discovering common checkpoints in the development of T2D and sarcopenia as possible shared therapeutic targets for both diseases. Current treatment for T2D with biguanides, incretins and insulin may already convey a protective effect on the development of sarcopenia. Furthermore, attention should be given to early diagnosis of sarcopenia within the population of people with T2D, given the sizeable physical and medical burden it encompasses. A combination of simple diagnostic techniques could be used at regular diabetes check‐ups to identify sarcopenia at an early stage and start lifestyle modifications and treatment as soon as possible.

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Irisin is a predictor of sarcopenic obesity in type 2 diabetes mellitus

Cited by 31 publications

References 46 publications

Multifactorial Mechanism of Sarcopenia and Sarcopenic Obesity. Role of Physical Exercise, Microbiota and Myokines

Multifactorial Mechanism of Sarcopenia and Sarcopenic Obesity. Role of Physical Exercise, Microbiota and Myokines

Exercise Therapy for People With Sarcopenic Obesity: Myokines and Adipokines as Effective Actors

Pathophysiological interactions between sarcopenia and type 2 diabetes: A two‐way street influencing diagnosis and therapeutic options

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