Irisin in metabolic diseases
Fibronectin type III domain-containing protein 5, the precursor of irisin, is a protein that is encoded by the FNDC5 gene.[5] Irisin is a cleaved version of FNDC5, named after the Greek messenger goddess Iris.[6]
Fibronectin domain-containing protein 5 is a membrane protein comprising a short cytoplasmic domain, a transmembrane segment, and an ectodomain consisting of a ~100 kDa fibronectin type III (FNIII) domain.
Irisin is a myokine/adipokine induced by the exercise in mice and humans, which is proposed to induce "browning" of white adipose tissue, its primary target, thus increasing thermogenesis and energy expenditure. Since its identification, irisin has been linked to favorable effects on metabolic diseases, including obesity, type 2 diabetes mellitus (T2DM), lipid metabolism and cardiovascular disease (CVD), nonalcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS), and metabolic bone diseases. Generally, despite the promising profile of irisin in rodents, its effects on human are less recognized.
Review:
Most, but not all studies show a positive association between irisin and indices of adiposity. In T2DM, NAFLD, and CVD, most observational studies reported lower irisin levels in patients than controls. Regarding metabolic bone diseases, irisin is positively associated with bone mineral density and strength in athletes, and inversely associated with osteoporotic fractures in postmenopausal osteoporosis. In PCOS, data remain largely conflicting. Irisin does not seem to be further reduced when two metabolic diseases, e.g., T2DM and NAFLD, or obesity and NAFLD exist though more data are needed. Furthermore, it seems that diverse confounders may have affected the results of different clinical studies.
Conclusion:
Irisin remains an appealing molecule from a pathophysiological point of view and an appealing therapeutic target for metabolic diseases, albeit much research is still needed.
Keywords:
Cardiovascular disease; Diabetes; Irisin; Myokine; Nonalcoholic fatty liver disease; Obesity
Source: US National Library of MedicineNational Institutes of Health
Exercise‐induced irisin release as a determinant of the metabolic response to exercise training in obese youth: the EXIT trial
Overview protocol
Participants underwent a screening and baseline assessment of body composition, fitness and physical activity level, muscle strength, and medical history. After completing the screening visit, participants performed an acute bout of aerobic exercise, and 1 week later an acute bout of resistance exercise, to quantify the irisin response to an acute exercise session. Following those two acute exercise sessions, all participants performed a 6‐week resistance exercise intervention to determine the metabolic response to chronic resistance exercise training (Fig. 1).
(A) Change in circulating plasma irisin during an acute bout of resistance training and an acute bout of aerobic training. Baseline and 45 min resistance‐EX; P = 0.182; Baseline and 45 min aerobic‐EX; P = 0.028. (B) Percentage change in circulating plasma irisin during an acute bout of resistance training and an acute bout of aerobic training. difference from baseline in resistance‐EX: P = 0.162; Difference from baseline; aerobic‐EX:P = 0.013.
Conclusion
In conclusion, results of our study suggest that the metabolic response to endurance exercise training varies considerably among obese youth. Acute increases in plasma irisin explain a portion of the metabolic response to endurance exercise training in obese youth. More studies with larger sample sizes are needed to confirm our results and to explore other adipomyokines and metabolic adaptations to exercise training in obese youth.
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