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• W3136647871 abstract "Background & aims Sarcopenic obesity (SO) increases the risk of mortality more than sarcopenia or obesity alone. Sarcopenia weakens the peripheral and respiratory muscles, leading to respiratory complications. It also induces mitochondrial dysfunction in the peripheral muscle; however, whether mitochondrial dysfunction in respiratory muscles differs among individuals with obesity, sarcopenia, and SO remains unknown. We evaluated the deterioration of respiratory muscle strength and mitochondrial function among normal, sarcopenia, obesity, and SO subjects. Methods Twenty-five patients who underwent lung resections were enrolled between April 2017 and January 2021, and their intercostal muscles were harvested. Based on their L3 muscle index and visceral fat area, the patients were divided into four groups (normal, obesity, sarcopenia, and SO). The clinical data, mRNA expression, and protein expressions associated with mitochondrial biogenesis/fusion/fission in the intercostal muscles were compared among the four groups. Results The respiratory muscle strength was evaluated using peak expiratory flow rate (PEFR). The PEFR values of the four groups were not significantly different. The levels of pAkt/Akt and mTOR (a marker of protein synthesis) were not significantly different among the four groups; however, those in the SO group were substantially lower than those in the sarcopenia or obesity groups. The levels of Atrogen-1 and MuRF1 (a marker of protein degradation) were not significantly different among the four groups; however, those in the SO group were substantially higher than those in the sarcopenia or obesity groups. Expression of PGC1-α (a marker of mitochondrial biogenesis) in the SO group was significantly lower than that in the normal group. MFN1 and MFN2 (marker of mitochondrial fusion) levels were significantly lower in the SO group than those in the normal group. DRP1 (a marker of mitochondrial fission) level in the SO group was substantially lower than that in the normal group. The expression of TNF-α (a pro-inflammatory cytokine) in the SO group was substantially lower than that in the normal group. Conclusion Our results suggest that the deterioration of protein synthesis and degradation of mitochondrial function in the respiratory muscles was most prominent in the SO before the weakening of the respiratory muscles. The deterioration mechanism may differentially regulate obesity, sarcopenia, and SO. Sarcopenic obesity (SO) increases the risk of mortality more than sarcopenia or obesity alone. Sarcopenia weakens the peripheral and respiratory muscles, leading to respiratory complications. It also induces mitochondrial dysfunction in the peripheral muscle; however, whether mitochondrial dysfunction in respiratory muscles differs among individuals with obesity, sarcopenia, and SO remains unknown. We evaluated the deterioration of respiratory muscle strength and mitochondrial function among normal, sarcopenia, obesity, and SO subjects. Twenty-five patients who underwent lung resections were enrolled between April 2017 and January 2021, and their intercostal muscles were harvested. Based on their L3 muscle index and visceral fat area, the patients were divided into four groups (normal, obesity, sarcopenia, and SO). The clinical data, mRNA expression, and protein expressions associated with mitochondrial biogenesis/fusion/fission in the intercostal muscles were compared among the four groups. The respiratory muscle strength was evaluated using peak expiratory flow rate (PEFR). The PEFR values of the four groups were not significantly different. The levels of pAkt/Akt and mTOR (a marker of protein synthesis) were not significantly different among the four groups; however, those in the SO group were substantially lower than those in the sarcopenia or obesity groups. The levels of Atrogen-1 and MuRF1 (a marker of protein degradation) were not significantly different among the four groups; however, those in the SO group were substantially higher than those in the sarcopenia or obesity groups. Expression of PGC1-α (a marker of mitochondrial biogenesis) in the SO group was significantly lower than that in the normal group. MFN1 and MFN2 (marker of mitochondrial fusion) levels were significantly lower in the SO group than those in the normal group. DRP1 (a marker of mitochondrial fission) level in the SO group was substantially lower than that in the normal group. The expression of TNF-α (a pro-inflammatory cytokine) in the SO group was substantially lower than that in the normal group. Our results suggest that the deterioration of protein synthesis and degradation of mitochondrial function in the respiratory muscles was most prominent in the SO before the weakening of the respiratory muscles. The deterioration mechanism may differentially regulate obesity, sarcopenia, and SO." @default.
• W3136647871 created "2021-03-29" @default.
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• W3136647871 date "2021-05-01" @default.
• W3136647871 modified "2023-09-24" @default.
• W3136647871 title "Deterioration of mitochondrial function in the human intercostal muscles differs among individuals with sarcopenia, obesity, and sarcopenic obesity" @default.
• W3136647871 cites W1493752155 @default.
• W3136647871 cites W1500436940 @default.
• W3136647871 cites W1570973990 @default.
• W3136647871 cites W1765706571 @default.
• W3136647871 cites W1777399276 @default.
• W3136647871 cites W1950561972 @default.
• W3136647871 cites W1969521541 @default.
• W3136647871 cites W1974422758 @default.
• W3136647871 cites W1977394375 @default.
• W3136647871 cites W1981614332 @default.
• W3136647871 cites W1985139869 @default.
• W3136647871 cites W2001819241 @default.
• W3136647871 cites W2002049655 @default.
• W3136647871 cites W2008589619 @default.
• W3136647871 cites W2017389761 @default.
• W3136647871 cites W2018384297 @default.
• W3136647871 cites W2021708686 @default.
• W3136647871 cites W2048046939 @default.
• W3136647871 cites W2048952126 @default.
• W3136647871 cites W2050112567 @default.
• W3136647871 cites W2055418044 @default.
• W3136647871 cites W2063111478 @default.
• W3136647871 cites W2083241104 @default.
• W3136647871 cites W2087393295 @default.
• W3136647871 cites W2090711760 @default.
• W3136647871 cites W2091214639 @default.
• W3136647871 cites W2093524310 @default.
• W3136647871 cites W2097022747 @default.
• W3136647871 cites W2102332997 @default.
• W3136647871 cites W2114063620 @default.
• W3136647871 cites W2118871284 @default.
• W3136647871 cites W2119027356 @default.
• W3136647871 cites W2122540540 @default.
• W3136647871 cites W2125078269 @default.
• W3136647871 cites W2127424726 @default.
• W3136647871 cites W2128677681 @default.
• W3136647871 cites W2141840873 @default.
• W3136647871 cites W2143410022 @default.
• W3136647871 cites W2145280166 @default.
• W3136647871 cites W2148366507 @default.
• W3136647871 cites W2148428406 @default.
• W3136647871 cites W2151698573 @default.
• W3136647871 cites W2162321723 @default.
• W3136647871 cites W2165718181 @default.
• W3136647871 cites W2169091672 @default.
• W3136647871 cites W2169501919 @default.
• W3136647871 cites W2170157817 @default.
• W3136647871 cites W2171217650 @default.
• W3136647871 cites W2176777883 @default.
• W3136647871 cites W2253924460 @default.
• W3136647871 cites W2268277946 @default.
• W3136647871 cites W2288712562 @default.
• W3136647871 cites W2326966452 @default.
• W3136647871 cites W2513613066 @default.
• W3136647871 cites W2529245535 @default.
• W3136647871 cites W2553464641 @default.
• W3136647871 cites W2617233822 @default.
• W3136647871 cites W2626238074 @default.
• W3136647871 cites W2747906925 @default.
• W3136647871 cites W2777880900 @default.
• W3136647871 cites W2791350230 @default.
• W3136647871 cites W2874175429 @default.
• W3136647871 cites W2884388698 @default.
• W3136647871 cites W2900946585 @default.
• W3136647871 cites W2909130616 @default.
• W3136647871 cites W2912987768 @default.
• W3136647871 cites W2923886615 @default.
• W3136647871 cites W2950169360 @default.
• W3136647871 cites W3093074122 @default.
• W3136647871 doi "https://doi.org/10.1016/j.clnu.2021.03.009" @default.
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