Obesity is associated with bioenergetic dysfunction of peripheral muscles; however, little is known regarding the impact of obesity on the diaphragm. We hypothesized that obesity would be associated with diaphragm dysfunction attributable to mitochondrial oxygen consumption and structural and ultrastructural changes. Wistar rat litters were culled to 3 pups to induce early postnatal overfeeding and consequent obesity. Control animals were obtained from unculled litters. From postnatal day 150, diaphragm ultrasonography, computed tomography, high-resolution respirometry, immunohistochemical, biomolecular and ultrastructural histological analyses were performed. The diaphragms of obese animals, compared to those of controls, exhibited presented changes in morphology as increased thickening fraction, diaphragm excursion and diaphragm dome height, as well as increased mitochondrial respiratory capacity coupled to ATP synthesis and maximal respiratory capacity. Fatty acid synthase expression was also higher in obese animals, suggesting a source of energy for the respiratory chain. Myosin heavy chain-IIA was increased, indicating shift from glycolytic toward oxidative muscle fiber profile. Diaphragm tissue also exhibited ultrastructural changes, such as compact, round, and swollen mitochondria with fainter cristae and more lysosomal bodies. Dynamin-1 expression in the diaphragm was reduced in obese rats, suggesting decreased mitochondrial fission. Furthermore, gene expressions of peroxisome gamma proliferator-activated receptor co-activator-1α and superoxide dismutase-2 were lower in obese animals than in controls, which may indicate a predisposition to oxidative injury. In conclusion, in the obesity model used herein, muscle fiber phenotype was altered in a manner likely associated with increased mitochondrial respiratory capability, suggesting respiratory adaptation to increased metabolic demand.

中文翻译：

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实验肥胖对隔膜结构，功能和生物代谢的影响。

肥胖与周围肌肉的生物能功能障碍有关。然而，关于肥胖对the肌的影响知之甚少。我们假设肥胖将与线粒体耗氧以及结构和超微结构的变化引起的structural肌功能障碍有关。将Wistar大鼠窝淘汰为3只幼崽，以诱导出生后早期的过度喂养和随之而来的肥胖。对照动物获自未清除的垫料。从出生后第150天开始，进行diaphragm膜超声检查，计算机断层扫描，高分辨率呼​​吸测定，免疫组织化学，生物分子和超微结构的组织学分析。与对照组相比，肥胖动物的diaphragm肌表现出形态上的变化，即增厚率，diaphragm肌偏移和diaphragm肌穹顶高度增加，以及增加的线粒体呼吸能力以及ATP合成和最大呼吸能力。肥胖动物中脂肪酸合酶的表达也较高，这暗示了呼吸链的能量来源。肌球蛋白重链-IIA增加，表明从糖酵解转变为氧化性肌纤维分布。横tissue膜组织还表现出超微结构变化，例如线粒体紧凑，圆形和肿胀，ista部较薄，溶酶体较小。肥胖大鼠隔膜中的Dynamin-1表达降低，表明线粒体裂变减少。此外，肥胖动物中过氧化物酶体γ增殖物激活受体共激活因子1α和超氧化物歧化酶-2的基因表达低于对照组，这可能表明易患氧化损伤。结论，