Department of Sports Science and Clinical Biomechanics, Faculty of Health Sciences, University of Southern Denmark, Odense, Denmark.
Steno Diabetes Center Odense, Odense University Hospital, Odense, Denmark.
J Physiol. 2023 May;601(10):1797-1815. doi: 10.1113/JP284386. Epub 2023 Apr 17.
Intramuscular lipid droplets (LDs) and mitochondria are essential organelles in cellular communication and metabolism, supporting local energy demands during muscle contractions. While insulin resistance impacts cellular functions and systems within the skeletal muscle, it remains unclear whether the interaction of LDs and mitochondria is affected by exercise and the role of obesity and type 2 diabetes. By employing transmission electron microscopy (TEM), we aimed to investigate the effects of 1 h of ergometry cycling on LD morphology, subcellular distribution and mitochondrial contact in skeletal muscle fibres of patients with type 2 diabetes and glucose-tolerant lean and obese controls, matched for equal exercise intensities. Exercise did not change LD volumetric density, numerical density, profile size or subcellular distribution. However, evaluated as the magnitude of inter-organelle contact, exercise increased the contact between LDs and mitochondria with no differences between the three groups. This effect was most profound in the subsarcolemmal space of type 1 muscle fibres, and here the absolute contact length increased on average from ∼275 to ∼420 nm. Furthermore, the absolute contact length before exercise (ranging from ∼140 to ∼430 nm) was positively associated with the fat oxidation rate during exercise. In conclusion, we showed that acute exercise did not mediate changes in the LD volume fractions, numbers or size but increased the contact between LDs and mitochondria, irrespective of obesity or type 2 diabetes. These data suggest that the increased LD-mitochondria contact with exercise is not disturbed in obesity or type 2 diabetes. KEY POINTS: Type 2 diabetes is associated with altered interactivity between lipid droplets (LDs) and mitochondria in the skeletal muscle. Physical contact between the surface of LDs and the surrounding mitochondrial network is considered favourable for fat oxidation. We show that 1 h of acute exercise increases the length of contact between LDs and mitochondria, irrespective of obesity or type 2 diabetes. This contact length between LDs and mitochondria is not associated with a net decrease in the LD volumetric density after the acute exercise. However, it correlates with the fat oxidation rate during exercise. Our data establish that exercise mediates contact between LDs and the mitochondrial network and that this effect is not impaired in individuals with type 2 diabetes or obesity.
肌内脂质滴（LDs）和线粒体是细胞通讯和代谢中的重要细胞器，在肌肉收缩期间支持局部能量需求。虽然胰岛素抵抗会影响骨骼肌中的细胞功能和系统，但尚不清楚 LDs 和线粒体之间的相互作用是否会受到运动的影响，以及肥胖和 2 型糖尿病的作用。通过使用透射电子显微镜（TEM），我们旨在研究 1 小时的运动自行车对 2 型糖尿病患者和葡萄糖耐受的瘦型和肥胖型对照者骨骼肌纤维中 LD 形态、亚细胞分布和线粒体接触的影响，这些患者的运动强度相等。运动并没有改变 LD 体积密度、数值密度、形态大小或亚细胞分布。然而，作为细胞器间接触程度来评估，运动增加了 LDs 和线粒体之间的接触，但三组之间没有差异。这种影响在 1 型肌纤维的肌膜下空间最为明显，在此空间，细胞器间的绝对接触长度平均从约 275nm 增加到约 420nm。此外，运动前的绝对接触长度（范围约为 140nm 至 430nm）与运动期间脂肪氧化率呈正相关。总之，我们表明，急性运动并没有介导 LD 体积分数、数量或大小的变化，但增加了 LDs 和线粒体之间的接触，与肥胖或 2 型糖尿病无关。这些数据表明，肥胖或 2 型糖尿病并不干扰运动引起的 LD-线粒体接触增加。关键点：2 型糖尿病与骨骼肌中脂质滴（LDs）和线粒体之间的相互作用改变有关。LD 表面与周围线粒体网络之间的物理接触被认为有利于脂肪氧化。我们表明，1 小时的急性运动增加了 LDs 和线粒体之间的接触长度，与肥胖或 2 型糖尿病无关。这种急性运动后，LD 体积密度没有净减少，LD 与线粒体之间的接触长度也没有变化。然而，它与运动期间的脂肪氧化率相关。我们的数据表明，运动介导了 LDs 与线粒体网络之间的接触，并且这种效应在 2 型糖尿病或肥胖个体中没有受损。
