Acute exercise increases the contact between lipid droplets and mitochondria independently of obesity and type 2 diabetes

Abstract

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.

Role of Perilipins in Oxidative Stress—Implications for Cardiovascular Disease

“…Contrary to maladaptive remodeling, physiological cardiac hypertrophy is considered harmless, completely reversible, and mostly occurs in response to increased workload such as exercise. Mounting evidence supports the notion that ROS as well as Plin levels are tightly regulated during exercise-induced adaptations [128][129][130][131][132]. Further investigations are needed to elucidate the interplay between Plins and ROS in the context of exercise and physiological hypertrophy.…”

Physically active pregnancies: Insights from the placenta

“…Yet, physically active participants with insufficient gestational weight gain showed a greater LD coverage on the fetal placental side, suggesting that PA promotes the accumulation of LD at the fetal side in cases of inadequate weight gain. While PA boosts LD-mitochondria interactions in skeletal muscle (de Almeida et al, 2023), with increased contact between LD and mitochondria facilitating increased direct transfer of fatty acids (FA) to the mitochondria for oxidation, this interaction in placental tissue has yet to be explored. Further, proteins coating LD such as the perilipin (PLIN) family are integral in FA storage and release, and findings in skeletal muscle suggest differential expression in response to PA (Peters et al, 2012;Pourteymour et al, 2015).…”