Posgrado en Biología Experimental, Depto. de Ciencias de la Salud, Universidad Autónoma Metropolitana Unidad Iztapalapa, CDMX 09340, Mexico.
Laboratorio de Bioenergética y Envejecimiento Celular, Depto. de Ciencias de la Salud, Universidad Autónoma Metropolitana, Unidad Iztapalapa, CDMX 09340, Mexico.
Oxid Med Cell Longev. 2021 Aug 14;2021:5294266. doi: 10.1155/2021/5294266. eCollection 2021.
Osteosarcopenic obesity (OSO) is characterized by bone density, mass, and muscle strength loss, in conjunction with adipose tissue increase. OSO impairs physical activity and mobility, provoking autonomy loss; also, it is known that augmenting body fat in the elderly decreases life expectancy. The main factors influencing this health deterioration are the inflammatory environment induced by adipose tissue and its infiltration into muscle tissue, which leads to oxidative stress generation. Currently, there are several treatments to delay OSO, among which exercise training stands out because it improves muscle fiber quality and quantity and decreases adipose tissue. We have recently demonstrated that the combined treatment between moderate exercise and metformin slows sarcopenia's onset by a mechanism that includes adipose reduction and REDOX regulation. On the other hand, tert-butylhydroquinone (tBHQ) is a well-known antioxidant that counteracts oxidative stress. Therefore, to slow down obesity's harmful effects on muscle mass and bone mineral density, we performed different interventions, including combining a Fartlek-type exercise routine with metformin and tBHQ administration, in a model of middle-aged female Wistar rats with obesity induced with a hypercaloric diet. Our results showed that the combined exercise-metformin-tBHQ treatment increased muscle mass and strength, decreased body weight, body mass index, and fat percentage, and improved redox status, thus increasing animal survival.
骨肌减少型肥胖症(OSO)的特点是骨密度、质量和肌肉力量下降,同时脂肪组织增加。OSO 会损害身体活动和移动能力,导致自主能力丧失;此外,已知老年人体内脂肪增加会降低预期寿命。影响这种健康恶化的主要因素是脂肪组织引起的炎症环境及其对肌肉组织的浸润,这导致氧化应激的产生。目前,有几种治疗方法可以延缓 OSO,其中运动训练尤为突出,因为它可以改善肌肉纤维的质量和数量,减少脂肪组织。我们最近的研究表明,中等强度运动和二甲双胍联合治疗通过减少脂肪和调节氧化还原来延缓肌少症的发生,这一机制包括减少脂肪和调节氧化还原。另一方面,叔丁基对苯二酚(tBHQ)是一种众所周知的抗氧化剂,可以对抗氧化应激。因此,为了减缓肥胖对肌肉质量和骨矿物质密度的有害影响,我们在肥胖诱导的中年雌性 Wistar 大鼠模型中进行了不同的干预,包括将法特莱克式运动与二甲双胍和 tBHQ 联合使用。我们的结果表明,联合运动-二甲双胍-tBHQ 治疗增加了肌肉质量和力量,降低了体重、体重指数和脂肪百分比,并改善了氧化还原状态,从而提高了动物的存活率。