Favourable alterations in adipose remodelling induced by exercise training without weight loss: exploring the role of microvascular endothelial function.
Favourable alterations in adipose remodelling induced by exercise training without weight loss: exploring the role of microvascular endothelial function.
复制标题
无体重减轻的运动训练诱导脂肪重构的有利改变：探索微血管内皮功能的作用。
DOI：
10.1113/jp283091
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发表时间：
2022-08
影响因子：
5.5
通讯作者：
Clayton, Zachary S.
中科院分区：
文献类型：
--
作者：
Maurer, Grace S.;Clayton, Zachary S.
肥胖是美国的一个主要健康问题，与心血管和代谢疾病的患病率增加有关。大约三分之一的美国人口是肥胖，强调肥胖作为一个相关的生物医学问题，需要立即关注。肥胖与脂肪细胞/脂肪组织功能障碍相关，其部分特征在于脂肪细胞肥大和增生、不利的细胞外基质重塑、纤维化和增加的炎症（Unamuno et al. 2018).脂肪组织炎症是由脂肪组织内的各种常驻细胞类型（如脂肪细胞、巨噬细胞、B细胞和T细胞）引起的，可以自分泌、旁分泌和内分泌方式发挥作用。例如，从脂肪细胞释放的促炎细胞因子肿瘤坏死因子α（TNFα）可作用于脂肪细胞上的细胞表面受体，进一步增加TNFα的产生（自分泌）。由功能失调的脂肪细胞分泌的各种激素、细胞因子和代谢物可对周围组织产生负面影响，使得从脂肪细胞释放的促炎细胞因子可促进组织如骨骼肌和肝脏中的炎症（旁分泌）。脂肪细胞相关的炎症也可导致细胞因子释放到体循环（内分泌）中。此外，功能失调的脂肪细胞储存新脂肪酸的能力有限，这导致体循环中脂肪酸的丰度更高，这可能进一步促进炎症。这些各种信号传导机制的损伤可引起局部（组织/细胞水平）胰岛素抵抗和化合物诱导全身性胰岛素抵抗。
Obesity is a major health problem in the United States and is associated with increased prevalence of cardiovascular and metabolic diseases. Approximately one-third of the United States population is obese, underscoring obesity as a relevant biomedical issue that requires immediate attention. Obesity is associated with adipocyte/adipose tissue dysfunction which is characterized, in part, by adipocyte hypertrophy and hyperplasia, adverse extracellular matrix remodeling, fibrosis, and increased inflammation (Unamuno et al., 2018).Adipose tissue inflammation, which is contributed to by a variety of resident cell types within adipose tissue–eg, adipocytes, macrophages, B cells, and T cells–can act in an autocrine, paracrine, and endocrine fashion. For example, the pro-inflammatory cytokine tumor-necrosis factor alpha (TNFα) released from adipocytes can act on cell surface receptors on adipocytes, further increasing TNFα production (autocrine). The various hormones, cytokines, and metabolites secreted by dysfunctional adipocytes can negatively impact the surrounding tissues, such that pro-inflammatory cytokines released from adipocytes can promote inflammation in tissues such as skeletal muscle and the liver (paracrine). Adipocyte-related inflammation can also cause the release of cytokines into the systemic circulation (endocrine). Additionally, dysfunctional adipocytes have a limited ability to store new fatty acids, which results in a greater abundance of fatty acids in the systemic circulation, which can further promote inflammation. Impairments in these various signaling mechanisms can cause local (tissue/cellular level) insulin resistance and compound to induce systemic insulin resistance.