Hypothesis: Postprandial remnant lipoproteins are the causal factors that induce the insulin resistance associated with obesity
Hypothesis: Postprandial remnant lipoproteins are the causal factors that induce the insulin resistance associated with obesity
复制标题
假设：餐后残余脂蛋白是诱发与肥胖相关的胰岛素抵抗的致病因素
DOI：
10.1016/j.cca.2018.06.029
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发表时间：
2018
影响因子：
5
通讯作者：
Tanaka Akira
中科院分区：
文献类型：
--
作者：
Nakajima Katsuyuki;Tokita Yoshiharu;Tanaka Akira
长期以来，我们认为血浆中残余脂蛋白（RLP）的显著增加是脂蛋白代谢紊乱导致肥胖和胰岛素抵抗的结果。因此，认为胰岛素抵抗引起并促进RLP形成。相反，该假说认为RLP诱导胰岛素抵抗是与过量脂肪摄入相关的肥胖的结果。脂肪摄入后血浆TG升高的大部分是RLP中的TG（RLP-TG），餐后RLP的大部分是VLDL残留，而不是CM残留。RLP是新形成的脂蛋白，主要用于抵抗饥饿的能量供应，就像碳水化合物摄入后的血糖。由于携带apoE、LPL和Lp（a）的RLP作为VLDL受体的配体起作用，因此RLP与内脏脂肪脂肪细胞中的VLDL受体相互作用并储存为TG，类似于过量血糖。然而，过量的VLDL残余物诱导肥胖及其相关的胰岛素抵抗，其作为代谢多米诺效应的引发剂起着重要作用，类似于血糖主要作为能量供应以防止饥饿。
We have long thought that remnant lipoproteins (RLP) in plasma are significantly increased as the result of disturbed lipoprotein metabolism followed by obesity and insulin resistance. Therefore, it was believed that insulin resistance causes and enhances RLP formation. In contrast, this hypothesis states that RLP induces insulin resistance as the result of obesity associated with the excessive fat intake. The majority of plasma TG increased after fat intake is TG in RLP (RLP-TG) and the majority of postprandial RLP is VLDL remnants, not CM remnants. RLP is newly formed lipoproteins primarily for energy supply against starvation, like blood sugar after carbohydrate intake. Since RLP bearing apoE, LPL and Lp(a) function as ligands for the VLDL receptor, RLP interacts with the VLDL receptor in visceral fat adipocytes and stored as TG similar to excessive blood sugar. However, the excessive VLDL remnants induces obesity and its associated insulin resistance, which plays a major role as the initiator of metabolic domino effects, similar to blood sugar primarily serving as an energy supply to protect against starvation.