Diabetes, Obesity and Atherosclerosis: Three Buds of One Stem MS-X

N. Chandra
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Abstract

Ideally insulin and leptin signaling share a common route and ditch each other depending on their surge in their affected physiological state. As a result, insulin and leptin resistances are simultaneous phenomena and no matter to induce other while the one is precipitated. Thus, the preponderance of running obesity and type-2 diabetes hand to hand is deeply expected. The (Figure 2) shows the common signaling road of both the ligands. Report shows that obesity reduces tyrosine phosphorylation of insulin receptor [12]. This affects insulin signaling and hence initiates insulin resistance. On the other hand, report also shows an association of insulin and LDL receptors [12-15] and this association keeps LDL receptor non-functional [12-15] making the system prone to vessel LDL accumulation. Yadav et al. has shown a decrease of LDL receptor mRNA level with increase of leptin concentration as well as two receptor association [14]. Repressed LDL receptor will reduce LDL clearance from blood vessels and the receptor-complex will keep receptors non-functional with concomitant Crimson Publishers Wings to the Research Mini Review
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糖尿病、肥胖和动脉粥样硬化:一茎三芽MS-X
理想情况下,胰岛素和瘦素信号共享一条共同的途径,并根据它们受影响的生理状态的激增而相互抛弃。因此,胰岛素抵抗和瘦素抵抗是同时发生的现象,一方沉淀,另一方诱导。因此,跑步型肥胖和2型糖尿病的优势是可以预见的。(图2)显示了这两种配体的共同信号通路。有报道表明,肥胖可降低胰岛素受体酪氨酸磷酸化[12]。这会影响胰岛素信号传导,从而引发胰岛素抵抗。另一方面,也有报道显示胰岛素和LDL受体存在关联[12-15],这种关联使LDL受体失去功能[12-15],使系统易于血管LDL积累。Yadav等研究表明,LDL受体mRNA水平随着瘦素浓度的升高而降低,两受体存在关联[14]。受抑制的LDL受体将减少LDL从血管中的清除,受体复合物将使受体失去功能
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