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职业迁徙
个人简介
Research in my laboratory focuses on studies of insulin action and how insulin’s action is altered by insulin resistance, obesity, and diabetes mellitus. Specific studies currently underway involve measuring insulin’s action to regulate its delivery to skeletal muscle by acting on endothelial and smooth muscle cells. Insulin relaxes smooth muscle cells associated with terminal arterioles and dilates microvascular vessels to enhance tissue perfusion, thereby increasing the delivery of both insulin and glucose to the tissues. This vasodilator effect appears to be secondary to insulin’s action on the endothelial cell to increase nitric oxide production via the activation of the enzyme nitric oxide synthase.
We have also demonstrated the second effect of insulin on the endothelial cell. This involves insulin promoting its uptake at the luminal surface of the endothelial cell and which then transports the insulin across to the abluminal surface of the cell, where it is released and becomes available to act on target tissues like adipocytes and myocytes. We have experimental evidence that insulin’s ability to cause smooth muscle relaxation and promote its transport is impaired in states of insulin resistance (e.g., obesity, type 2 diabetes). This step involving insulin transport across the endothelium appears to be the rate-limiting step for overall insulin action on skeletal muscle (which is the major target tissue for insulin-mediated glucose disposal).
We are also studying how these processes are affected by the action of other growth factors (growth hormone and IGF-I). A major hypothesis that we are exploring is that a significant fraction of the insulin resistance which is encountered in skeletal muscle in states like obesity, diabetes, and hypertension is attributable to impaired action of insulin on the microvasculature in addition to any effect on the muscle cell per se.
We have also demonstrated the second effect of insulin on the endothelial cell. This involves insulin promoting its uptake at the luminal surface of the endothelial cell and which then transports the insulin across to the abluminal surface of the cell, where it is released and becomes available to act on target tissues like adipocytes and myocytes. We have experimental evidence that insulin’s ability to cause smooth muscle relaxation and promote its transport is impaired in states of insulin resistance (e.g., obesity, type 2 diabetes). This step involving insulin transport across the endothelium appears to be the rate-limiting step for overall insulin action on skeletal muscle (which is the major target tissue for insulin-mediated glucose disposal).
We are also studying how these processes are affected by the action of other growth factors (growth hormone and IGF-I). A major hypothesis that we are exploring is that a significant fraction of the insulin resistance which is encountered in skeletal muscle in states like obesity, diabetes, and hypertension is attributable to impaired action of insulin on the microvasculature in addition to any effect on the muscle cell per se.
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Abigail G Wolpe,Melissa A Luse, Christopher Baryiames, Wyatt J Schug, Jacob B Wolpe,Scott R Johnstone,Luke S Dunaway, Zuzanna J Juśkiewicz, Skylar A Loeb,Henry R Askew Page,Yen-Lin Chen,Vikram Sabapathy,
Science signalingno. 821 (2024): eadg2622-eadg2622
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