View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues
Clinical Medicine Research
Volume 7, Issue 5, September 2018, Pages: 124-130
Received: Aug. 20, 2018; Accepted: Oct. 31, 2018; Published: Nov. 26, 2018
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Ming Li, Department of Physiology, Tulane University, New Orleans, USA
You Lu, Department of Physiology, Tulane University, New Orleans, USA
Alun Rongxiang Wang, Department of Pathology, Tulane University, New Orleans, USA
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Curl rent hypotheses of insulin resistance mostly emphasize cellular mechanisms in peripheral tissues. Although received broad recognition, these opinions may have overlooked the interaction between pancreatic endocrine cells and the peripheral tissues in the process of establishment and maintenance of insulin resistance in the whole body. It has been suggested that basal hyperinsulinemia is the root cause of insulin resistance. Basal insulin release does not share the same intracellular mechanism of high glucose stimulated insulin release; instead, it is regulated by local Ca2+ fluctuation and activation of the cAMP-Epac2/Rap1 signaling pathway. Basal insulin release is controlled by the interaction between pancreatic head β-cells and pancreatic tail α-cells, which release insulin and glucagon, respectively. In diabetes, an elevated basal insulin level would mitigate the sensitivity of peripheral tissues to insulin; the decreased insulin sensitivity and elevated plasma glucose concentration could further stimulate more basal insulin release partially by increasing T-type Ca2+ channel expression and activity in β-cells. This interaction forms a positive feedback loop. Therefore, T-type Ca2+ channel antagonists can potentially be employed to break this positive feedback loop, thus reversing insulin resistance.
nsulin Resistance, Hyperinsulinemia, T-type Ca2+ Channel
To cite this article
Ming Li, You Lu, Alun Rongxiang Wang, View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues, Clinical Medicine Research. Vol. 7, No. 5, 2018, pp. 124-130. doi: 10.11648/j.cmr.20180705.14
Copyright © 2018 Authors retain the copyright of this article.
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