View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues

Ming Li; You Lu; Alun Rongxiang Wang

doi:doi:10.11648/j.cmr.20180705.14

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View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues

Ming Li, You Lu, Alun Rongxiang Wang

Published in Clinical Medicine Research (Volume 7, Issue 5)

Received: 20 August 2018 Accepted: 31 October 2018 Published: 26 November 2018

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Abstract

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.

Published in	Clinical Medicine Research (Volume 7, Issue 5)
DOI	10.11648/j.cmr.20180705.14
Page(s)	124-130
Creative Commons	This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.
Copyright	Copyright © The Author(s), 2018. Published by Science Publishing Group

Keywords

nsulin Resistance, Hyperinsulinemia, T-type Ca²⁺ Channel

References

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APA Style

Ming Li, You Lu, Alun Rongxiang Wang. (2018). View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues. Clinical Medicine Research, 7(5), 124-130. https://doi.org/10.11648/j.cmr.20180705.14

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ACS Style

Ming Li; You Lu; Alun Rongxiang Wang. View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues. Clin. Med. Res. 2018, 7(5), 124-130. doi: 10.11648/j.cmr.20180705.14

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AMA Style

Ming Li, You Lu, Alun Rongxiang Wang. View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues. Clin Med Res. 2018;7(5):124-130. doi: 10.11648/j.cmr.20180705.14

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@article{10.11648/j.cmr.20180705.14,
  author = {Ming Li and You Lu and Alun Rongxiang Wang},
  title = {View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues},
  journal = {Clinical Medicine Research},
  volume = {7},
  number = {5},
  pages = {124-130},
  doi = {10.11648/j.cmr.20180705.14},
  url = {https://doi.org/10.11648/j.cmr.20180705.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20180705.14},
  abstract = {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.},
 year = {2018}
}

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TY  - JOUR
T1  - View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues
AU  - Ming Li
AU  - You Lu
AU  - Alun Rongxiang Wang
Y1  - 2018/11/26
PY  - 2018
N1  - https://doi.org/10.11648/j.cmr.20180705.14
DO  - 10.11648/j.cmr.20180705.14
T2  - Clinical Medicine Research
JF  - Clinical Medicine Research
JO  - Clinical Medicine Research
SP  - 124
EP  - 130
PB  - Science Publishing Group
SN  - 2326-9057
UR  - https://doi.org/10.11648/j.cmr.20180705.14
AB  - 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.
VL  - 7
IS  - 5
ER  -

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Author Information

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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Plain Text BibTeX RIS

APA Style

Ming Li, You Lu, Alun Rongxiang Wang. (2018). View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues. Clinical Medicine Research, 7(5), 124-130. https://doi.org/10.11648/j.cmr.20180705.14

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ACS Style

Ming Li; You Lu; Alun Rongxiang Wang. View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues. Clin. Med. Res. 2018, 7(5), 124-130. doi: 10.11648/j.cmr.20180705.14

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AMA Style

Ming Li, You Lu, Alun Rongxiang Wang. View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues. Clin Med Res. 2018;7(5):124-130. doi: 10.11648/j.cmr.20180705.14

Copy | Download

@article{10.11648/j.cmr.20180705.14,
  author = {Ming Li and You Lu and Alun Rongxiang Wang},
  title = {View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues},
  journal = {Clinical Medicine Research},
  volume = {7},
  number = {5},
  pages = {124-130},
  doi = {10.11648/j.cmr.20180705.14},
  url = {https://doi.org/10.11648/j.cmr.20180705.14},
  eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cmr.20180705.14},
  abstract = {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.},
 year = {2018}
}

Copy | Download

TY  - JOUR
T1  - View Insulin Resistance from an Interaction Between Pancreatic Islets and Peripheral Tissues
AU  - Ming Li
AU  - You Lu
AU  - Alun Rongxiang Wang
Y1  - 2018/11/26
PY  - 2018
N1  - https://doi.org/10.11648/j.cmr.20180705.14
DO  - 10.11648/j.cmr.20180705.14
T2  - Clinical Medicine Research
JF  - Clinical Medicine Research
JO  - Clinical Medicine Research
SP  - 124
EP  - 130
PB  - Science Publishing Group
SN  - 2326-9057
UR  - https://doi.org/10.11648/j.cmr.20180705.14
AB  - 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.
VL  - 7
IS  - 5
ER  -

Copy | Download