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Glucagon secretion and signaling in the development of diabetes

Overview of attention for article published in Frontiers in Physiology, January 2012
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  • Good Attention Score compared to outputs of the same age (77th percentile)
  • High Attention Score compared to outputs of the same age and source (80th percentile)

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4 X users
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1 Facebook page
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1 Wikipedia page

Citations

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Title
Glucagon secretion and signaling in the development of diabetes
Published in
Frontiers in Physiology, January 2012
DOI 10.3389/fphys.2012.00349
Pubmed ID
Authors

Herbert Y. Gaisano, Patrick E. MacDonald, Mladen Vranic

Abstract

Normal release of glucagon from pancreatic islet α-cells promotes glucose mobilization, which counteracts the hypoglycemic actions of insulin, thereby ensuring glucose homeostasis. In treatment of diabetes aimed at rigorously reducing hyperglycemia to avoid chronic complications, the resulting hypoglycemia triggering glucagon release from α-cells is frequently impaired, with ensuing hypoglycemic complications. This review integrates the physiology of glucagon secretion regulating glucose homeostasis in vivo to single α-cell signaling, and how both become perturbed in diabetes. α-cells within the social milieu of the islet micro-organ are regulated not only by intrinsic signaling events but also by paracrine regulation, particularly by adjacent insulin-secreting β-cells and somatostatin-secreting δ-cells. We discuss the intrinsic α-cell signaling events, including glucose sensing and ion channel regulation leading to glucagon secretion. We then discuss the complex crosstalk between the islet cells and the breakdown of this crosstalk in diabetes contributing to the dysregulated glucagon secretion. Whereas, there are many secretory products released by β- and δ-cells that become deficient or excess in diabetes, we discuss the major ones, including the better known insulin and lesser known somatostatin, which act as putative paracrine on/off switches that very finely regulate α-cell secretory responses in health and diabetes. Of note in several type 1 diabetes (T1D) rodent models, blockade of excess somatostatin actions on α-cell could normalize glucagon secretion sufficient to attain normoglycemia in response to hypoglycemic assaults. There has been slow progress in fully elucidating the pathophysiology of the α-cell in diabetes because of the small number of α-cells within an islet and the islet mass becomes severely reduced and inflamed in diabetes. These limitations are just now being surmounted by new approaches.

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X Demographics

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 182 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Mexico 2 1%
Switzerland 1 <1%
United Kingdom 1 <1%
Italy 1 <1%
Canada 1 <1%
Iraq 1 <1%
Unknown 175 96%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 41 23%
Student > Master 31 17%
Student > Doctoral Student 15 8%
Researcher 15 8%
Student > Bachelor 14 8%
Other 27 15%
Unknown 39 21%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 44 24%
Agricultural and Biological Sciences 38 21%
Medicine and Dentistry 33 18%
Chemistry 5 3%
Nursing and Health Professions 5 3%
Other 14 8%
Unknown 43 24%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 5. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 24 March 2021.
All research outputs
#5,849,842
of 22,675,759 outputs
Outputs from Frontiers in Physiology
#2,641
of 13,467 outputs
Outputs of similar age
#52,354
of 244,088 outputs
Outputs of similar age from Frontiers in Physiology
#59
of 309 outputs
Altmetric has tracked 22,675,759 research outputs across all sources so far. This one has received more attention than most of these and is in the 73rd percentile.
So far Altmetric has tracked 13,467 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.5. This one has done well, scoring higher than 80% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 244,088 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 77% of its contemporaries.
We're also able to compare this research output to 309 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 80% of its contemporaries.