Evidence map›Paper›PMID 26389599›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2015

ACE2 deficiency reduces β-cell mass and impairs β-cell proliferation in obese C57BL/6 mice.

Robin Shoemaker, Frederique Yiannikouris, Sean Thatcher, Lisa Cassis

Abstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.0field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
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  6. Article
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  8. Review
  9. COVID-19 induced Diabetes: A novel presentation.Diabetes research and clinical practice · 2022
    Review
  10. Review
  11. Children With Short Stature Display ReducedFrontiers in endocrinology · 2022
    Article
  12. Diabetes and COVID-19; A Bidirectional Interplay.Frontiers in endocrinology · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Robin ShoemakerDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
Frederique YiannikourisDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
Sean ThatcherDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky.
Lisa CassisDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, Kentucky lcassis@uky.edu.
University of Kentucky · US

Funding

WU P&FP30DK020579 · NIDDK · WASHINGTON UNIVERSITY · PI Jennifer Lynn Powers Carson · 2013 to 2026
$27.1M
The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2012 to 2017
$13.7M
Angiotensin: A Link Between Obesity and HypertensionR01HL073085 · NHLBI · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2003 to 2017
$5.0M
NHLBI NIH HHS R01 HL073085NIDDK NIH HHS P30 DK020579NIGMS NIH HHS P20 GM-103527NIGMS NIH HHS P20 GM103527PHS HHS R01 73085
6 · The paper itself

Abstract

Drugs that inhibit the renin-angiotensin system (RAS) decrease the onset of type 2 diabetes (T2D). Pancreatic islets express RAS components, including angiotensin-converting enzyme 2 (ACE2), which cleaves angiotensin II (Ang II) to angiotensin-(1-7) [Ang-(1-7)]. Overexpression of ACE2 in pancreas of diabetic mice improved glucose homeostasis. The purpose of this study was to determine if deficiency of endogenous ACE2 contributes to islet dysfunction and T2D. We hypothesized that ACE2 deficiency potentiates the decline in β-cell function and augments the development of diet-induced T2D. Male Ace2(+/y) or Ace2(-/y) mice were fed a low-fat (LF) or high-fat (HF) diet for 1 or 4 mo. A subset of 1-mo HF-fed mice were infused with Sal (Sal), losartan (Los), or Ang-(1-7). At 4 mo, while both genotypes of HF-fed mice developed a similar level of insulin resistance, adaptive hyperinsulinemia was reduced in Ace2(-/y) vs. Ace2(+/y) mice. Similarly, in vivo glucose-stimulated insulin secretion (GSIS) was reduced in 1-mo HF-fed Ace2(-/y) compared with Ace2(+/y) mice, resulting in augmented hyperglycemia. The average islet area was significantly smaller in both LF- and HF-fed Ace2(-/y) vs. Ace2(+/y) mice. Additionally, β-cell mass and proliferation were reduced significantly in HF-fed Ace2(-/y) vs. Ace2(+/y) mice. Neither infusion of Los nor Ang-(1-7) was able to correct impaired in vivo GSIS of HF-fed ACE2-deficient mice. These results demonstrate a critical role for endogenous ACE2 in the adaptive β-cell hyperinsulinemic response to HF feeding through regulation of β-cell proliferation and growth.

Indexed as

Angiotensin-Converting Enzyme 2AnimalsCell CountCell ProliferationDiet, High-FatFemaleGlucose IntoleranceInsulinInsulin-Secreting CellsInsulin SecretionMaleMiceMice, Inbred C57BLMice, KnockoutMice, ObeseObesityAce2 protein, mouseAngiotensin-Converting Enzyme 2InsulinPeptidyl-Dipeptidase AACE2diabetesβ-cell

Identifiers

PMID26389599
PMCPMC4593774
OpenAlexW2298465989

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.