Evidence map›Paper›PMID 27866224›Full record

ArticleDiabetologia2017

The beneficial effects of empagliflozin, an SGLT2 inhibitor, on atherosclerosis in ApoE

Ji Hye Han, Tae Jung Oh, Ghayoung Lee, Hyo Jin Maeng, Dong Hwa Lee, Kyoung Min Kim, Sung Hee Choi, Hak Chul Jang, Hye Seung Lee, Kyong Soo Park and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed, 5 pooled it
11.6field-weighted citation impact, top 1% 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

153 citing papers in PubMed, 5 syntheses or guidelines pooled it, 280 citations in OpenAlex.

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  19. Type 2 diabetes mellitus.Nature reviews. Disease primers · 2026
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93 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 2 countries.

Ji Hye HanDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Tae Jung OhDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Ghayoung LeeDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Hyo Jin MaengDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Dong Hwa LeeDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Kyoung Min KimDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Sung Hee ChoiDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Hak Chul JangDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070.
Hye Seung LeeDepartment of Pathology, Seoul National University College of Medicine and Seoul National University Bundang Hospital, Seongnam, South Korea.
Kyong Soo ParkDepartment of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea.
Young-Bum KimDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Soo LimDepartment of Internal Medicine, Seoul National University College of Medicine and Seoul National University Bundang Hospital, 300 Gumi-dong, Bundang-gu, Seongnam-city, South Korea, 463-070. limsoo@snu.ac.kr.
Seoul National University Bundang Hospital · KRHarvard University · USSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisA recent large clinical study has shown that empagliflozin has a lower rate of cardiovascular and all-cause mortality when compared with placebo in patients with type 2 diabetes. We investigated the effect of empagliflozin (compared with glimepiride) on the progression of atherosclerosis, and its possible mechanisms of action.

methodsForty-eight 5-week-old male ApoE

resultsAfter 8 weeks of treatment, the empagliflozin and glimepiride groups exhibited decreased blood glucose levels. Atherosclerotic plaque areas in the aortic arch/valve were significantly smaller in the empagliflozin groups than in the control or glimepiride groups. Insulin resistance and circulating concentrations of TNF-α, IL-6, monocyte chemoattractant protein-1 (MCP-1), serum amyloid A and urinary microalbumin decreased after empagliflozin treatment, and this significantly correlated with plaque size. Empagliflozin treatment reduced weight and fat mass, lipid droplets in the liver, fat cell size, mRNA expression of Tnf, Il6 and Mcp-1 (also known as Ccl2) and the infiltration of inflammatory cells in plaque and adipose tissue compared with the control or glimepiride group. Empagliflozin treatment increased adiponectin levels. CONCLUSIONS/

interpretationImprovements in inflammation and insulin resistance seem to be mechanisms involved in the mitigation of atherosclerosis by empagliflozin.

Indexed as

Sodium-Glucose Transporter 2 InhibitorsAdipose TissueAnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticApolipoproteins EAtherosclerosisBenzhydryl CompoundsBlotting, WesternCD11c AntigenCD68 MoleculeCell LineCell ProliferationDiabetes Mellitus, Type 2Diet, WesternGlucosidesAntigens, CDAntigens, Differentiation, MyelomonocyticApolipoproteins EBenzhydryl CompoundsCD11c AntigenCD68 antigen, humanCD68 MoleculeempagliflozinGlucosidesSodium-Glucose Transporter 2 InhibitorsAtherosclerosisInsulin resistanceSodium glucose cotransporterType 2 diabetes

Identifiers

PMID27866224
OpenAlexW2555543235

What Socratic 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 Socratic graph.