Evidence map›Paper›PMID 33611885›Full record

ArticleDiabetes & metabolism journal2021

Ipragliflozin, an SGLT2 Inhibitor, Ameliorates High-Fat Diet-Induced Metabolic Changes by Upregulating Energy Expenditure through Activation of the AMPK/ SIRT1 Pathway.

Ji-Yeon Lee, Minyoung Lee, Ji Young Lee, Jaehyun Bae, Eugene Shin, Yong-Ho Lee, Byung-Wan Lee, Eun Seok Kang, Bong-Soo Cha

Open access · goldAbstract read
In one paragraph

Article in Diabetes & metabolism journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

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  18. Immunomodulatory Effects of SGLT2 Inhibitors-Targeting Inflammation and Oxidative Stress in Aging.International journal of environmental research and public health · 2023
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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

9 authors at 1 institution in 1 country.

Ji-Yeon Lee *Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Minyoung Lee *Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Ji Young Lee *Department of Molecular, Cellular and Cancer Biology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Seoul, Korea.
Jaehyun BaeDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Eugene ShinInstitute of Endocrine Research, Yonsei University College of Medicine, Seoul, Korea.
Yong-Ho LeeDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Byung-Wan LeeDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Eun Seok KangDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Bong-Soo ChaDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul, Korea.
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSodium-glucose co-transporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs that exhibit multiple extraglycemic effects. However, there are conflicting results regarding the effects of SGLT2 inhibition on energy expenditure and thermogenesis. Therefore, we investigated the effect of ipragliflozin (a selective SGLT2 inhibitor) on energy metabolism.

methodsSix-week-old male 129S6/Sv mice with a high propensity for adipose tissue browning were randomly assigned to three groups: normal chow control, 60% high-fat diet (HFD)-fed control, and 60% HFD-fed ipragliflozin-treated groups. The administration of diet and medication was continued for 16 weeks.

resultsThe HFD-fed mice became obese and developed hepatic steatosis and adipose tissue hypertrophy, but their random glucose levels were within the normal ranges; these features are similar to the metabolic features of a prediabetic condition. Ipragliflozin treatment markedly attenuated HFD-induced hepatic steatosis and reduced the size of hypertrophied adipocytes to that of smaller adipocytes. In the ipragliflozin treatment group, uncoupling protein 1 (Ucp1) and other thermogenesis-related genes were significantly upregulated in the visceral and subcutaneous adipose tissue, and fatty acid oxidation was increased in the brown adipose tissue. These effects were associated with a significant reduction in the insulin-to-glucagon ratio and the activation of the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1) pathway in the liver and adipose tissue.

conclusionSGLT2 inhibition by ipragliflozin showed beneficial metabolic effects in 129S6/Sv mice with HFD-induced obesity that mimics prediabetic conditions. Our data suggest that SGLT2 inhibitors, through their upregulation of energy expenditure, may have therapeutic potential in prediabetic obesity.

Indexed as

Sodium-Glucose Transporter 2 InhibitorsAMP-Activated Protein KinasesAnimalsDiet, High-FatEnergy MetabolismGlucosidesMaleMiceSirtuin 1ThiophenesAMP-Activated Protein KinasesGlucosidesipragliflozinSirt1 protein, mouseSirtuin 1Sodium-Glucose Transporter 2 InhibitorsThiophenesAdipose tissueObesitySodium-glucose transporter 2 inhibitorsThermogenesis

Identifiers

PMID33611885
PMCPMC8640151
OpenAlexW3129683874

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.