Evidence map›Paper›PMID 26963613›Full record

ArticlePloS one2016

Dapagliflozin, a Sodium-Glucose Co-Transporter 2 Inhibitor, Acutely Reduces Energy Expenditure in BAT via Neural Signals in Mice.

Yumiko Chiba, Tetsuya Yamada, Sohei Tsukita, Kei Takahashi, Yuichiro Munakata, Yuta Shirai, Shinjiro Kodama, Yoichiro Asai, Takashi Sugisawa, Kenji Uno and 4 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05459701 (The Hepato-protective Effect of Dapagliflozin in Type 2 Diabetes Mellitus Patients), which is not on this map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.3field-weighted citation impact, top 8% 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.

NCT05459701 phase4completedstarted 2022, after this paper: background citation

The Hepato-protective Effect of Dapagliflozin in Type 2 Diabetes Mellitus Patients (T2DM) With Nonalcoholic Fatty Liver Disease (NAFLD)

Ran2022Enrolled50Registered outcomes3Posted comparisons0ConditionsNonalcoholic Fatty Liver Disease, Type 2 DiabetesArmsDapagliflozin 10mg Tab, Placebo
PMID 26914659PMID 23707905other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 72 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. New and future heart failure drugs.Nature cardiovascular research · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Renoprotective Effects of SGLT2 Inhibitors.Heart failure clinics · 2022
    Review
  15. Review
  16. Review
  17. Review
  18. Diabetes, Heart Failure and Beyond: Elucidating the Cardioprotective Mechanisms of Sodium Glucose Cotransporter 2 (SGLT2) Inhibitors.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2022
    Review
  19. Article
  20. Article
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

14 authors at 2 institutions in 1 country.

Yumiko ChibaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Tetsuya YamadaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Sohei TsukitaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Kei TakahashiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yuichiro MunakataDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yuta ShiraiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Shinjiro KodamaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Yoichiro AsaiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Takashi SugisawaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Kenji UnoDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Shojiro SawadaDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Junta ImaiDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Kazuhiro NakamuraDepartment of Integrative Physiology, Nagoya University Graduate School of Medicine, Nagoya, 466-8550, Japan.
Hideki KatagiriDepartment of Metabolism and Diabetes, Tohoku University Graduate School of Medicine, Sendai, 980-8575, Japan.
Tohoku University · JPNagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Selective sodium glucose cotransporter-2 inhibitor (SGLT2i) treatment promotes urinary glucose excretion, thereby reducing blood glucose as well as body weight. However, only limited body weight reductions are achieved with SGLT2i treatment. Hyperphagia is reportedly one of the causes of this limited weight loss. However, the effects of SGLT2i treatment on systemic energy expenditure have not been fully elucidated. Herein, we investigated the acute effects of dapagliflozin, a SGLT2i, on systemic energy expenditure in mice. Eighteen hours after dapagliflozin treatment oxygen consumption and brown adipose tissue (BAT) expression of ucp1, a thermogenesis-related gene, were significantly decreased as compared to those after vehicle treatment. In addition, dapagliflozin significantly suppressed norepinephrine (NE) turnover in BAT and c-fos expression in the rostral raphe pallidus nucleus (rRPa) which contains the sympathetic premotor neurons responsible for thermogenesis. These findings indicate that the dapagliflozin-mediated acute decrease in energy expenditure involves a reduction in BAT thermogenesis via decreased sympathetic nerve activity from the rRPa. Furthermore, common hepatic branch vagotomy abolished the reductions in ucp1 expression and NE contents in BAT and c-fos expression in the rRPa. In addition, alterations in hepatic carbohydrate metabolism, such as decreases in glycogen contents and upregulation of phosphoenolpyruvate carboxykinase, manifested prior to the suppression of BAT thermogenesis, e.g. 6 hours after dapagliflozin treatment. Collectively, these results suggest that SGLT2i treatment acutely suppresses energy expenditure in BAT via regulation of an inter-organ neural network consisting of the common hepatic vagal branch and sympathetic nerves.

Indexed as

Sodium-Glucose Transporter 2 InhibitorsAdipose Tissue, BrownAnimalsBenzhydryl CompoundsCarbohydrate MetabolismEnergy MetabolismGene Expression RegulationGlucosidesGlycogenIon ChannelsLiverMaleMiceMidbrain Raphe NucleiMitochondrial ProteinsProto-Oncogene Proteins c-fosBenzhydryl CompoundsdapagliflozinGlucosidesGlycogenIon ChannelsMitochondrial ProteinsProto-Oncogene Proteins c-fosSlc5a2 protein, mouseSodium-Glucose Transporter 2Sodium-Glucose Transporter 2 InhibitorsUcp1 protein, mouseUncoupling Protein 1

Identifiers

PMID26963613
PMCPMC4786146
OpenAlexW2295311043

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.