Evidence map›Paper›PMID 32423964›Full record

ArticleBMJ open diabetes research & care2020

Insulin enhances renal glucose excretion: relation to insulin sensitivity and sodium-glucose cotransport.

Ele Ferrannini, Ricardo Pereira-Moreira, Marta Seghieri, Eleni Rebelos, Aglécio L Souza, Valeria B Chueire, Caterina Arvia, Elza Muscelli

Open access · goldAbstract read
In one paragraph

Article in BMJ open diabetes research & care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

6 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Human Glucose Transporters in Renal Glucose Homeostasis.International journal of molecular sciences · 2021
    Review
  5. Review
  6. Insulin: Trigger and Target of Renal Functions.Frontiers in cell and developmental biology · 2020
    Review
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

8 authors at 4 institutions in 2 countries.

Ele Ferrannini *Institute of Clinical Physiology, CNR, Pisa, Italy ferranni@ifc.cnr.it.ORCID 0000-0002-1384-1584
Ricardo Pereira-Moreira *Department of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Marta SeghieriDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Eleni RebelosDepartment of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Aglécio L SouzaDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Valeria B ChueireDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Caterina ArviaFondazione Toscana Gabriele Monasterio, Pisa, Italy.
Elza MuscelliDepartment of Internal Medicine, School of Medical Sciences, University of Campinas, Campinas, Brazil.
Universidade Estadual de Campinas (UNICAMP) · BRUniversity of Pisa · ITFondazione Toscana Gabriele Monasterio · ITIstituto di Fisiologia Clinica · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionInsulin regulates renal glucose production and utilization; both these fluxes are increased in type 2 diabetes (T2D). Whether insulin also controls urinary glucose excretion is not known.

methodsWe applied the pancreatic clamp technique in 12 healthy subjects and 13 T2D subjects. Each participant received a somatostatin infusion and a variable glucose infusion to achieve (within 1 hour) and maintain glycemia at 22 mmol/L for 3 hours; next, a constant insulin infusion (240 pmol/min/kg) was added for another 3 hours. Urine was collected separately in each period for glucose and creatinine determination.

resultsDuring saline, glucose excretion was lower in T2D than controls in absolute terms (0.49 (0.32) vs 0.69 (0.18) mmol/min, median (IQR), p=0.01) and as a fraction of filtered glucose (16.2 (6.4) vs 19.9 (7.5)%, p<0.001). With insulin, whole-body glucose disposal rose more in controls than T2D (183 (48) vs 101 (48) µmol/kg

conclusionsAcute exogenous insulin infusion jointly stimulates renal glucose and sodium excretion, indicating that the effect may be mediated by SGLTs. This action is resistant in patients with diabetes, accounting for their increased retention of glucose and sodium, and is not abolished by partial SGLT2 inhibition by empagliflozin.

Indexed as

Diabetes Mellitus, Type 2Insulin ResistanceGlucoseHumansInsulinSodiumGlucoseInsulinSodiumglucose transportinsulinkidneysodium glucose cotransporter

Identifiers

PMID32423964
PMCPMC7245398
OpenAlexW3027861866

What OpenQuestion holds

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LicenceCC BY-NC
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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.