Evidence mapPaperPMID 37481263Full record

ArticleThe Journal of clinical endocrinology and metabolism2023

Emergence of a New Glucoregulatory Mechanism for Glycemic Control With Dapagliflozin/Exenatide Therapy in Type 2 Diabetes.

Eugenio Cersosimo, Mariam Alatrach, Carolina Solis-Herrera, Gozde Baskoy, John Adams, Andrea Hansis-Diarte, Amalia Gastaldelli, Alberto Chavez, Curtis Triplitt, Ralph A DeFronzo

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. SGLT2 inhibitors: cardiorenal metabolic drugs for the ages.The Journal of clinical investigation · 2024
    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

10 authors at 1 institution in 1 country.

Eugenio CersosimoDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.ORCID 0000-0002-2573-0208
Mariam AlatrachDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
Carolina Solis-HerreraDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.ORCID 0000-0002-6215-9418
Gozde BaskoyDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
John AdamsDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
Andrea Hansis-DiarteDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
Amalia GastaldelliDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
Alberto ChavezDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
Curtis TriplittDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
Ralph A DeFronzoDepartment of Medicine, Division of Diabetes, University of Texas Health Science Center and Texas Diabetes Institute, University Health System, San Antonio, TX 78229, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Ketones, Muscle Metabolism, and SGLT2 InhibitorsR01DK107680 · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · 2025 to 2025
$583k
NIDDK NIH HHS R01 DK107680NIH/NIDDK RO1-DK107680-05
6 · The paper itself

Abstract

contextThis study addresses the development of a new glucoregulatory mechanism in type 2 diabetes (T2D) patients treated with SGLT-2 inhibitors, which is independent of glucose, insulin and glucagon. The data suggest the presence of a potential trigger factor (s) arising in the kidney that stimulates endogenous glucose production (EGP) during sustained glycosuria.

objectiveTo investigate effects of SGLT-2 inhibitor therapy together with GLP-1 receptor agonist on EGP and glucose kinetics in patients with T2D. Our hypothesis was that increased EGP in response to SGLT2i-induced glycosuria persists for a long period and is not abolished by GLP-1 RA stimulation of insulin secretion and glucagon suppression.

methodsSeventy-five patients received a 5-hour dual-tracer oral glucose tolerance test (OGTT) (intravenous 3-(3H)-glucose oral (1-14C)-glucose): (1) before/after 1 of dapagliflozin (DAPA); exenatide (EXE), or both, DAPA/EXE (acute study), and (2) after 1 and 4 months of therapy with each drug.

resultsIn the acute study, during the OGTT plasma glucose (PG) elevation was lower in EXE (Δ = 42 ± 1 mg/dL) than DAPA (Δ = 72 ± 3), and lower in DAPA/EXE (Δ = 11 ± 3) than EXE and DAPA. EGP decrease was lower in DAPA (Δ = -0.65 ± 0.03 mg/kg/min) than EXE (Δ = -0.96 ± 0.07); in DAPA/EXE (Δ = -0.84 ± 0.05) it was lower than EXE, higher than DAPA. At 1 month, similar PG elevations (EXE, Δ = 26 ± 1 mg/dL; DAPA, Δ = 62 ± 2, DAPA/EXE, Δ = 27 ± 1) and EGP decreases (DAPA, Δ = -0.60 ± 0.05 mg/kg/min; EXE, Δ = -0.77 ± 0.04; DAPA/EXE, Δ = -0.72 ± 0.03) were observed. At 4 months, PG elevations (EXE, Δ = 55 ± 2 mg/dL; DAPA, Δ = 65 ± 6; DAPA/EXE, Δ = 46 ± 2) and lower EGP decrease in DAPA (Δ = -0.66 ± 0.04 mg/kg/min) vs EXE (Δ = -0.84 ± 0.05) were also comparable; in DAPA/EXE (Δ = -0.65 ± 0.03) it was equal to DAPA and lower than EXE. Changes in plasma insulin/glucagon could not explain higher EGP in DAPA/EXE vs EXE mg/kg/min.

conclusionOur findings provide strong evidence for the emergence of a new long-lasting, glucose-independent, insulin/glucagon-independent, glucoregulatory mechanism via which SGLT2i-induced glycosuria stimulates EGP in patients with T2D. SGLT2i plus GLP-1 receptor agonist combination therapy is accompanied by superior glycemic control vs monotherapy.

Indexed as

Diabetes Mellitus, Type 2GlycosuriaSodium-Glucose Transporter 2 InhibitorsBenzhydryl CompoundsBlood GlucoseExenatideGlucagonGlucagon-Like Peptide-1 Receptor AgonistsGlucoseGlucosidesGlycemic ControlHumansHypoglycemic AgentsInsulinBenzhydryl CompoundsBlood GlucosedapagliflozinExenatideGlucagonGlucagon-Like Peptide-1 Receptor AgonistsGlucoseGlucosidesHypoglycemic AgentsInsulinSodium-Glucose Transporter 2 Inhibitorsendogenous glucose productionGLP-1 receptor agonistsglucose regulationkidneySGLT-2 inhibitorstype 2 diabetes

Identifiers

PMID37481263
PMCPMC12187005
OpenAlexW4385071434

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.