Evidence mapPaperPMID 39439079Full record

ArticleJournal of the peripheral nervous system : JPNS2024

Glucose-lowering medication associated with weight loss may limit the progression of diabetic neuropathy in type 2 diabetes.

Georgios Ponirakis, Ibrahim Al-Janahi, Einas Elgassim, Rawan Hussein, Ioannis N Petropoulos, Hoda Gad, Adnan Khan, Hadeel B Zaghloul, Mashhood A Siddique, Hamda Ali and 18 more

Abstract read
In one paragraph

Article in Journal of the peripheral nervous system : JPNS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Assessing corneal dendritic cells in glucose dysregulation small-fibre neuropathy.Journal of the peripheral nervous system : JPNS · 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

28 authors.

Georgios PonirakisDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.ORCID https://orcid.org/0000-0002-6936-1248
Ibrahim Al-JanahiNational Diabetes Center, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Einas ElgassimDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Rawan HusseinDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Ioannis N PetropoulosDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Hoda GadDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Adnan KhanDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.ORCID https://orcid.org/0000-0003-4647-6672
Hadeel B ZaghloulDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Mashhood A SiddiqueNational Diabetes Center, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Hamda AliNational Diabetes Center, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Fatima F S MohamedDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Lina H M AhmedDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Youssra DakrouryDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Abeer M M El ShewehyDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Ruba SaeidDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Fadwa MahjoubDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Shaikha N Al-ThaniDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Farheen AhmedDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Moayad HomssiDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Salah MahmoudDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Nebras H HadidDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Aisha Al ObaidanDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Iuliia SalivonNational Diabetes Center, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Ziyad R MahfoudDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.
Mahmoud A ZirieNational Diabetes Center, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Yousuf Al-AnsariNational Diabetes Center, Hamad General Hospital, Hamad Medical Corporation, Doha, Qatar.
Stephen L AtkinRoyal College of Surgeons in Ireland Bahrain, Adliya, Bahrain.
Rayaz A MalikDepartment of Medicine, Weill Cornell Medicine-Qatar, Qatar Foundation, Doha, Qatar.ORCID https://orcid.org/0000-0002-7188-8903

Funding

Qatar National Research Fund BMRP-5726113101Qatar National Research Fund NPRP 8-315-3-065
6 · The paper itself

Abstract

aimObesity is a major risk factor for diabetic peripheral neuropathy (DPN) in type 2 diabetes (T2D). This study investigated the effect of glucose lowering medication associated with weight change on DPN.

methodsParticipants with T2D were grouped based on whether their glucose lowering medications were associated with weight gain (WG) or weight loss (WL). They underwent clinical, metabolic testing and assessment of neuropathic symptoms, vibration perception threshold (VPT), sudomotor function and corneal confocal microscopy (CCM) at baseline and follow-up between 4 and 7 years.

resultsOf 76 participants, 69.7% were on glucose lowering medication associated with WG, and 30.3% were on glucose lowering medication associated with WL. At baseline, participants in the WG group had a significantly longer duration of diabetes (p < .01), higher douleur neuropathique en 4 (DN4) score (p < .0001) and VPT (p = .01) compared with those in the WL group. Over a 56-month period, participants in the WG group showed no significant change in body weight (p = .11), HbA1c (p = .18), triglycerides (p = .42), DN4 (p = .11), VPT (p = .15) or Sudoscan (p = .43), but showed a decline in corneal nerve fiber density (CNFD), corneal nerve branch density (CNBD) and corneal nerve fiber length (CNFL) (p < .0001). Participants in the WL group showed a reduction in weight (p = .01) and triglycerides (p < .05), no change in DN4 (p = .30), VPT (p = .31) or Sudoscan (p = .17) and a decline in the corneal nerve branch density (p < .01).

conclusionsParticipants treated with glucose lowering medication associated with weight gain had worse neuropathy and greater loss of corneal nerves during follow-up, compared to patients treated with medication associated with weight loss.

Indexed as

Diabetes Mellitus, Type 2Diabetic NeuropathiesHypoglycemic AgentsWeight LossAgedDisease ProgressionFemaleFollow-Up StudiesHumansMaleMiddle AgedObesityHypoglycemic Agentscorneal confocal microscopydiabetic peripheral neuropathyglucose lowering medicationtype 2 diabetesweight change

Identifiers

PMID39439079
PMCPMC11625975

What Socratic holds

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Registered trials

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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.