Evidence map›Paper›PMID 32998869›Full record

ArticleBMJ open diabetes research & care2020

Oral administration of NPC43 counters hyperglycemia and activates insulin receptor in streptozotocin-induced type 1 diabetic mice.

Zi-Jian Lan, Zhenmin Lei, Lucinda Nation, Xian Li, Alexandros Yiannikouris, Thirupathi Reddy Yerramreddy, Hayley Kincaid, Katie Eastridge, Rijin Xiao, Ryan Goettl and 1 more

Abstract 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 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Ginsenoside Rg1 Ameliorates Pancreatic Injuries via the AMPK/mTOR Pathway in vivo and in vitro.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
    Article
  4. Activation of Insulin Signaling by Botanical Products.International journal of molecular sciences · 2021
    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

11 authors.

Zi-Jian Lan *Division of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA zlan@alltech.com rpower@alltech.com.ORCID 0000-0002-5904-6834
Zhenmin LeiDepartment of OB/GYN, University of Louisville School of Medicine, Louisville, Kentucky, USA.
Lucinda NationDivision of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA.
Xian LiDepartment of OB/GYN, University of Louisville School of Medicine, Louisville, Kentucky, USA.
Alexandros YiannikourisChemistry Department, Alltech, Inc, Nicholasville, Kentucky, USA.
Thirupathi Reddy YerramreddyChemistry Department, Alltech, Inc, Nicholasville, Kentucky, USA.
Hayley KincaidDivision of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA.
Katie EastridgeDivision of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA.
Rijin XiaoDivision of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA.
Ryan GoettlDivision of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA.
Ronan Power *Division of Life Sciences, Alltech, Inc, Nicholasville, Kentucky, USA zlan@alltech.com rpower@alltech.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionAdenosine, 5'-Se-methyl-5'-seleno-,2',3'-diacetate (NPC43) is a recently identified small, non-peptidyl molecule which restores normal insulin signaling in a mouse model of type 2 diabetes (Lan RESEARCH DESIGN AND

methodsIn this study, STZ was intraperitoneally injected into wild-type mice to induce hyperglycemia and hypoinsulinemia, the main features of T1D. These STZ-induced T1D mice were given NPC43 orally or intraperitoneally and blood glucose levels were measured using a glucometer. Protein levels of phosphorylated and total Insrβ, protein kinase B (Akt) and AS160 (critical for glucose uptake) in the skeletal muscle and liver of STZ-induced T1D mice following oral NPC43 treatment were determined by western blot analysis. In addition, hepatic expression of activated Insr in STZ-induced T1D mice after intraperitoneal NPC43 treatment was measured by ELISA. Student's t-test was used for statistical analysis.

resultsOral administration of NPC43 at a dose of 5.4 or 10.8 mg/kg body weight (mpk) effectively lowered blood glucose levels in STZ-induced T1D mice at ≥1 hour post-treatment and the glucose-lowering activity of oral NPC43 persisted for 5 hours. Blood glucose levels were also reduced in STZ-induced T1D mice following intraperitoneal NPC43 (5.4 mpk) treatment. Protein levels of phosphorylated Insrβ, Akt and AS160 were significantly increased in the skeletal muscle and liver of STZ-induced T1D mice after oral NPC43 (5.4 mpk) treatment. In addition, activation of hepatic Insr was observed in STZ-induced T1D mice following intraperitoneal NPC43 (5.4 mpk) treatment.

conclusionsWe conclude that NPC43 is a de facto fast-acting oral and injectable insulin mimetic which activates Insr and mitigates hyperglycemia in a mouse model of T1D.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2HyperglycemiaAdministration, OralAnimalsMiceReceptor, InsulinStreptozocinReceptor, InsulinStreptozocindiabetes mellitusexperimentalhyperglycemiamicepharmacology

Identifiers

PMID32998869
PMCPMC7528369

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.