Evidence map›Paper›PMID 35163806›Full record

ReviewInternational journal of molecular sciences2022

Physiologic Insulin Resensitization as a Treatment Modality for Insulin Resistance Pathophysiology.

Frank Greenway, Brian Loveridge, Richard M Grimes, Tori R Tucker, Michael Alexander, Scott A Hepford, Justin Fontenot, Candi Nobles-James, Carol Wilson, Adam M Starr and 3 more

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Pathology of Diabetes-Induced Immune Dysfunction.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Review
  7. 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

13 authors at 5 institutions in 1 country.

Frank GreenwayClinical Trials Unit, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808, USA.
Brian LoveridgeDiabetes Relief, Layton, UT 84041, USA.
Richard M GrimesDepartment of Internal Medicine, McGovern Medical School, University of Texas Health Science Center, Houston, TX 77030, USA.
Tori R TuckerDepartment of Development and Cell Biology, University of California Irvine, Irvine, CA 92617, USA.
Michael AlexanderDepartment of Surgery, University of California Irvine, Orange, CA 92868, USA.
Scott A HepfordWell Cell Global LLC, Houston, TX 77079, USA.
Justin FontenotLafayette Arthritis and Endocrine Clinic, Lafayette, LA 70506, USA.
Candi Nobles-JamesDivision of Endocrinology, Mercer University School of Medicine, Macon, GA 31207, USA.
Carol WilsonWell Cell Support LLC, Houston, TX 77079, USA.
Adam M StarrDepartment of Orthopedic Surgery, Asheville Orthopedic Associates P.A, Asheville, NC 28801, USA.
Mohammed AbdelsaidBiomedical Sciences Department, Mercer University School of Medicine, Savannah, GA 31404, USA.
Stanley T LewisEselle Health, Inc., La Jolla, CA 92037, USA.
Jonathan R T LakeyDepartment of Surgery, University of California Irvine, Orange, CA 92868, USA.
University of California, Irvine · USMercer University · USAsheville Cardiology Associates · USLouisiana State University · USThe University of Texas Health Science Center at Houston · US

Funding

Tracking & Evaluation CoreU54GM104940 · NIGMS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI Peter Todd Katzmarzyk · 2012 to 2026
$69.1M
National Institute of Genetic Engineering and Biotechnology 1 U54 GM104940NIGMS NIH HHS U54 GM104940
6 · The paper itself

Abstract

Prevalence of type 2 diabetes increased from 2.5% of the US population in 1990 to 10.5% in 2018. This creates a major public health problem, due to increases in long-term complications of diabetes, including neuropathy, retinopathy, nephropathy, skin ulcers, amputations, and atherosclerotic cardiovascular disease. In this review, we evaluated the scientific basis that supports the use of physiologic insulin resensitization. Insulin resistance is the primary cause of type 2 diabetes. Insulin resistance leads to increasing insulin secretion, leading to beta-cell exhaustion or burnout. This triggers a cascade leading to islet cell destruction and the long-term complications of type 2 diabetes. Concurrent with insulin resistance, the regular bursts of insulin from the pancreas become irregular. This has been treated by the precise administration of insulin more physiologically. There is consistent evidence that this treatment modality can reverse the diabetes-associated complications of neuropathy, diabetic ulcers, nephropathy, and retinopathy, and that it lowers HbA1c. In conclusion, physiologic insulin resensitization has a persuasive scientific basis, significant treatment potential, and likely cost benefits.

Indexed as

Insulin ResistanceDiabetes Mellitus, Type 2Glycated HemoglobinHumansInsulin, Regular, HumanInsulin SecretionPancreasGlycated Hemoglobinhemoglobin A1c protein, humanInsulin, Regular, Humancardiovascular diseasechronic kidney diseaseCKDdiabetesinsulin infusioninsulin resistancemetabolic disordernephropathyneuropathyobesityphysiologic insulin resensitizationPIRretinopathytreatment modality

Identifiers

PMID35163806
PMCPMC8836751
OpenAlexW4211246034

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.