Evidence map›Paper›PMID 32128655›Full record

ReviewReviews in endocrine & metabolic disorders2020

Type 2 diabetes - unmet need, unresolved pathogenesis, mTORC1-centric paradigm.

Jacob Bar-Tana

Open access · hybridAbstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Weight of time: exploring the link between obesity and aging.Aging clinical and experimental research · 2025
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
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  11. DNA methylation profile of liver of mice conceived byJournal of developmental origins of health and disease · 2022
    Article
  12. The TWEAK/Fn14/CD163 axis-implications for metabolic disease.Reviews in endocrine & metabolic disorders · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Acne Comorbidities.Clinical, cosmetic and investigational dermatology · 2022
    Review
  17. Article
  18. Review
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Jacob Bar-TanaHebrew University Medical School, 91120, Jerusalem, Israel. jacobb@ekmd.huji.ac.il.ORCID http://orcid.org/0000-0002-7697-9679
Hebrew University of Jerusalem · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The current paradigm of type 2 diabetes (T2D) is gluco-centric, being exclusively categorized by glycemic characteristics. The gluco-centric paradigm views hyperglycemia as the primary target, being driven by resistance to insulin combined with progressive beta cells failure, and considers glycemic control its ultimate treatment goal. Most importantly, the gluco-centric paradigm considers the non-glycemic diseases associated with T2D, e.g., obesity, dyslipidemia, hypertension, macrovascular disease, microvascular disease and fatty liver as 'risk factors' and/or 'outcomes' and/or 'comorbidities', rather than primary inherent disease aspects of T2D. That is in spite of their high prevalence (60-90%) and major role in profiling T2D morbidity and mortality. Moreover, the gluco-centric paradigm fails to realize that the non-glycemic diseases of T2D are driven by insulin and, except for glycemic control, response to insulin in T2D is essentially the rule rather than the exception. Failure of the gluco-centric paradigm to offer an exhaustive unifying view of the glycemic and non-glycemic diseases of T2D may have contributed to T2D being still an unmet need. An mTORC1-centric paradigm maintains that hyperactive mTORC1 drives the glycemic and non-glycemic disease aspects of T2D. Hyperactive mTORC1 is proposed to act as double-edged agent, namely, to interfere with glycemic control by disrupting the insulin receptor-Akt transduction pathway, while concomitantly driving the non-glycemic diseases of T2D. The mTORC1-centric paradigm may offer a novel perspective for T2D in terms of pathogenesis, clinical focus and treatment strategy.

Indexed as

Diabetes ComplicationsDiabetes Mellitus, Type 2AnimalsHumansMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 1Insulin resistanceMammalian target of rapamycin (mTOR)Metabolic syndromeType 2 diabetes

Identifiers

PMID32128655
PMCPMC7560924
OpenAlexW3009816666

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.