Evidence map›Paper›PMID 30104701›Full record

ReviewNature reviews. Molecular cell biology2018

Metabolites as regulators of insulin sensitivity and metabolism.

Qin Yang, Archana Vijayakumar, Barbara B Kahn

Registry-linked trialAbstract readReview
In one paragraph

Review in Nature reviews. Molecular cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07284316 (Effect of a Multidomain Intervention Plus Turmeric on the Prevention of Cognitive Decline in People Over 55 Years of Age With Insulin Resistance), which is not on this map. Cited by 369 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
369citing papers in PubMed, 2 pooled it
16.0field-weighted citation impact, top 1% 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.

NCT07284316 phase2 / phase3active not recruitingnot on this mapstarted 2025, after this paper: background citation

Effect of a Multidomain Intervention Plus Turmeric on the Prevention of Cognitive Decline in People Over 55 Years of Age With Insulin Resistance: A Randomized Clinical Trial

TypeinterventionalSponsorInstituto Mexicano del Seguro SocialRan2025 to 2027Enrolled100ConditionsCognitive Decline, Subjective Cognitive Impairment, Insulin ResistanceArmsTurmeric extract, Control: Placebo. 500mg gelatin in capsules 2 times a day
3 · Its place in the literature

Who cites it

369 citing papers in PubMed, 2 syntheses or guidelines pooled it, 688 citations in OpenAlex.

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  18. O-Acetyl-Serine Supplementation Enhances Insulin Secretion and Improves Postprandial Glycaemia in Lean and Prediabetic Mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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309 more citing papers are in PubMed but not listed here.

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

3 authors at 3 institutions in 1 country.

Qin YangDepartment of Medicine and Physiology, UC Irvine Diabetes Center, Center for Epigenetics and Metabolism, University of California at Irvine, Irvine, CA, USA. qin.yang@uci.edu.
Archana VijayakumarDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.
Barbara B KahnDivision of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. bkahn@bidmc.harvard.edu.
Beth Israel Deaconess Medical Center · USHarvard University · USUniversity of California, Irvine · US

Funding

Regulation of the biosynthesis of a novel class of anti-diabetic lipidsR01DK106210 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B., SAGHATELIAN, ALAN · 2016 to 2024
$6.6M
GLUCOSE TRANSPORTER REGULATION IN OBESITY AND DIABETESR01DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 1992 to 2020
$4.4M
A PSGL-1 Glycopeptide Mimetic for Treatment of Metabolic SyndromeR01DK107405 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CHAIKOF, ELLIOT, KAHN, BARBARA B. · 2016 to 2019
$2.5M
Nicotinamide N-methyltransferase is a novel regulator of energy expenditureR01DK100385 · NIDDK · UNIVERSITY OF CALIFORNIA-IRVINE · PI YANG, QIN · 2014 to 2018
$1.7M
NIDDK NIH HHS R01 DK043051NIDDK NIH HHS R01 DK100385NIDDK NIH HHS R01 DK106210NIDDK NIH HHS R01 DK107405
6 · The paper itself

Abstract

The cause of insulin resistance in obesity and type 2 diabetes mellitus (T2DM) is not limited to impaired insulin signalling but also involves the complex interplay of multiple metabolic pathways. The analysis of large data sets generated by metabolomics and lipidomics has shed new light on the roles of metabolites such as lipids, amino acids and bile acids in modulating insulin sensitivity. Metabolites can regulate insulin sensitivity directly by modulating components of the insulin signalling pathway, such as insulin receptor substrates (IRSs) and AKT, and indirectly by altering the flux of substrates through multiple metabolic pathways, including lipogenesis, lipid oxidation, protein synthesis and degradation and hepatic gluconeogenesis. Moreover, the post-translational modification of proteins by metabolites and lipids, including acetylation and palmitoylation, can alter protein function. Furthermore, the role of the microbiota in regulating substrate metabolism and insulin sensitivity is unfolding. In this Review, we discuss the emerging roles of metabolites in the pathogenesis of insulin resistance and T2DM. A comprehensive understanding of the metabolic adaptations involved in insulin resistance may enable the identification of novel targets for improving insulin sensitivity and preventing, and treating, T2DM.

Indexed as

AnimalsDiabetes Mellitus, Type 2GlucoseGlucose Metabolism DisordersHumansInsulinInsulin ResistanceLipid MetabolismLiverMetabolic Networks and PathwaysMetabolomicsObesityReceptor, InsulinSignal TransductionGlucoseInsulinReceptor, Insulin

Identifiers

PMID30104701
PMCPMC6380503
OpenAlexW2886808233

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.