Evidence mapPaperPMID 32191645Full record

Trial reportThe Journal of clinical investigation2020

Free fatty acid processing diverges in human pathologic insulin resistance conditions.

Hilal Sekizkardes, Stephanie Therese Chung, Shaji Chacko, Morey W Haymond, Megan Startzell, Mary Walter, Peter J Walter, Marissa Lightbourne, Rebecca J Brown

4 registry-linked trialsOpen access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 4 registered trials, which are not on this map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.4field-weighted citation impact, top 3% 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.

NCT00001987 recruitingnot on this map

Natural History of Disorders of Insulin Resistance

TypeobservationalSponsorNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Ran1976Enrolled1,200ConditionsDiabetes Mellitus, Severe Insulin ResistanceArmsHR-pQCT scan
NCT00085982 phase2active not recruitingnot on this map

Phase II Trial of Effect of Metreleptin Therapy in Severe Insulin Resistance

TypeinterventionalSponsorNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Ran2003 to 2030Enrolled11ConditionsSevere Insulin ResistanceArmsMetreleptin
NCT01778556 phase2completednot on this map

Short Term Effects of Leptin Withdrawal or Initiation in Lipodystrophy Independent of Energy Intake

TypeinterventionalSponsorNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Ran2013 to 2018Enrolled25ConditionsLipodystrophyArmsMetreleptin
NCT02457897 phase2completednot on this map

Thyroid Hormone to Induce Non-Insulin Mediated Glucose Disposal in Patients With Insulin Receptor Mutations

TypeinterventionalSponsorNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)Ran2015 to 2018Enrolled7ConditionsInsulin Resistance, Diabetes Mellitus, Abnormal Glucose MetabolismArmsLiothyronine
3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 59 citations in OpenAlex.

  1. Trial
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  14. Protective Effects of Curcumin and its AnaloguesCurrent medicinal chemistry · 2024
    Review
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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

9 authors at 3 institutions in 2 countries.

Hilal SekizkardesNational Institute of Child Health and Human Development.
Stephanie Therese ChungNational Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.
Shaji ChackoChildren's Nutrition Research Center, Department of Pediatrics, US Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston, Texas, USA.
Morey W HaymondChildren's Nutrition Research Center, Department of Pediatrics, US Department of Agriculture/Agricultural Research Service, Baylor College of Medicine, Houston, Texas, USA.
Megan StartzellNational Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.
Mary WalterNational Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.
Peter J WalterNational Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.
Marissa LightbourneNational Institute of Child Health and Human Development.
Rebecca J BrownNational Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, Maryland, USA.
National Institute of Diabetes and Digestive and Kidney Diseases · USChildren's Nutrition Research Center at Baylor College of Medicine · USHealth and Human Development (2HD) Research Network · CM

Funding

Clinical Mass Spectrometry CoreZICDK075039 · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · 2025 to 2025
$3.3M
Molecular and Clinical Studies of Insulin ResistanceZIADK047050 · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · 2025 to 2025
$833k
Clinical utility of leptin therapy in syndromic forms of insulin resistance.ZIADK047052 · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · 2025 to 2025
$417k
6 · The paper itself

Abstract

BACKGROUNDPostreceptor insulin resistance (IR) is associated with hyperglycemia and hepatic steatosis. However, receptor-level IR (e.g., insulin receptor pathogenic variants, INSR) causes hyperglycemia without steatosis. We examined 4 pathologic conditions of IR in humans to examine pathways controlling lipid metabolism and gluconeogenesis.METHODSCross-sectional study of severe receptor IR (INSR, n = 7) versus postreceptor IR that was severe (lipodystrophy, n = 14), moderate (type 2 diabetes, n = 9), or mild (obesity, n = 8). Lipolysis (glycerol turnover), hepatic glucose production (HGP), gluconeogenesis (deuterium incorporation from body water into glucose), hepatic triglyceride (magnetic resonance spectroscopy), and hepatic fat oxidation (plasma β-hydroxybutyrate) were measured.RESULTSLipolysis was 2- to 3-fold higher in INSR versus all other groups, and HGP was 2-fold higher in INSR and lipodystrophy versus type 2 diabetes and obesity (P < 0.001), suggesting severe adipose and hepatic IR. INSR subjects had a higher contribution of gluconeogenesis to HGP, approximately 77%, versus 52% to 59% in other groups (P = 0.0001). Despite high lipolysis, INSR subjects had low hepatic triglycerides (0.5% [interquartile range 0.1%-0.5%]), in contrast to lipodystrophy (10.6% [interquartile range 2.8%-17.1%], P < 0.0001). β-hydroxybutyrate was 2- to 7-fold higher in INSR versus all other groups (P < 0.0001), consistent with higher hepatic fat oxidation.CONCLUSIONThese data support a key pathogenic role of adipose tissue IR to increase glycerol and FFA availability to the liver in both receptor and postreceptor IR. However, the fate of FFA diverges in these populations. In receptor-level IR, FFA oxidation drives gluconeogenesis rather than being reesterified to triglyceride. In contrast, in postreceptor IR, FFA contributes to both gluconeogenesis and hepatic steatosis.TRIAL REGISTRATIONClinicalTrials.gov NCT01778556, NCT00001987, and NCT02457897.FUNDINGNational Institute of Diabetes and Digestive and Kidney Diseases, US Department of Agriculture/Agricultural Research Service 58-3092-5-001.

Indexed as

Insulin ResistanceLipolysisAdipose TissueAdolescentAdultAntigens, CDChildCross-Sectional StudiesFatty AcidsFemaleHumansLipodystrophyMaleMiddle AgedReceptor, InsulinAntigens, CDFatty AcidsINSR protein, humanReceptor, InsulinAdipose tissueEndocrinologyGlucose metabolismInsulin

Identifiers

PMID32191645
PMCPMC7324196
OpenAlexW3012007437

What Socratic holds

Textmetadata
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.