Evidence mapPaperPMID 1874938Full record

ArticleThe Journal of clinical endocrinology and metabolism1991

Mechanism of insulin resistance in insulin-dependent diabetes mellitus: a major role for reduced skeletal muscle blood flow.

A D Baron, M Laakso, G Brechtel, S V Edelman

2 registry-linked trialsAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
7.0field-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.

NCT02633488 nacompletedstarted 2014, after this paper: background citation

Effect of Metformin on Insulin Sensitivity and Pan-Arterial Vascular Function in Adults With Metabolic Syndrome

Ran2014Enrolled19Registered outcomes1Posted comparisons1ConditionsInsulin Sensitivity, Metabolic SyndromeArmsMetformin, Placebos
Open the trial in the graph
NCT04133922 early_phase1withdrawnstarted 2019, after this paper: background citation

Effect of GLP-1 on Microvascular Insulin Responses in Type 1 Diabetes

Ran2019Enrolled0Registered outcomes5Posted comparisons0ConditionsInsulin Sensitivity/Resistance, Type 1 DiabetesArmsDextrose 20 % in Water, GLP-1, Insulin
Open the trial in the graph
3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 214 citations in OpenAlex.

  1. Beneficial vascular effects of oral phosphatidylserine supplementation in type 2 diabetes.Journal of applied physiology (Bethesda, Md. : 1985) · 2026
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  11. Sympathetic transduction to blood pressure during euglycemic-hyperinsulinemia in young healthy adults: role of burst amplitude.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  12. Impact of sex and diet-induced weight loss on vascular insulin sensitivity in type 2 diabetes.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  13. Vascular deficits contributing to skeletal fragility in type 1 diabetes.Frontiers in clinical diabetes and healthcare · 2023
    Review
  14. New insights into mechanisms of endothelial insulin resistance in type 2 diabetes.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  15. Review
  16. ADAM17 cleaves the insulin receptor ectodomain on endothelial cells and causes vascular insulin resistance.American journal of physiology. Heart and circulatory physiology · 2022
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  17. Review
  18. Role of the arterial baroreflex in the sympathetic response to hyperinsulinemia in adult humans.American journal of physiology. Endocrinology and metabolism · 2022
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  20. Article

2 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

4 authors at 4 institutions in 1 country.

A D BaronDepartment of Medicine, Veterans Administration Medical Center, San Diego, California 92161.
M Laakso
G Brechtel
S V Edelman
Indiana University – Purdue University Indianapolis · USUniversity Medical Center · USUniversity of California, San Diego · USUniversity of California San Diego Medical Center · US

Funding

ZOVIRAX CREAM TO TREAT HERPES LABIALIS IN ADOLESCENTSM01RR000827 · UNIVERSITY OF CALIFORNIA SAN DIEGO · 1985 to 2005
$47.5M
ROLE OF HEMODYNAMICS IN IN VIVO INSULIN RESISTANCER37DK042469 · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · 1999 to 2003
$1.1M
INSULIN RESISTANCE IN NON-INSULIN-DEPENDENT DIABETESF05TW003969 · UNIVERSITY OF CALIFORNIA SAN DIEGO · 1987 to 1988
ROLE OF HEMODYNAMICS IN IN VIVO INSULIN RESISTANCER01DK042469 · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · 1995 to 1998
ROLE OF HEMODYNAMICS IN IN VIVO INSULIN RESISTANCER29DK042469 · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · 1990 to 1994
FIC NIH HHS TW-03969-01NCRR NIH HHS MO1-RR-00827NIDDK NIH HHS DK-42469
6 · The paper itself

Abstract

To define the kinetic mechanisms of insulin resistance (IR) in insulin-dependent diabetes (IDDM), we studied seven control (C) and five IDDM (glycohemoglobin, 14 +/- 2+) men matched for age (36 +/- 2 vs. 37 +/- 3 yr), lean body mass (59 +/- 2 vs. 58 +/- 3 kg), and leg volume (mean +/- SEM, 10.4 +/- 0.3 vs. 9.8 +/- 0.5 L). Maximal capacity (Vmax) and affinity (Km) for glucose uptake in whole body (WBGU) and leg skeletal muscle (LGU) were measured during a 120 mU/m2.min insulin infusion, and blood glucose was clamped at about 4, 7, 12, and 21 mmol/L. LGU = femoral arterio-venous glucose difference (FAVGD) X leg blood flow (LBF). Compared to C, IDDMs had about 35% lower rates of WBGU at all glucose levels (P less than 0.01). The FAVGD (millimoles per L) in C vs. IDDM was 1.23 +/- 0.05 vs. 1.06 +/- 0.09, 2.44 +/- 0.11 vs. 2.24 +/- 0.16, 2.91 +/- 0.18 vs. 2.91 +/- 0.30, and 3.27 +/- 0.12 vs. 3.35 +/- 0.4 (P = NS at each glucose). LBF (decaliters per min) was reduced in IDDM vs. C [2.8 +/- 0.5 vs. 4.3 +/- 0.4 (P less than 0.05), 3.1 +/- 0.4 vs. 5.1 +/- 0.7 (P less than 0.05), 2.7 +/- 0.2 vs. 6.3 +/- 0.8 (P less than 0.01), and 3.1 +/- 0.7 vs. 6.5 +/- 0.8 (P less than 0.01) at each glucose level]. Kinetic analysis revealed that 1) the Vmax for WBGU and LGU were reduced in IDDM vs. C (P less than 0.05), and 2) the Vmax for skeletal muscle glucose extraction (FAVGD) was identical in C and IDDM (3.6 mmol/L). The Km values for WBGU, LGU, and glucose extraction were not different in C and IDDM (approximately 6 mmol/L). Thus, in IDDM 1) decreased glucose uptake is due to reduced skeletal muscle glucose uptake; 2) muscle glucose extraction is normal, but blood flow is reduced; and thus, 3) in IDDM, IR is due to reduced glucose and insulin delivery (blood flow) to skeletal muscle. This represents a novel mechanism for in vivo IR.

Indexed as

AdultBlood GlucoseDiabetes Mellitus, Type 1FemaleGlucoseHumansInsulinInsulin ResistanceMaleMusclesRegional Blood FlowBlood GlucoseGlucoseInsulin

Identifiers

PMID1874938
OpenAlexW2050753633

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.