Evidence map›Paper›PMID 25277390›Full record

Trial reportDiabetes2015

Central nervous insulin administration does not potentiate the acute glucoregulatory impact of concurrent mild hyperinsulinemia.

Volker Ott, Hendrik Lehnert, Josefine Staub, Kathrin Wönne, Jan Born, Manfred Hallschmid

Abstract readRandomized Controlled Trial
PubMed Publisher
In one paragraph

Trial report in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. Hypothalamus-liver talks: whispers in the language of metabolism.Reviews in endocrine & metabolic disorders · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Insulin action in the brain regulates both central and peripheral functions.American journal of physiology. Endocrinology and metabolism · 2021
    Review
  8. Review
  9. Article
  10. Molecular Mechanisms of Hypothalamic Insulin Resistance.International journal of molecular sciences · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Intranasal Insulin Improves Age-Related Cognitive Deficits and Reverses Electrophysiological Correlates of Brain Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016
    Article
  16. Review
  17. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Volker OttDepartment of Neuroendocrinology, University of Lübeck, Lübeck, Germany.
Hendrik LehnertDepartment of Internal Medicine I, University of Lübeck, Lübeck, Germany.
Josefine StaubDepartment of Neuroendocrinology, University of Lübeck, Lübeck, Germany.
Kathrin WönneDepartment of Neuroendocrinology, University of Lübeck, Lübeck, Germany.
Jan BornInstitute for Medical Psychology and Behavioral Neurobiology, University of Tübingen, Tübingen, Germany German Center for Diabetes Research, Tübingen, Germany Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen (IDM), Tübingen, Germany.
Manfred HallschmidInstitute for Medical Psychology and Behavioral Neurobiology, University of Tübingen, Tübingen, Germany German Center for Diabetes Research, Tübingen, Germany Institute for Diabetes Research and Metabolic Diseases of the Helmholtz Centre Munich at the University of Tübingen (IDM), Tübingen, Germany manfred.hallschmid@uni-tuebingen.de.
University of Lübeck · DEHeinrich Heine University Düsseldorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experiments in rodents suggest that hypothalamic insulin signaling essentially contributes to the acute control of peripheral glucose homeostasis. Against this background, we investigated in healthy humans whether intranasal (IN) insulin, which is known to effectively reach the brain compartment, impacts systemic glucose metabolism. Twenty overnight-fasted healthy, normal-weight men were IN administered 210 and 420 international units [IU] (10 and 20 IU every 15 min) of the insulin analog aspart (ins-asp) and placebo, respectively, during experimental sessions lasting 6 h. The use of ins-asp rather than human insulin enabled us to disentangle exogenous and endogenous insulin kinetics. IN insulin dose-dependently decreased plasma glucose concentrations while reducing C-peptide and attenuating endogenous insulin levels. However, we also observed a slight dose-dependent permeation of ins-asp into the circulation. In control experiments mimicking the systemic but not the central nervous uptake of the IN 210 IU dose via intravenous infusion of ins-asp at a dose of 0.12 IU/kg/24 h (n = 10), we obtained essentially identical effects on fasting plasma glucose concentrations. This pattern indicates that sustained IN insulin administration to the human brain to enhance central nervous insulin signaling does not acutely alter systemic glucose homeostasis beyond effects accounted for by concurrent mild hyperinsulinemia.

Indexed as

AdultBlood GlucoseC-PeptideFastingFemaleHumansHyperinsulinismInfusions, IntravenousInsulinMaleYoung AdultBlood GlucoseC-PeptideInsulin

Identifiers

PMID25277390
OpenAlexW2118240765

What Socratic holds

Textmetadata
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 Socratic graph.