Evidence map›Paper›PMID 21752898›Full record

Trial reportThe Journal of clinical endocrinology and metabolism2011

Glucose ingestion selectively amplifies ACTH and cortisol secretory-burst mass and enhances their joint synchrony in healthy men.

Ali Iranmanesh, Donna Lawson, Barbara Dunn, Johannes D Veldhuis

Abstract readClinical Trial
In one paragraph

Trial report in The Journal of clinical endocrinology and metabolism, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 42% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

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  8. Glucocorticoid Receptor Signaling in Diabetes.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Glucose can promote a glucocorticoid resistance state.Journal of cellular and molecular medicine · 2012
    Article
  11. Glucose ingestion acutely lowers pulsatile LH and basal testosterone secretion in men.American journal of physiology. Endocrinology and metabolism · 2012
    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

4 authors at 1 institution in 1 country.

Ali IranmaneshEndocrine Section, Medical Service, Salem Veterans Affairs Medical Center, Salem, Virginia 24153, USA.
Donna Lawson
Barbara Dunn
Johannes D Veldhuis
Mayo Clinic · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
Obesity and Energy Metabolism CoreP30DK050456 · NIDDK · UNIVERSITY OF MINNESOTA TWIN CITIES · PI BERNLOHR, DAVID A · 1995 to 2015
$17.0M
Ensemble Control of ACTH Secretion: Impact of GenderR01DK073148 · NIDDK · MAYO CLINIC ROCHESTER · PI VELDHUIS, JOHANNES D · 2007 to 2011
$1.4M
NCRR NIH HHS 1 UL 1 RR024150NCRR NIH HHS UL1 RR024150NIDDK NIH HHS DK050456NIDDK NIH HHS DK073148NIDDK NIH HHS P30 DK050456NIDDK NIH HHS R01 DK073148
6 · The paper itself

Abstract

contextGlucose intake is associated with a variable increase in adrenal glucocorticoid secretion. HYPOTHESIS: Glucose ingestion elevates cortisol secretion by 1) augmenting pulsatile ACTH release; and/or 2) enhancing ACTH-cortisol synchrony or dose-responsiveness. SUBJECTS: Fifty-eight healthy men ages 19-78 yr with computed tomography-estimated abdominal visceral fat participated in the study. LOCATION: The study was conducted at the Clinical Translational-Research Center and Veterans Affairs Medical Center.

methodsWe conducted frequent sampling of plasma ACTH and cortisol concentrations after glucose vs. water ingestion in the fasting state, as well as deconvolution, approximate entropy, linear-regression, and dose-response analysis. OUTCOMES: After water ingestion, age was a negative correlate of the mass of ACTH (P = 0.009; R(2) = 0.119) and of cortisol (P < 0.001; R(2) = 0.269) secreted per burst. Glucose ingestion abolished both relationships but amplified pulsatile ACTH (P = 0.009) and cortisol (P = 0.001) secretion. Glucose exposure selectively augmented the mass of ACTH (P < 0.001) and of cortisol (P = 0.004) secreted per burst without altering burst number or basal secretion. The increment in pulsatile ACTH strongly predicted the increment in pulsatile cortisol (P < 10(-4); R(2) = 0.325) secretion. Abdominal visceral fat positively forecast the glucose-induced increment in cortisol secretory-burst mass (P = 0.019). According to approximate entropy analysis, glucose input also enhanced the joint synchrony of ACTH-cortisol secretory patterns (P ≤ 0.001). Caloric intake did not affect analytical dose-response estimates of ACTH potency and efficacy or adrenal sensitivity.

conclusionConjoint augmentation of the mass of ACTH and cortisol secreted per burst and enhancement of ACTH-cortisol synchrony underlie glucose-induced glucocorticoid secretion in healthy men. Visceral adiposity is a predictor of the glucose-stimulated increment in burst-like cortisol output, suggesting an additional possible mechanism for increased cardiovascular risk in abdominal obesity.

Indexed as

Administration, OralAdrenocorticotropic HormoneAdultAgedGlucoseHumansHydrocortisoneHypothalamo-Hypophyseal SystemMaleMiddle AgedPituitary-Adrenal SystemAdrenocorticotropic HormoneGlucoseHydrocortisone

Identifiers

PMID21752898
PMCPMC3167666
OpenAlexW2025368620

What OpenQuestion 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 OpenQuestion graph.