Evidence map›Paper›PMID 27045985›Full record

ArticleThe Journal of clinical endocrinology and metabolism2016

Elevated Glucose Oxidation, Reduced Insulin Secretion, and a Fatty Heart May Be Protective Adaptions in Ischemic CAD.

J C Hannukainen, R Lautamäki, A Mari, J P Pärkkä, M Bucci, M A Guzzardi, S Kajander, T Tuokkola, J Knuuti, P Iozzo

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 26% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Relationship of fat in the pancreas with cardiovascular disease: A systematic review and meta-analysis.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025
    Pooled it
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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

10 authors at 3 institutions in 2 countries.

J C HannukainenTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
R LautamäkiTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
A MariTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
J P PärkkäTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
M BucciTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
M A GuzzardiTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
S KajanderTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
T TuokkolaTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
J KnuutiTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
P IozzoTurku PET Center (J.C.H., R.L., J.P.P., M.B., S.K., T.T., J.K., P.I.), University of Turku, 20014 Turku, Finland; Heart Center (R.L.), Turku University Hospital, 20520 Turku, Finland; Institute of Neuroscience (A.M.), National Research Council, 35127 Padua, Italy; and Institute of Clinical Physiology (M.A.G., P.I.), National Research Council, 56124 Pisa, Italy.
University of Turku · FITurku PET Centre · FINational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInsulin resistance, β-cell dysfunction, and ectopic fat deposition have been implicated in the pathogenesis of coronary artery disease (CAD) and type 2 diabetes, which is common in CAD patients. We investigated whether CAD is an independent predictor of these metabolic abnormalities and whether this interaction is influenced by superimposed myocardial ischemia. METHODS AND

resultsWe studied CAD patients with (n = 8) and without (n = 14) myocardial ischemia and eight non-CAD controls. Insulin sensitivity and secretion and substrate oxidation were measured during fasting and oral glucose tolerance testing. We used magnetic resonance imaging/spectroscopy, positron emission and computerized tomography to characterize CAD, cardiac function, pericardial and abdominal adipose tissue, and myocardial, liver, and pancreatic triglyceride contents. Ischemic CAD was characterized by elevated oxidative glucose metabolism and a proportional decline in β-cell insulin secretion and reduction in lipid oxidation. Cardiac function was preserved in CAD groups, whereas cardiac fat depots were elevated in ischemic CAD compared to non-CAD subjects. Liver and pancreatic fat contents were similar in all groups and related with surrounding adipose masses or systemic insulin sensitivity.

conclusionsIn ischemic CAD patients, glucose oxidation is enhanced and correlates inversely with insulin secretion. This can be seen as a mechanism to prevent glucose lowering because glucose is required in oxygen-deprived tissues. On the other hand, the accumulation of cardiac triglycerides may be a physiological adaptation to the limited fatty acid oxidative capacity. Our results underscore the urgent need of clinical trials that define the optimal/safest glycemic range in situations of myocardial ischemia.

Indexed as

Adaptation, PhysiologicalLipid MetabolismAbdominal FatAdiposityAgedBlood GlucoseCase-Control StudiesCoronary Artery DiseaseCytoprotectionFemaleGlucoseHeartHumansInsulinInsulin SecretionMaleBlood GlucoseGlucoseInsulinTriglycerides

Identifiers

PMID27045985
PMCPMC4929844
OpenAlexW2317552219

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.