Evidence map›Paper›PMID 23709089›Full record

ArticleEndocrinology2013

High-fat feeding-induced hyperinsulinemia increases cardiac glucose uptake and mitochondrial function despite peripheral insulin resistance.

Anisha A Gupte, Laurie J Minze, Maricela Reyes, Yuelan Ren, Xukui Wang, Gerd Brunner, Mohamad Ghosn, Andrea M Cordero-Reyes, Karen Ding, Domenico Pratico and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. The role of acetylation in obesity-induced cardiac metabolic alterations.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Impairment of Mitochondrial Respiration in Metabolic Diseases: An Overview.International journal of molecular sciences · 2022
    Review
  9. Functional resilience of C57BL/6J mouse heart to dietary fat overload.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 1 country.

Anisha A GupteMethodist Diabetes and Metabolism Institute, Houston, TX, USA.
Laurie J Minze
Maricela Reyes
Yuelan Ren
Xukui Wang
Gerd Brunner
Mohamad Ghosn
Andrea M Cordero-Reyes
Karen Ding
Domenico Pratico
Joel Morrisett
Zheng-Zheng Shi
Dale J Hamilton
Christopher J Lyon
Willa A Hsueh
Cornell University · USBaylor College of Medicine · USHouston Methodist · USRice University · USTemple University · US

Funding

Inhibition of OLA1: A Novel Strategy for Anti-Metastasis TherapyR01CA155069 · NCI · METHODIST HOSPITAL RESEARCH INSTITUTE · PI SHI, ZHENG-ZHENG · 2011 to 2015
$1.6M
NCI NIH HHS R01 CA155069
6 · The paper itself

Abstract

In obesity, reduced cardiac glucose uptake and mitochondrial abnormalities are putative causes of cardiac dysfunction. However, high-fat diet (HFD) does not consistently induce cardiac insulin resistance and mitochondrial damage, and recent studies suggest HFD may be cardioprotective. To determine cardiac responses to HFD, we investigated cardiac function, glucose uptake, and mitochondrial respiration in young (3-month-old) and middle-aged (MA) (12-month-old) male Ldlr(-/-) mice fed chow or 3 months HFD to induce obesity, systemic insulin resistance, and hyperinsulinemia. In MA Ldlr(-/-) mice, HFD induced accelerated atherosclerosis and nonalcoholic steatohepatitis, common complications of human obesity. Surprisingly, HFD-fed mice demonstrated increased cardiac glucose uptake, which was most prominent in MA mice, in the absence of cardiac contractile dysfunction or hypertrophy. Moreover, hearts of HFD-fed mice had enhanced mitochondrial oxidation of palmitoyl carnitine, glutamate, and succinate and greater basal insulin signaling compared with those of chow-fed mice, suggesting cardiac insulin sensitivity was maintained, despite systemic insulin resistance. Streptozotocin-induced ablation of insulin production markedly reduced cardiac glucose uptake and mitochondrial dysfunction in HFD-fed, but not in chow-fed, mice. Insulin injection reversed these effects, suggesting that insulin may protect cardiac mitochondria during HFD. These results have implications for cardiac metabolism and preservation of mitochondrial function in obesity.

Indexed as

Age FactorsAnimalsAtherosclerosisBlotting, WesternDiet, High-FatFatty LiverGlucoseGlutamic AcidHyperinsulinismHypoglycemic AgentsInsulinInsulin ResistanceMaleMiceMice, Inbred C57BLMice, KnockoutGlucoseGlutamic AcidHypoglycemic AgentsInsulinMitochondrial ProteinsPalmitoylcarnitineReceptors, LDLStreptozocinSuccinic Acid

Identifiers

PMID23709089
PMCPMC5398492
OpenAlexW2088769904

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.