Evidence map›Paper›PMID 28123939›Full record

ArticleMolecular metabolism2017

Global IP6K1 deletion enhances temperature modulated energy expenditure which reduces carbohydrate and fat induced weight gain.

Qingzhang Zhu, Sarbani Ghoshal, Richa Tyagi, Anutosh Chakraborty

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

30 citing papers in PubMed, 44 citations in OpenAlex.

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  16. Whole BodyInternational journal of molecular sciences · 2022
    Article
  17. Article
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  19. Inositol phosphate kinases in the eukaryote landscape.Advances in biological regulation · 2021
    Article
  20. Review
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 2 institutions in 1 country.

Qingzhang ZhuDepartment of Metabolism and Aging, The Scripps Research Institute, Jupiter, FL, 33458, USA.
Sarbani GhoshalDepartment of Metabolism and Aging, The Scripps Research Institute, Jupiter, FL, 33458, USA.
Richa TyagiThe Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA.
Anutosh ChakrabortyDepartment of Metabolism and Aging, The Scripps Research Institute, Jupiter, FL, 33458, USA. Electronic address: achakrab@scripps.edu.
Scripps Research Institute · USJohns Hopkins University · US

Funding

Inositol hexakisphosphate kinase-1 As a Novel Target in ObesityR01DK103746 · NIDDK · SCRIPPS FLORIDA · PI CHAKRABORTY, ANUTOSH · 2015 to 2019
$1.9M
NIDDK NIH HHS R01 DK103746
6 · The paper itself

Abstract

objectiveIP6 kinases (IP6Ks) regulate cell metabolism and survival. Mice with global (IP6K1-KO) or adipocyte-specific (AdKO) deletion of IP6K1 are protected from diet induced obesity (DIO) at ambient (23 °C) temperature. AdKO mice are lean primarily due to increased AMPK mediated thermogenic energy expenditure (EE). Thus, at thermoneutral (30 °C) temperature, high fat diet (HFD)-fed AdKO mice expend energy and gain body weight, similar to control mice. IP6K1 is ubiquitously expressed; thus, it is critical to determine to what extent the lean phenotype of global IP6K1-KO mice depends on environmental temperature. Furthermore, it is not known whether IP6K1 regulates AMPK mediated EE in cells, which do not express UCP1.

methodsQ-NMR, GTT, food intake, EE, QRT-PCR, histology, mitochondrial oxygen consumption rate (OCR), fatty acid metabolism assays, and immunoblot studies were conducted in IP6K1-KO and WT mice or cells.

resultsGlobal IP6K1 deletion mediated enhancement in EE is impaired albeit not abolished at 30 °C. As a result, IP6K1-KO mice are protected from DIO, insulin resistance, and fatty liver even at 30 °C. Like AdKO, IP6K1-KO mice display enhanced adipose tissue browning. However, unlike AdKO mice, thermoneutrality only partly abolishes browning in IP6K1-KO mice. Cold (5 °C) exposure enhances carbohydrate expenditure, whereas 23 °C and 30 °C promote fat oxidation in HFD-KO mice. Furthermore, IP6K1 deletion diminishes cellular fat accumulation via activation of the AMPK signaling pathway.

conclusionsGlobal deletion of IP6K1 ameliorates obesity and insulin resistance irrespective of the environmental temperature conditions, which strengthens its validity as an anti-obesity target.

Indexed as

AdipocytesAnimalsDiet, High-FatEatingEnergy MetabolismInsulin ResistanceMaleMiceMice, KnockoutObesityPhosphotransferases (Phosphate Group Acceptor)Signal TransductionTemperatureThermogenesisWeight GainIhpk1 protein, mousePhosphotransferases (Phosphate Group Acceptor)DiabetesEnergy expenditureIP6KObesityβ-oxidation

Identifiers

PMID28123939
PMCPMC5220553
OpenAlexW2558411440

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.