Evidence map›Paper›PMID 19296465›Full record

ArticleHepatology (Baltimore, Md.)2009

Loss of protein kinase Cbeta function protects mice against diet-induced obesity and development of hepatic steatosis and insulin resistance.

Wei Huang, Rishipal Bansode, Madhu Mehta, Kamal D Mehta

Open access · bronzeAbstract read
In one paragraph

Article in Hepatology (Baltimore, Md.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

33 citing papers in PubMed, 67 citations in OpenAlex.

  1. Hepatic protein kinase Cβ antagonizing p38American journal of physiology. Gastrointestinal and liver physiology · 2025
    Article
  2. Review
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  4. Ubiquitination and deubiquitination in the regulation of NJournal of molecular medicine (Berlin, Germany) · 2024
    Review
  5. Review
  6. Article
  7. Article
  8. Review
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  11. Increased intracellular CaProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  12. Protein Kinase C β: a New Target Therapy to Prevent the Long-Term Atypical Antipsychotic-Induced Weight Gain.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  13. PKCβ: Expanding role in hepatic adaptation of cholesterol homeostasis to dietary fat/cholesterol.American journal of physiology. Gastrointestinal and liver physiology · 2017
    Review
  14. Review
  15. Article
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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

4 authors at 1 institution in 1 country.

Wei HuangDepartment of Molecular and Cellular Biochemistry, Dorothy M. Davis Heart & Lung Research Institute, The Ohio State University College of Medicine, Columbus, OH 43210, USA.
Rishipal Bansode
Madhu Mehta
Kamal D Mehta
The Ohio State University · US

Funding

Role of PKCbeta in Diet-induced HypercholesterolemiaR01HL079091 · NHLBI · OHIO STATE UNIVERSITY · PI MEHTA, KAMAL D · 2005 to 2010
$1.9M
NHLBI NIH HHS HL079091NHLBI NIH HHS R01 HL079091
6 · The paper itself

Abstract

Obesity is an energy balance disorder in which intake is greater than expenditure, with most excess calories stored as triglyceride (TG). We previously reported that mice lacking the beta-isoform of protein kinase C (PKCbeta), a diacylglycerol- and phospholipid-dependent kinase, exhibit marked reduction in the whole body TG content, including white adipose tissue (WAT) mass. To investigate the role of this signaling kinase in metabolic adaptations to severe dietary stress, we studied the impact of a high-fat diet (HFD) on PKCbeta expression and the effect of PKCbeta deficiency on profound weight gain. We report herein that HFD selectively increased PKCbeta expression in obesity-prone C57BL/6J mice, specifically in WAT; the expression levels were little or unchanged in the liver, muscle, kidney, and heart. Basal PKCbeta expression was also found to be elevated in WAT of obese ob/ob mice. Remarkably, mice lacking PKCbeta were resistant to HFD-induced obesity, showing significantly reduced WAT and slightly higher core body temperatures. Unlike lean lipodystrophic mouse models, these mice did not have fatty livers, nor did they exhibit insulin resistance. Moreover, PKCbeta(-/-) mice exhibited changes in lipid metabolism gene expression, and such alterations were accompanied by significant changes in serum adipokines. These observations suggest that PKCbeta deficiency induced a unique metabolic state congruous with obesity resistance, thus raising the possibility that dysregulation of PKCbeta expression could contribute to dietary fat-induced obesity and related disorders.

Indexed as

Insulin ResistanceLipid MetabolismAdipokinesAdipose Tissue, WhiteAnimalsDietary FatsFatty AcidsFatty LiverGene ExpressionIsoenzymesLiverMaleMiceMice, Inbred C57BLMice, KnockoutObesityAdipokinesDietary FatsFatty AcidsIsoenzymesProtein Kinase CProtein Kinase C beta

Identifiers

PMID19296465
PMCPMC2728215
OpenAlexW1966792793

What OpenQuestion holds

Textmetadata
LicenceTDM
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.