Evidence map›Paper›PMID 17372192›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2007

Loss of the Par-1b/MARK2 polarity kinase leads to increased metabolic rate, decreased adiposity, and insulin hypersensitivity in vivo.

Jonathan B Hurov, Mei Huang, Lynn S White, Jochen Lennerz, Cheol Soo Choi, You-Ree Cho, Hyo-Jeong Kim, Julie L Prior, David Piwnica-Worms, Lewis C Cantley and 3 more

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.4field-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

46 citing papers in PubMed, 76 citations in OpenAlex.

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  8. Review
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  13. Metabolic control of regulatory T cell (Treg) survival and function by Lkb1.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  14. Article
  15. Article
  16. ssc-miR-7134-3p regulates fat accumulation in castrated male pigs by targetingInternational journal of biological sciences · 2017
    Article
  17. Partitioning-Defective 1a/b Depletion Impairs Glomerular and Proximal Tubule Development.Journal of the American Society of Nephrology : JASN · 2016
    Article
  18. Article
  19. Protein Scaffolds Control Localized Protein Kinase Cζ Activity.The Journal of biological chemistry · 2016
    Article
  20. 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

13 authors at 6 institutions in 2 countries.

Jonathan B HurovDepartment of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110-1093, USA.
Mei Huang
Lynn S White
Jochen Lennerz
Cheol Soo Choi
You-Ree Cho
Hyo-Jeong Kim
Julie L Prior
David Piwnica-Worms
Lewis C Cantley
Jason K Kim
Gerald I Shulman
Helen Piwnica-Worms
Howard Hughes Medical Institute · USPennsylvania State University · USWashington University in St. Louis · USYale University · USBeth Israel Deaconess Medical Center · USMallinckrodt (Ireland) · IE

Funding

Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Nicholas O. Davidson · 2000 to 2026
$30.8M
WU-MDACC Inter-Institutional Molecular Imaging CenterP50CA094056 · NCI · WASHINGTON UNIVERSITY · PI KOPAN, RAPHAEL · 2002 to 2016
$26.3M
Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
PROTEIN KINASE SIGNALING PATHWAYSR01GM056203 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI CANTLEY, LEWIS C. · 1997 to 2012
$4.5M
Interleukin-10 and Regulation of Skeletal Muscle Insulin ActionR01DK080756 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2008 to 2012
$1.6M
NCI NIH HHS P50 CA094056NCI NIH HHS P50 CA94056NIDDK NIH HHS DK52574NIDDK NIH HHS P30 DK052574NIDDK NIH HHS R01 DK040936NIDDK NIH HHS R01 DK080756NIDDK NIH HHS U24 DK059635NIDDK NIH HHS U24 DK-59635NIGMS NIH HHS R01 GM056203NIGMS NIH HHS R01 GM56203PHS HHS P30 57521
6 · The paper itself

Abstract

Obesity is a major factor central to the development of insulin resistance and type 2 diabetes. The identification and characterization of genes involved in regulation of adiposity, insulin sensitivity, and glucose uptake are key to the design and development of new drug therapies for this disease. In this study, we show that the polarity kinase Par-1b/MARK2 is required for regulating glucose metabolism in vivo. Mice null for Par-1b were lean, insulin hypersensitive, resistant to high-fat diet-induced weight gain, and hypermetabolic. (18)F-FDG microPET and hyperinsulinemic-euglycemic clamp analyses demonstrated increased glucose uptake into white and brown adipose tissue, but not into skeletal muscle of Par-1b null mice relative to wild-type controls. Taken together, these data indicate that Par-1b is a regulator of glucose metabolism and adiposity in the whole animal and may be a valuable drug target for the treatment of both type 2 diabetes and obesity.

Indexed as

Gene Expression RegulationAdipose TissueAdiposityAnimalsCell Cycle ProteinsFemaleGlucoseInsulinInsulin ResistanceMaleMiceMice, Inbred C57BLMice, KnockoutObesityProtein Serine-Threonine KinasesTime FactorsCell Cycle ProteinsGlucoseInsulinMark2 protein, mouseProtein Serine-Threonine Kinases

Identifiers

PMID17372192
PMCPMC1838456
OpenAlexW1996894913

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.