Evidence map›Paper›PMID 27143553›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2016

Loss of CTRP5 improves insulin action and hepatic steatosis.

Xia Lei, Susana Rodriguez, Pia S Petersen, Marcus M Seldin, Caitlyn E Bowman, Michael J Wolfgang, G William Wong

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-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

31 citing papers in PubMed, 48 citations in OpenAlex.

  1. CTRP10 is required for optimal motor function.The Journal of biological chemistry · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. CTRP11 contributes modestly to systemic metabolism and energy balance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  11. CTRP14 inactivation alters physical activity and food intake response to fasting and refeeding.American journal of physiology. Endocrinology and metabolism · 2022
    Article
  12. Article
  13. Article
  14. CTRP4 ablation impairs associative learning and memory.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  15. Review
  16. Article
  17. Loss of CTRP4 alters adiposity and food intake behaviors in obese mice.American journal of physiology. Endocrinology and metabolism · 2020
    Article
  18. Adiponectin and related C1q/TNF-related proteins bind selectively to anionic phospholipids and sphingolipids.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  19. 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

7 authors at 2 institutions in 1 country.

Xia LeiDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Susana RodriguezDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Pia S PetersenDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Marcus M SeldinDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Caitlyn E BowmanDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland.
Michael J WolfgangDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland; and Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland.
G William WongDepartment of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland; Center for Metabolism and Obesity Research, Johns Hopkins University School of Medicine, Baltimore, Maryland gwwong@jhmi.edu.
Johns Hopkins University · USJohns Hopkins Medicine · US

Funding

CTRP and Metabolic ControlR01DK084171 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI Guang William Wong · 2010 to 2026
$8.0M
Regulation of Neuronal Lipid Homeostasis By ThioesterasesR01NS072241 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2011 to 2020
$4.0M
NIDDK NIH HHS R01 DK084171NINDS NIH HHS R01 NS072241
6 · The paper itself

Abstract

The gene that encodes C1q/TNF-related protein 5 (CTRP5), a secreted protein of the C1q family, is mutated in individuals with late-onset retinal degeneration. CTRP5 is widely expressed outside the eye and also circulates in plasma. Its physiological role in peripheral tissues, however, has yet to be elucidated. Here, we show that Ctrp5 expression is modulated by fasting and refeeding, and by different diets, in mice. Adipose expression of CTRP5 was markedly upregulated in obese and diabetic humans and in genetic and dietary models of obesity in rodents. Furthermore, human CTRP5 expression in the subcutaneous fat depot positively correlated with BMI. A genetic loss-of-function mouse model was used to address the metabolic function of CTRP5 in vivo. On a standard chow diet, CTRP5-deficient mice had reduced fasting insulin but were otherwise comparable with wild-type littermate controls in body weight and adiposity. However, when fed a high-fat diet, CTRP5-deficient animals had attenuated hepatic steatosis and improved insulin action. Loss of CTRP5 also improved the capacity of chow-fed aged mice to respond to subsequent high-fat feeding, as evidenced by decreased insulin resistance. In cultured adipocytes and myotubes, recombinant CTRP5 treatment attenuated insulin-stimulated Akt phosphorylation. Our results provide the first genetic and physiological evidence for CTRP5 as a negative regulator of glucose metabolism and insulin sensitivity. Inhibition of CTRP5 action may result in the alleviation of insulin resistance associated with obesity and diabetes.

Indexed as

Adipose TissueAdultAnimalsCollagenDown-RegulationFatty LiverFemaleHumansInsulinInsulin ResistanceLiverMaleMiceMice, Inbred C57BLMice, KnockoutMiddle AgedC1QTNF5 protein, humanCollagenInsulinadipokineC1QTNF5C1q/TNF-related protein 5diabetesinsulin sensitivityobesity

Identifiers

PMID27143553
PMCPMC4935138
OpenAlexW2345656359

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.