Evidence map›Paper›PMID 26171590›Full record

ArticlePhysiology & behavior2015

Lipid transport in cholecystokinin knockout mice.

Alexandra King, Qing Yang, Sarah Huesman, Therese Rider, Chunmin C Lo

Abstract read
In one paragraph

Article in Physiology & behavior, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Energy homeostasis in apolipoprotein AIV and cholecystokinin-deficient mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Article
  10. Article
  11. 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

5 authors at 2 institutions in 1 country.

Alexandra KingDepartment of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH, United States.
Qing YangDepartment of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH, United States.
Sarah HuesmanDepartment of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH, United States.
Therese RiderDepartment of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH, United States.
Chunmin C LoDepartment of Pathology and Laboratory Medicine, Metabolic Diseases Institute, University of Cincinnati, Cincinnati, OH, United States; Department of Biomedical Science, Diabetes Institute, Ohio University, Athens, OH, United States. Electronic address: locm@uc.edu.
University of Cincinnati · USOhio University · US

Funding

Food intake and energy metabolism regulated by apo AIV and CCKK01DK083550 · NIDDK · UNIVERSITY OF CINCINNATI · PI LO, CHUNMIN C. · 2009 to 2013
$559k
Apolipoprotein AIV regulates CCK secretion and potentiates CCK-induced satiationR03DK097436 · NIDDK · UNIVERSITY OF CINCINNATI · PI LO, CHUNMIN C. · 2013 to 2014
$159k
NIDDK NIH HHS DK83550NIDDK NIH HHS DK97436NIDDK NIH HHS K01 DK083550NIDDK NIH HHS R03 DK097436
6 · The paper itself

Abstract

Cholecystokinin (CCK) is released in response to lipid feeding and regulates pancreatic digestive enzymes vital to the absorption of nutrients. Our previous reports demonstrated that cholecystokinin knockout (CCK-KO) mice fed for 10 weeks of HFD had reduced body fat mass, but comparable glucose uptake by white adipose tissues and skeletal muscles. We hypothesized that CCK is involved in energy homeostasis and lipid transport from the small intestine to tissues in response to acute treatment with dietary lipids. CCK-KO mice with comparable fat absorption had increased energy expenditure and were resistant to HFD-induced obesity. Using intraduodenal infusion of butter fat and intravenous infusion using Liposyn III, we determined the mechanism of lipid transport from the small intestine to deposition in lymph and adipocytes in CCK-KO mice. CCK-KO mice had delayed secretion of Apo B48-chylomicrons, lipid transport to the lymphatic system, and triglyceride (TG)-derived fatty acid uptake by epididymal fat in response to acute treatment of intraduodenal lipids. In contrast, CCK-KO mice had comparable TG clearance and lipid uptake by white adipocytes in response to TGs in chylomicron-like emulsion. Thus, we concluded that CCK is important for lipid transport and energy expenditure to control body weight in response to dietary lipid feeding.

Indexed as

AdipocytesAdipose TissueAnimalsApolipoprotein B-48Body WeightCholecystokininChylomicronsDietary FatsDiet, High-FatEnergy IntakeEnergy MetabolismIntestine, SmallLipid MetabolismLiverLymphatic SystemMaleApolipoprotein B-48CholecystokininChylomicronsDietary FatsFat absorptionFatty acid uptakeLymphWhite adipose tissues

Identifiers

PMID26171590
PMCPMC4587287
OpenAlexW782185990

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.