Evidence map›Paper›PMID 24784138›Full record

ArticleThe Journal of biological chemistry2014

Intestine-specific deletion of acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2 protects mice from diet-induced obesity and glucose intolerance.

David W Nelson, Yu Gao, Mei-I Yen, Chi-Liang Eric Yen

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.6field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 79 citations in OpenAlex.

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  20. Mechanisms underlying reduced weight gain in intestinal fatty acid-binding protein (IFABP) null mice.American journal of physiology. Gastrointestinal and liver physiology · 2020
    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

4 authors at 1 institution in 1 country.

David W NelsonFrom the Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706.
Yu GaoFrom the Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706.
Mei-I YenFrom the Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706.
Chi-Liang Eric YenFrom the Department of Nutritional Sciences, University of Wisconsin, Madison, Wisconsin 53706 yen@nutrisci.wisc.edu.
University of Wisconsin–Madison · US

Funding

TRAINING IN NUTRITIONT32DK007665 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI GUY E GROBLEWSKI, Chi- Liang Eric Yen · 1993 to 2026
$9.2M
Intestinal Triacylglycerol Metabolism and Energy BalanceR01DK088210 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI YEN, CHI- LIANG ERIC · 2011 to 2015
$1.7M
NIDDK NIH HHS R01 DK088210NIDDK NIH HHS R01DK088210NIDDK NIH HHS T32 DK007665NIDDK NIH HHS T32DK007665
6 · The paper itself

Abstract

The absorption of dietary fat involves the re-esterification of digested triacylglycerol in the enterocytes, a process catalyzed by acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2. Mice without a functional gene encoding MGAT2 (Mogat2(-/-)) are protected from diet-induced obesity. Surprisingly, these mice absorb normal amounts of dietary fat but increase their energy expenditure. MGAT2 is expressed in tissues besides intestine, including adipose tissue in both mice and humans. To test the hypothesis that intestinal MGAT2 regulates systemic energy balance, we generated and characterized mice deficient in MGAT2 specifically in the small intestine (Mogat2(IKO)). We found that, like Mogat2(-/-) mice, Mogat2(IKO) mice also showed a delay in fat absorption, a decrease in food intake, and a propensity to use fatty acids as fuel when first exposed to a high fat diet. Mogat2(IKO) mice increased energy expenditure although to a lesser degree than Mogat2(-/-) mice and were protected against diet-induced weight gain and associated comorbidities, including hepatic steatosis, hypercholesterolemia, and glucose intolerance. These findings illustrate that intestinal lipid metabolism plays a crucial role in the regulation of systemic energy balance and may be a feasible intervention target. In addition, they suggest that MGAT activity in extraintestinal tissues may also modulate energy metabolism.

Indexed as

AnimalsDietary FatsEatingEnergy MetabolismFatty LiverGene DeletionGlucose IntoleranceHumansHypercholesterolemiaIntestinal AbsorptionIntestinesMiceMice, KnockoutN-AcetylglucosaminyltransferasesObesityalpha-1,6-mannosyl-glycoprotein beta-1,2-N-acetylglucosaminyltransferaseDietary FatsN-AcetylglucosaminyltransferasesDiacylglycerolDietEnergy MetabolismLipid AbsorptionTriacylglycerol

Identifiers

PMID24784138
PMCPMC4067168
OpenAlexW1975254771

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.