ArticlePloS one2014
Intestine-targeted DGAT1 inhibition improves obesity and insulin resistance without skin aberrations in mice.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Molecular Effects of Physical Activity and Body Composition: A Systematic Review and Meta-Analysis.International journal of environmental research and public health · 2025Pooled it
- Detection of theAnimals : an open access journal from MDPI · 2026Article
- Pharmacologic Inhibition of Macrophage Triglyceride Biosynthesis Pathways Does Not Improve Mycobacterium tuberculosis Control in Infected Mice.The Journal of infectious diseases · 2025Article
- DNA methylation analysis to differentiate reference, breed, and parent-of-origin effects in the bovine pangenome era.GigaScience · 2024Article
- Metabolic reprogramming and lipid droplets are involved in Zika virus replication in neural cells.Journal of neuroinflammation · 2023Article
- Intestine-specific DGAT1 deficiency improves atherosclerosis in apolipoprotein E knockout mice by reducing systemic cholesterol burden.Atherosclerosis · 2020Article
- Lipidomics in the Study of Hypertension in Metabolic Syndrome.Current hypertension reports · 2017Review
- Novel role of a triglyceride-synthesizing enzyme: DGAT1 at the crossroad between triglyceride and cholesterol metabolism.Biochimica et biophysica acta · 2016Article
- Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDiacylglycerol O-acyltransferase 1 (DGAT1) catalyzes the final committed step in triglyceride biosynthesis. DGAT1 null mice are known to be resistant to diet-induced obesity, and more insulin sensitive relative to the wild-type; however, the mice exhibit abnormalities in the skin. This work determined whether the intestine-targeted DGAT1 inhibitor could improve obesity and insulin resistance without skin aberrations in mice. DESIGN AND
methodsWe synthesized 2 DGAT1 inhibitors: Compound A, described in the patent application from the Japan Tobacco, and Compound B (A-922500), reported by Abbott Laboratories. Both compounds were evaluated for inhibitory activities against DGAT1 enzymes and effects on the skin in mice in vivo. Compound B was further investigated for effects on obesity and insulin resistance in diet-induced-obese (DIO) mice.
resultsThe 2 compounds comparably inhibited the DGAT1 enzyme activity and the cellular triglyceride synthesis in vitro, while they showed different distribution patterns in mice in vivo. Compound A, which distributed systemically, caused skin aberrations, while Compound B, which preferentially distributed to the intestine, improved obesity and insulin resistance without skin aberrations in DIO mice.
conclusionsOur results suggest that the intestine is the key tissue in which DGAT1 plays a role in promoting obesity and insulin resistance.
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