ArticleCellular and molecular gastroenterology and hepatology2022
FACI Is a Novel CREB-H-Induced Protein That Inhibits Intestinal Lipid Absorption and Reverses Diet-Induced Obesity.
Article in Cellular and molecular gastroenterology and hepatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 15 citations in OpenAlex.
- Review
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- Oncogenic role of C11orf86 in ovarian cancer involving hypoxia response and immune modulation.Discover oncology · 2026Article
- C1orf115 interacts with clathrin adaptors to undergo endocytosis and induces ABCA1 to promote enteric cholesterol efflux.Cellular and molecular life sciences : CMLS · 2025Article
- Cgref1 is a CREB-H-regulated hepatokine that promotes hepaticInternational journal of biological sciences · 2025Article
- Amelioration of non-alcoholic fatty liver disease by targeting adhesion G protein-coupled receptor F1 (eLife · 2023Article
- Circadian PER1 controls daily fat absorption with the regulation of PER1-PKA on phosphorylation of bile acid synthetase.Journal of lipid research · 2023Article
- FACI is a novel clathrin adaptor protein 2-binding protein that facilitates low-density lipoprotein endocytosis.Cell & bioscience · 2023Article
- Aberrant splicing events caused by insertion of genes of interest into expression vectors.International journal of biological sciences · 2022Article
- Stress-induced Regulators of Intestinal Fat Absorption.Cellular and molecular gastroenterology and hepatology · 2022Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND &
aimsCREB-H is a key liver-enriched transcription factor governing lipid metabolism. Additional targets of CREB-H remain to be identified and characterized. Here, we identified a novel fasting- and CREB-H-induced (FACI) protein that inhibits intestinal lipid absorption and alleviates diet-induced obesity in mice.
methodsFACI was identified by reanalysis of existing transcriptomic data. Faci
resultsFACI expression was enriched in liver and intestine. FACI is a phospholipid-binding protein that localizes to plasma membrane and recycling endosomes. Hepatic transcription of Faci was regulated by not only CREB-H, but also nutrient-responsive transcription factors sterol regulatory element-binding protein 1 (SREBP1), hepatocyte nuclear factor 4α (HNF4α), peroxisome proliferator-activated receptor γ coactivator-1α (PGC1α), and CREB, as well as fasting-related cyclic adenosine monophosphate (cAMP) signaling. Genetic knockout of Faci in mice showed an increase in intestinal fat absorption. In accordance with this, Faci deficiency aggravated high-fat diet-induced obesity, hyperlipidemia, steatosis, and other obesity-related metabolic dysfunction in mice.
conclusionsFACI is a novel CREB-H-induced protein. Genetic disruption of Faci in mice showed its inhibitory effect on fat absorption and obesity. Our findings shed light on a new target of CREB-H implicated in lipid homeostasis.
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