Targeted deletion of fibrinogen like protein 1 reveals a novel role in energy substrate utilization
Open accessAbstract
Fibrinogen like protein 1(Fgl1) is a secreted protein with mitogenic activity on primary hepatocytes. Fgl1 is expressed in the liver and its expression is enhanced following acute liver injury. In animals with acute liver failure, administration of recombinant Fgl1 results in decreased mortality supporting the notion that Fgl1 stimulates hepatocyte proliferation and/or protects hepatocytes from injury. However, because Fgl1 is secreted and detected in the plasma, it is possible that the role of Fgl1 extends far beyond its effect on hepatocytes. In this study, we show that Fgl1 is additionally expressed in brown adipose tissue. We find that signals elaborated following liver injury also enhance the expression of Fgl1 in brown adipose tissue suggesting that there is a cross talk between the injured liver and adipose tissues. To identify extra hepatic effects, we generated Fgl1 deficient mice. These mice exhibit a phenotype suggestive of a global metabolic defect: Fgl1 null mice are heavier than wild type mates, have abnormal plasma lipid profiles, fasting hyperglycemia with enhanced gluconeogenesis and exhibit differences in white and brown adipose tissue morphology when compared to wild types. Because Fgl1 shares structural similarity to Angiopoietin like factors 2, 3, 4 and 6 which regulate lipid metabolism and energy utilization, we postulate that Fgl1 is a member of an emerging group of proteins with key roles in metabolism and liver regeneration.
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Hepassocin is secreted predominantly from the liver, but is also expressed in adipose tissue where it is suggested to regulate lipid metabolism.
“Hepassocin is secreted predominantly from the liver, but is also expressed in adipose tissue where it is suggested to regulate lipid metabolism [219].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [219]
Liver injury in mice enhances expression of hepassocin in adipose tissues, suggesting crosstalk between liver and adipose tissue.
“Liver injury in mice enhances the expression of hepassocin in adipose tissues, suggesting crosstalk between the liver and adipose tissue, although its role in obesity remains obscure [219].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [219]
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- Authors
- Demchev, V., Malana, G., Vangala, D., Stoll, J., Desai, A., Kang, H. W., Li, Y., Nayeb-Hashemi, H., Niepel, M., Cohen, D. E., & Ukomadu, C.
- Affiliations
- Brigham and Women's Hospital (US)
- Corresponding author
- Ukomadu, Chinweike
- Venue
- PLoS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-03-06
- Volume
- 8
- Issue
- 3
- Pages
- e58084
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC3590190
- OpenAlex
- W2120167012
- Cited by
- 89
- References
- 36
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 14 · 2023: 10 · 2022: 14 · 2021: 9 · 2020: 9 · 2019: 7 · 2018: 3 · 2017: 3 · 2016: 5 · 2015: 3
- FWCI
- 1.86
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- American Heart Association
- Brigham and Women's Hospital
- National Institutes of Health (NIH T32, T32 grant, DK‐48873, DK034854)
- Harvard Digestive Diseases Center, Harvard University (DK034854)
- National Institute of Diabetes and Digestive and Kidney Diseases (R29DK048873, DK56628, DK07477, R01DK056626, R37DK048873, DK080789, T32DK007477, R01DK080789, P30DK034854, R01DK048873, DK 48873)
- Topics
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- FGL1, brown adipose tissue, energy substrate utilization, liver injury, angiopoietin-like proteins, gluconeogenesis, fasting hyperglycemia, plasma lipid profile, adipose tissue morphology, liver regeneration
- MeSH terms
- Animals, Body Weight, Adipose Tissue, Brown, Calorimetry, Indirect, Cholesterol, Energy Metabolism, Fasting, Fatty Acids, Nonesterified, Feeding Behavior, Fibrinogen, Glucose, Hyperglycemia, Lipids, Liver, Organ Size, Gene Deletion, Mice, Knockout, Gene Targeting, Mice
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