LECT2 functions as a hepatokine that links obesity to skeletal muscle insulin resistance
Open accessAbstract
Recent articles have reported an association between fatty liver disease and systemic insulin resistance in humans, but the causal relationship remains unclear. The liver may contribute to muscle insulin resistance by releasing secretory proteins called hepatokines. Here we demonstrate that leukocyte cell-derived chemotaxin 2 (LECT2), an energy-sensing hepatokine, is a link between obesity and skeletal muscle insulin resistance. Circulating LECT2 positively correlated with the severity of both obesity and insulin resistance in humans. LECT2 expression was negatively regulated by starvation-sensing kinase adenosine monophosphate-activated protein kinase in H4IIEC hepatocytes. Genetic deletion of LECT2 in mice increased insulin sensitivity in the skeletal muscle. Treatment with recombinant LECT2 protein impaired insulin signaling via phosphorylation of Jun NH2-terminal kinase in C2C12 myocytes. These results demonstrate the involvement of LECT2 in glucose metabolism and suggest that LECT2 may be a therapeutic target for obesity-associated insulin resistance.
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LECT2 alters insulin signaling through the JNK pathway in myocytes, and expression of LECT2 in liver is negatively regulated by AMPK.
“LECT2 alters insulin signaling through the JNK pathway in myocytes, and the expression of LECT2 in the liver is negatively regulated by the energy-depletion sensor AMPK [239,248,249].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
There is a positive relationship between circulating LECT2 levels, BMI, and insulin resistance in humans.
“Interestingly, there is a positive relationship between circulating LECT2 levels, BMI, and insulin resistance in humans [239] (Table 1).”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
LECT2 is an energy-sensing hepatokine positively associated with hepatic inflammatory signaling, obesity, NAFLD, and insulin resistance.
“Leukocyte cell-derived chemotaxin 2 (LECT2) is an energy-sensing hepatokine that is positively associated with hepatic inflammatory signaling, obesity, NAFLD, and insulin resistance [239,240].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
LECT2-deficient mice show improved insulin sensitivity in skeletal muscle, while administration of recombinant LECT2 in mice leads to impaired insulin signaling and induced insulin resistance in skeletal muscle.
“LECT2-deficient mice showed improved insulin sensitivity in skeletal muscle, while administration of recombinant LECT2 in mice led to impaired insulin signaling and induced insulin resistance in skeletal muscle [239] (Figure 3).”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
LECT2-deficient mice exhibit increased glucose tolerance and insulin sensitivity.
“LECT2-deficient mice exhibited increased glucose tolerance and insulin sensitivity [239].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
Mice fed high-fat diets or exercised have increased or decreased serum and hepatic levels of LECT2, respectively.
“For example, mice that were fed high-fat diets or exercised had increased or decreased serum and hepatic levels of LECT2, respectively [239].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
LECT2-deficient mice exhibit increased insulin-stimulated AKT phosphorylation in skeletal muscle but not liver or adipose tissue, suggesting loss of LECT2 selectively improves insulin sensitivity in skeletal muscle.
“These mice also exhibited increased insulin-stimulated AKT phosphorylation in skeletal muscle but not in the liver or adipose tissue, suggesting that loss of LECT2 selectively improves insulin sensitivity in skeletal muscle [239].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [239]
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“…non-alcoholic fatty liver disease, fetuin-A, fibroblast growth factor-21, selenoprotein P, sex hormone-binding globulin, angiopoietin-related growth factor, leukocyte derived chemotaxin 2 Received: 19 January, 2016; revised: 10 May, 2016; accepted: 18 May, 2016; available on-line: 6 June, 2016”
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- Authors
- Lan, F., Misu, H., Chikamoto, K., Takayama, H., Kikuchi, A., Mohri, K., Takata, N., Hayashi, H., Matsuzawa-Nagata, N., Takeshita, Y., Noda, H., Matsumoto, Y., Ota, T., Nagano, T., Nakagen, M., Miyamoto, K.-I., Takatsuki, K., Seo, T., Iwayama, K., Tokuyama, K., Matsugo, S., Tang, H., Saito, Y., Yamagoe, S., Kaneko, S., & Takamura, T.
- Affiliations
- Kanazawa University (JP)
- Department of Disease Control and Homeostasis, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan
- Public Central Hospital of Matto Ishikawa (JP)
- Merck & Co., Inc., Rahway, NJ, USA (United States) (US)
- University of Tsukuba (JP)
- West China Hospital of Sichuan University (CN)
- Doshisha University (JP)
- National Institute of Infectious Diseases (JP)
- Corresponding author
- Takamura, Toshinari
- ORCID
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2014-04-12
- Volume
- 63
- Issue
- 5
- Pages
- 1649-1664
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- OpenAlex
- W2165318249
- Cited by
- 158
- References
- 60
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 16 · 2023: 16 · 2022: 22 · 2021: 14 · 2020: 11 · 2019: 16 · 2018: 15 · 2017: 11 · 2016: 12 · 2015: 6
- FWCI
- 7.30
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Diabetes (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion, cc-by-nc-nd)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Kanazawa University Repository for Academic Resources (DSpace) (Kanazawa University) (submittedVersion, cc-by-nc-nd)
- Funders
- Japan Society for the Promotion of Science (25282017, 26670229, 14J03079, 23591301, 26461329, 25292078, 25461334, 23590275)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- LECT2, hepatokines, obesity, skeletal muscle insulin resistance, AMPK, hepatic steatosis, JNK phosphorylation, insulin signaling, glucose metabolism, energy sensing, hepatocytes, muscle cells
- MeSH terms
- Animals, Glucose, Humans, Insulin, Insulin Resistance, Liver, Obesity, Phosphorylation, Severity of Illness Index, Signal Transduction, Muscle, Skeletal, Hepatocytes, Muscle Cells, Intercellular Signaling Peptides and Proteins, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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