Asprosin, a Fasting-Induced Glucogenic Protein Hormone
Open accessAbstract
Hepatic glucose release into the circulation is vital for brain function and survival during periods of fasting and is modulated by an array of hormones that precisely regulate plasma glucose levels. We have identified a fasting-induced protein hormone that modulates hepatic glucose release. It is the C-terminal cleavage product of profibrillin, and we name it Asprosin. Asprosin is secreted by white adipose, circulates at nanomolar levels, and is recruited to the liver, where it activates the G protein-cAMP-PKA pathway, resulting in rapid glucose release into the circulation. Humans and mice with insulin resistance show pathologically elevated plasma asprosin, and its loss of function via immunologic or genetic means has a profound glucose- and insulin-lowering effect secondary to reduced hepatic glucose release. Asprosin represents a glucogenic protein hormone, and therapeutically targeting it may be beneficial in type II diabetes and metabolic syndrome.
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Asprosin is a novel fasting-induced adipokine that promotes hepatic glucose production.
“Asprosin, a novel fasting‐induced adipokine that promotes hepatic glucose production, was recently identified 59.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [59]
Asprosin's promotion of glucose release is independent from glucagon receptor signaling and from the β-adrenergic receptor.
“This process is independent from glucagon receptor signaling and from the β‐adrenergic receptor 59.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [59]
Asprosin directly targets the liver to promote glucose release, without increasing plasma levels of glucagon, catecholamines, and glucocorticoids.
“Asprosin directly targets the liver to promote glucose release, without increasing plasma levels of glucagon, catecholamines, and glucocorticoids.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [59]
An antibody to sequester circulating asprosin improves the metabolic phenotype of obese insulin‐resistant mice.
“Moreover, the improvement of the metabolic phenotype of obese insulin‐resistant mice when using an antibody to sequester circulating asprosin makes this novel adipokine a potential therapeutic target against diabetes 59.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [59]
High plasma asprosin may contribute to the onset of hyperglycemia and insulin resistance in mice and humans.
“This observation suggests that high plasma asprosin may contribute to the onset of hyperglycemia and insulin resistance in mice and humans.”
From Inter‐organ communication: a gatekeeper for metabolic health (2019) · cites this paper as [59]
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Self-citation
- Authors
- Romere, C., Duerrschmid, C., Bournat, J., Constable, P., Jain, M., Xia, F., Saha, P. K., Del Solar, M., Zhu, B., York, B., Sarkar, P., Rendon, D. A., Gaber, M. W., LeMaire, S. A., Coselli, J. S., Milewicz, D. M., Sutton, V. R., Butte, N. F., Moore, D. D., & Chopra, A. R.
- Affiliations
- Baylor College of Medicine (US)
- The University of Texas Health Science Center at Houston (US)
- Corresponding author
- Chopra, Atul R.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2016-04
- Volume
- 165
- Issue
- 3
- Pages
- 566-579
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4852710
- OpenAlex
- W4240089340
- Cited by
- 591
- References
- 19
- Citations by year
- 2026: 80 · 2025: 72 · 2024: 83 · 2023: 91 · 2022: 80 · 2021: 52 · 2020: 50 · 2019: 31 · 2018: 27 · 2017: 15 · 2016: 8 · 2012: 1
- FWCI
- 25.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Vanderbilt University
- Johns Hopkins University
- National Institutes of Health (5p50hl083794-05, 5p60dk020593-31)
- National Heart, Lung, and Blood Institute (P50-HL083794)
- National Human Genome Research Institute (U54HG006542)
- National Institute of Diabetes and Digestive and Kidney Diseases (P60-DK020593, U24DK059637, K08DK102529, P30DK079638, P30DK020593)
- Common Fund
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Keywords
- asprosin, fasting, hepatic glucose production, insulin resistance, type 2 diabetes, metabolic syndrome, plasma glucose regulation
- MeSH terms
- Fibrillin-1, Cyclic AMP, Amino Acid Sequence, Animals, Antibodies, Circadian Rhythm, Fasting, Female, Fetal Growth Retardation, Glucose, Humans, Insulin, Liver, Male, Mice, Inbred C57BL, Mice, Obese, Microfilament Proteins, Molecular Sequence Data, Peptide Fragments, Progeria, Recombinant Proteins, Sequence Alignment, Cyclic AMP-Dependent Protein Kinases, Peptide Hormones, Mice, Adipose Tissue, White, Adipokines
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