Inactivating hepatic follistatin alleviates hyperglycemia
Open accessAbstract
Unsuppressed hepatic glucose production (HGP) contributes substantially to glucose intolerance and diabetes, which can be modeled by the genetic inactivation of hepatic insulin receptor substrate 1 (Irs1) and Irs2 (LDKO mice). We previously showed that glucose intolerance in LDKO mice is resolved by hepatic inactivation of the transcription factor FoxO1 (that is, LTKO mice)-even though the liver remains insensitive to insulin. Here, we report that insulin sensitivity in the white adipose tissue of LDKO mice is also impaired but is restored in LTKO mice in conjunction with normal suppression of HGP by insulin. To establish the mechanism by which white adipose tissue insulin signaling and HGP was regulated by hepatic FoxO1, we identified putative hepatokines-including excess follistatin (Fst)-that were dysregulated in LDKO mice but normalized in LTKO mice. Knockdown of hepatic Fst in the LDKO mouse liver restored glucose tolerance, white adipose tissue insulin signaling and the suppression of HGP by insulin; however, the expression of Fst in the liver of healthy LTKO mice had the opposite effect. Of potential clinical significance, knockdown of Fst also improved glucose tolerance in high-fat-fed obese mice, and the level of serum Fst was reduced in parallel with glycated hemoglobin in obese individuals with diabetes who underwent therapeutic gastric bypass surgery. We conclude that Fst is a pathological hepatokine that might be targeted for diabetes therapy during hepatic insulin resistance.
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Follistatin-overexpressing mice showed strong insulin resistance in WAT, increased hepatic glucose production, and glucose intolerance.
“Follistatin-overexpressing mice showed strong insulin resistance in WAT, increased hepatic glucose production, and glucose intolerance [200], which is in line with the higher levels observed in patients with T2DM.”
The extent to which follistatin improves glycaemic measures remains controversial.
“The extent to which follistatin might improve glycaemic measures remains controversial.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [116]
Inactivating hepatic follistatin in a mouse model improved WAT sensitivity and reduced hepatic glucose production.
“inactivating hepatic follistatin in a mouse model improved WAT sensitivity and reduced hepatic glucose production116.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [116]
After bariatric surgery, improvements in HbA1c were observed with reduced follistatin levels.
“After bariatric surgery, improvements in HbA1c have been observed in the setting of reduced levels of follistatin116.”
From Exerkines in health, resilience and disease (2022) · cites this paper as [116]
Overexpression of FST in mice results in insulin resistance in WAT, increased hepatic glucose production, and impaired whole-body glucose tolerance.
“Overexpression of FST in mice resulted in insulin resistance in WAT, increased hepatic glucose production, and impaired whole-body glucose tolerance, consistent with higher expression in patients with type 2 diabetes [77,196].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [196]
Knockdown of FST in mice improves insulin sensitivity.
“Furthermore, knockdown of FST in mice improved insulin sensitivity [29,196].”
From Hepatokines and metabolism: Deciphering communication from the liver (2021) · cites this paper as [196]
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Follistatin Alleviates Hepatic Steatosis in NAFLD via the mTOR Dependent Pathway
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Self-citationFollistatin and follistatin-like 3 in metabolic disorders
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The Regulation of Circulating Hepatokines by Fructose Ingestion in Humans
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The Reign of Follistatin in Tumors and Their Microenvironment: Implications for Drug Resistance
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Fructose and follistatin potentiate acute MASLD during complete hepatic insulin resistance
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Self-citationRegulation of Hepatic Follistatin Expression at Rest and during Exercise in Mice
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Publisher Correction: Inactivating hepatic follistatin alleviates hyperglycemia
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Self-citationStudies of Foxo1 over the Past 25 Years: Mechanisms of Insulin Resistance and Glucose Dysregulation
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- Authors
- Tao, R., Wang, C., Stöhr, O., Qiu, W., Hu, Y., Miao, J., Dong, X. C., Leng, S., Stefater, M., Stylopoulos, N., Lin, L., Copps, K. D., & White, M. F.
- Affiliations
- Boston Children's Hospital (US)
- Indiana University School of Medicine (US)
- ORCID
- Venue
- Nature Medicine
- Published
- 2018-06-04
- Volume
- 24
- Issue
- 7
- Pages
- 1058-1069
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC6039237
- OpenAlex
- W2805369292
- Cited by
- 104
- References
- 54
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 13 · 2023: 17 · 2022: 10 · 2021: 12 · 2020: 11 · 2019: 15 · 2018: 9
- FWCI
- 9.17
- Type
- journal article
- Language
- en
- Update notices
- correction (2018-08-15)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- IUScholarWorks (Indiana University) (submittedVersion)
- Purdue University Indianapolis (Indiana University) (submittedVersion)
- Funders
- National Institutes of Health (5r01dk098655-08)
- National Institute on Alcohol Abuse and Alcoholism (R21AA024550)
- National Eye Institute (P30EY012196)
- National Institute of General Medical Sciences (P50GM021700)
- National Institute of Diabetes and Digestive and Kidney Diseases (K99DK077505, R01DK107682, R01- DK098655, R00DK077505, R56DK098655, R01DK108642, R56DK091592, R01DK091592, R00DK100539)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › FOXO transcription factor regulation
- Keywords
- follistatin, hepatic glucose production, hyperglycemia, FOXO1, insulin resistance, insulin receptor substrate 2, hepatokines, impaired glucose tolerance, diabetes mellitus, obesity, gastric bypass, HbA1c, high-fat diet
- MeSH terms
- Forkhead Box Protein O1, Animals, Glucose, Humans, Hyperglycemia, Insulin Resistance, Liver, Mice, Inbred C57BL, Signal Transduction, Down-Regulation, Glucose Intolerance, Mice, Knockout, Follistatin, 3T3-L1 Cells, Bariatric Surgery, Mice, Adipose Tissue, White, Gene Knockdown Techniques
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