Liver-specific deletion of Ppp2cα enhances glucose metabolism and insulin sensitivity
Open accessAbstract
Protein phosphatase 2A (PP2A) is a key negative regulator of phosphatidylinositol 3-kinase/Akt pathway. Previous study showed that, in the liver, the catalytic subunit of PP2A (PP2Ac) is closely associated with insulin resistance syndrome, which is characterized by glucose intolerance and dyslipidemia. Here we studied the role of liver PP2Ac in glucose metabolism and evaluated whether PP2Ac is a suitable therapeutic target for treating insulin resistance syndrome. Liver-specific Ppp2cα knockout mice (Ppp2cα(loxp/loxp): Alb) exhibited improved glucose homeostasis compared with littermate controls in both normal and high-fat diet conditions, despite no significant changes in body weight and liver weight under chow diet. Ppp2cα(loxp/loxp): Alb mice showed enhanced glycogen deposition, serum triglyceride, cholesterol, low density lipoprotein and high density lipoprotein, activated insulin signaling, decreased expressions of gluconeogenic genes G6P and PEPCK, and lower liver triglyceride. Liver-specific Ppp2cα knockout mice showed enhanced glucose homeostasis and increased insulin sensitivity by activation of insulin signaling through Akt. These findings suggest that inhibition of hepatic Ppp2cα may be a useful strategy for the treatment of insulin resistance syndrome.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Increased insulin signaling included increased phosphorylation of AKT Ser473/Thr308, GSK-3α/β Ser21/Ser9, FoxO1 Ser264, and GS Ser641.
“Increased insulin signaling was exemplified by increased phosphorylation of AKT (Ser473, Thr308), GSK-3α/β (Ser21/Ser9), FoxO1 (Ser264) and GS (Ser641).”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [71]
These mice had normal body weights, normal liver-to-body weight ratios, and normal liver histology.
“The mice showed normal body weights, normal liver-body weight ratios and normal liver histology.”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [71]
The improved glucose tolerance could be prevented by prior treatment with wortmannin, a PI3K inhibitor.
“The improved glucose tolerance could be prevented by prior treatment with wortmannin, a PI3K inhibitor.”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [71]
The livers also showed improved glycogen storage and decreased lipid deposition.
“The livers also showed improved glycogen storage and decreased lipid deposition.”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [71]
Liver-specific deletion of Ppp2ca improved glucose tolerance and enhanced insulin sensitivity and signaling in liver, but not in muscle.
“Liver-specific deletion of Ppp2ca resulted in improved glucose tolerance and enhanced insulin sensitivity and signaling in liver, but not in muscle [71].”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [71]
Serum triglycerides, cholesterol, HDL, and LDL were increased on both normal chow and high-fat diets.
“increased levels of triglycerides (TGD), cholesterol (CHOL), and high-and low-density lipoproteins (HDL and LDL) in serum, both when mice were given normal chow or high-fat diets [71].”
From Physiologic functions of PP2A: Lessons from genetically modified mice (2019) · cites this paper as [71]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 43 · Cited by 31
- Authors
- Xian, L., Hou, S., Huang, Z., Tang, A., Shi, P., Wang, Q., Song, A., Jiang, S., Lin, Z., Guo, S., & Gao, X.
- Affiliations
- Model Animal Research Center (CN)
- Corresponding author
- Gao, Xiang
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2015-02-21
- Volume
- 7
- Issue
- 4
- Pages
- 223-232
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC4429087
- OpenAlex
- W221618059
- Cited by
- 31
- References
- 43
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 1 · 2023: 6 · 2022: 4 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 3 · 2016: 2 · 2015: 1
- FWCI
- 1.16
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (31100918)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- protein phosphatase 2A, liver-specific knockout, metabolic syndrome, glucose homeostasis, insulin sensitivity, Akt signaling, insulin signaling, hepatic glucose metabolism, gluconeogenesis, glycogen accumulation, dyslipidemia, high-fat diet, therapeutic target
- MeSH terms
- Protein Phosphatase 2C, Animals, Glucose, Homeostasis, Insulin, Insulin Resistance, Lipids, Liver, Phosphoprotein Phosphatases, Signal Transduction, Glucose Intolerance, Mice, Knockout, Proto-Oncogene Proteins c-akt, Mice, Diet, High-Fat
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 ›
Are you an author, or do you see a problem with this page? Request a review
