Abstract | BACKGROUND: METHODS: Eleven-week-old Gnmt-/- and wild-type (WT) mice with a C57BL/6 genetic background were used in this study. The metabolic defects of GNMT deficiency were measured by glucose and insulin tolerance tests, lipid homeostasis, gluconeogenesis, and insulin signaling. RESULTS: CONCLUSIONS: Our data indicate that hepatic GNMT regulates lipid and glucose homeostasis, and provide insight into the development of insulin resistance through modulating the PI3K/Akt pathway.
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Authors | Yi-Jen Liao, Tzong-Shyuan Lee, Yuh-Ching Twu, Shih-Ming Hsu, Ching-Ping Yang, Chung-Kwe Wang, Yu-Chih Liang, Yi-Ming Arthur Chen |
Journal | Journal of biomedical science
(J Biomed Sci)
Vol. 23
Issue 1
Pg. 69
(Oct 04 2016)
ISSN: 1423-0127 [Electronic] England |
PMID | 27716281
(Publication Type: Journal Article)
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Chemical References |
- Insulin
- Glycine N-Methyltransferase
- Phosphatidylinositol 3-Kinases
- Proto-Oncogene Proteins c-akt
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Topics |
- Animals
- Female
- Gluconeogenesis
- Glycine N-Methyltransferase
(deficiency, genetics)
- Insulin
(metabolism)
- Liver
(enzymology)
- Metabolic Syndrome
(genetics, metabolism)
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Phosphatidylinositol 3-Kinases
(genetics, metabolism)
- Proto-Oncogene Proteins c-akt
(genetics, metabolism)
- Signal Transduction
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