M
Mengyin Cai
Researcher at Sun Yat-sen University
Publications - 26
Citations - 912
Mengyin Cai is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Insulin & Adipose tissue. The author has an hindex of 11, co-authored 23 publications receiving 760 citations. Previous affiliations of Mengyin Cai include Lund University.
Papers
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Journal ArticleDOI
The many faces of diabetes: a disease with increasing heterogeneity
Tiinamaija Tuomi,Nicola Santoro,Sonia Caprio,Mengyin Cai,Jianping Weng,Leif Groop,Leif Groop +6 more
TL;DR: Diabetes is a much more heterogeneous disease than the present subdivision into types 1 and 2 assumes; type 1 and type 2 diabetes probably represent extremes on a range of diabetic disorders.
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Epigenetic regulation of the thioredoxin-interacting protein (TXNIP) gene by hyperglycemia in kidney
Yang De Marinis,Mengyin Cai,Mengyin Cai,Pradeep Bompada,David Atac,Olga Kotova,Martin Johansson,Eliana Garcia-Vaz,Maria F. Gomez,Markku Laakso,Leif Groop,Leif Groop +11 more
TL;DR: Glucose is a potent inducer of histone modifications, which could drive expression of proinflammatory genes and thereby predispose to diabetic kidney disease.
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SIRT1/HSF1/HSP pathway is essential for exenatide-alleviated, lipid-induced hepatic endoplasmic reticulum stress
TL;DR: The SIRT1/heat shock factor 1/HSP pathway is essential for exenatide‐alleviated, lipid‐induced ER stress and hepatic steatosis, which provides evidence for a molecular mechanism to support exen atide and incretin mimetics as promising therapeutics for obesity‐induced hepatic Steatosis.
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Diet‐induced obesity and insulin resistance are associated with brown fat degeneration in SIRT1‐deficient mice
TL;DR: The role of SIRT1 loss‐of‐function in diet‐induced obesity and insulin resistance and the mechanism involved in adipose tissue thermogenesis are investigated.
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Epigenetic regulation of glucose-stimulated osteopontin (OPN) expression in diabetic kidney
TL;DR: It is demonstrated that glucose is a potent inducer of histone acetylation and methylation, which in turn leads to upregulation of OPN gene expression, and treatment targeting histone marks may represent an alternative method to protect kidneys from deleterious effects of glucose.