Keyang Chen
Temple University
11 Papers
89 Citations
Keyang Chen is an academic researcher from Temple University. The author has contributed to research in topics: Insulin resistance & Tyrosine phosphorylation. The author has an hindex of 7, co-authored 11 publications. Previous affiliations of Keyang Chen include University of Gothenburg.
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Papers
Recent insights into factors affecting remnant lipoprotein uptake.
Kevin Jon Williams,Keyang Chen +1 more
TL;DR: Correct identification of hepatic remnant receptors has finally allowed investigations of their molecular dysregulation in diabetes and related conditions, and new work points to novel therapeutic targets to correct postprandial dyslipoproteinemia and its consequent arterial damage.
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Type 2 diabetes in mice induces hepatic overexpression of sulfatase 2, a novel factor that suppresses uptake of remnant lipoproteins
Keyang Chen,Ming-Lin Liu,Lana Schaffer,Mingzhen Li,Guenther Boden,Xiangdong Wu,Kevin Jon Williams +6 more
TL;DR: It is found that advanced glycosylation end products provoked a 10‐fold induction in SULF2 expression by cultured hepatocytes and an approximately 50% impairment in their catabolism of remnants and very low‐density lipoprotein, an effect that was entirely reversed by SulF2 knockdown.
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Inhibition of hepatic sulfatase‐2 In Vivo: A novel strategy to correct diabetic dyslipidemia
H. Carlijne Hassing,Hans L. Mooij,Shuling Guo,Brett P. Monia,Keyang Chen,Wim Kulik,Geesje M. Dallinga-Thie,Max Nieuwdorp,Erik S.G. Stroes,Kevin Jon Williams +9 more
TL;DR: In conclusion, inhibition of a single dys‐regulated molecule, SULF2, normalizes the VLDL‐binding capacity of their hepatocytes and abolishes postprandial hypertriglyceridemia in T2DM mice, providing a key proof of concept in vivo to support Sulf2 inhibition as an attractive strategy to improve metabolic dyslipidemia.
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The role of pathway-selective insulin resistance and responsiveness in diabetic dyslipoproteinemia.
TL;DR: A unified molecular explanation for fatty liver, atherogenic dyslipoproteinemia, hyperglycemia, and hence accelerated atherosclerosis and microvascular disease in T2DM, obesity, and related syndromes of positive caloric imbalance is suggested.
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