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Xueliang Du

Researcher at Albert Einstein College of Medicine

Publications -  27
Citations -  7836

Xueliang Du is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Diabetes mellitus & Insulin. The author has an hindex of 18, co-authored 23 publications receiving 7418 citations. Previous affiliations of Xueliang Du include Yeshiva University.

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The adipocyte-secreted protein Acrp30 enhances hepatic insulin action

TL;DR: It is proposed that Acrp30 is a potent insulin enhancer linking adipose tissue and whole-body glucose metabolism, which triggers a transient decrease in basal glucose levels in mice treated with streptozotocin.
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Structure-Function Studies of the Adipocyte-secreted Hormone Acrp30/Adiponectin IMPLICATIONS FOR METABOLIC REGULATION AND BIOACTIVITY

TL;DR: It is shown that there is a profound sexual dimorphism of Acrp30 levels and complex distribution in serum and a new model for in vivo activation of the protein, implicating a serum reductase activity is suggested.
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Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells

TL;DR: It is shown that hyperglycemia-induced overproduction of superoxide by the mitochondrial electron transport chain activates the three major pathways of hyperglycemic damage found in aortic endothelial cells by inhibiting GAPDH activity.
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Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy

TL;DR: In this article, the lipid-soluble thiamine derivative benfotiamine can inhibit three major biochemical pathways simultaneously, which might be clinically useful in preventing the development and progression of diabetic complications.
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Lower blood glucose, hyperglucagonemia, and pancreatic α cell hyperplasia in glucagon receptor knockout mice

TL;DR: The data indicate that glucagon is essential for maintenance of normal glycemia and postnatal regulation of islet and α and δ cell numbers and the lean phenotype of Gcgr−/− mice suggests glucagon action may be involved in the regulation of whole body composition.