Increased expression of GPI-specific phospholipase D in mouse models of type 1 diabetes

American Journal of Physiology - Endocrinology and Metabolism - Tập 281 Số 1 - Trang E147-E154 - 2001
Mark A. Deeg1, Rosario F. Bowen1, Monet D. Williams1, L. Karl Olson2, Elizabeth A. Kirk3, Renee Leboeuf3
1Departments of Medicine and of Biochemistry and Molecular Biology, Indiana University School of Medicine and the Richard L. Roudebush Veterans Affairs Medical Center, Indianapolis, Indiana 46202;
2Department of Physiology, Michigan State University, East Lansing, Michigan 48824; and
3Departments of Pathobiology, Nutritional Sciences, and Medicine, University of Washington, Seattle, Washington 98125

Tóm tắt

Glycosylphosphatidylinositol-specific phospholipase D (GPI-PLD) is a high-density lipoprotein-associated protein. However, the tissue source(s) for circulating GPI-PLD and whether serum levels are regulated are unknown. Because the diabetic state alters lipoprotein metabolism, and liver and pancreatic islets are possible sources of GPI-PLD, we hypothesized that GPI-PLD levels would be altered in diabetes. GPI-PLD serum activity and liver mRNA were examined in two mouse models of type 1 diabetes, a nonobese diabetic (NOD) mouse model and low-dose streptozotocin-induced diabetes in CD-1 mice. With the onset of hyperglycemia (2- to 5-fold increase over nondiabetic levels), GPI-PLD serum activity and liver mRNA increased 2- to 4-fold in both models. Conversely, islet expression of GPI-PLD was absent as determined by immunofluorescence. Insulin may regulate GPI-PLD expression, because insulin treatment of diabetic NOD mice corrected the hyperglycemia along with reducing serum GPI-PLD activity and liver mRNA. Our data demonstrate that serum GPI-PLD levels are altered in the diabetic state and are consistent with liver as a contributor to circulating GPI-PLD.

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Thông tin xuất bản

American Journal of Physiology - Endocrinology and Metabolism

Tập 281 Số 1

E147-E154

Thông tin tác giả