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Central Nervous System Neuropeptide Y Signaling Modulates VLDL Triglyceride Secretion
Author(s) -
John M. Stafford,
Fang Yu,
Richard L. Printz,
Alyssa H. Hasty,
Larry L. Swift,
Kevin D. Niswender
Publication year - 2008
Publication title -
diabetes
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.219
H-Index - 330
eISSN - 1939-327X
pISSN - 0012-1797
DOI - 10.2337/db07-1702
Subject(s) - endocrinology , medicine , neuropeptide y receptor , very low density lipoprotein , adipose tissue , agonist , energy homeostasis , receptor , biology , lipoprotein , neuropeptide , cholesterol
Elevated triglyceride (TG) is the major plasma lipid abnormality in obese and diabetic patients and contributes to cardiovascular morbidity in these disorders. We sought to identify novel mechanisms leading to hypertriglyceridemia. Resistance to negative feedback signals from adipose tissue in key central nervous system (CNS) energy homeostatic circuits contributes to the development of obesity. Because triglycerides both represent the largest energy depot in the body and are elevated in both the plasma and adipose in obesity and diabetes, we hypothesized that the same neural circuits that regulate energy balance also regulate the secretion of TGs into plasma.

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