期刊
CIRCULATION RESEARCH
卷 116, 期 8, 页码 1293-1295出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/CIRCRESAHA.115.305937
关键词
adipokines; blood pressure; obesity
资金
- NIDDK NIH HHS [P01 DK088761, R01-DK55758, P01-DK088761, R01-DK099110, R01 DK099110, R01 DK055758] Funding Source: Medline
Obese individuals often struggle with increases in blood pressure (BP) that ultimately lead to an enhanced cardiovascular disease (CVD) risk. The mechanistic basis for this association has remained largely unknown. Although a large number of metabolic signals are altered in obese individuals, including dyslipidemia, associated changes in sphingolipids, and an overall increase in subclinical inflammation, none of these parameters are thought to greatly influence BP. Recent data suggest that the adipokine leptin, whose circulating levels are typically proportional to fat mass, is a major driving force for the obesity-associated increases in BP. The effects of leptin on BP are mediated by neuronal circuits, including leptin-responsive neurons in the dorsomedial hypothalamic (DMH) nucleus.
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