Abstract
Background: Endothelial dysfunction signals the initiation and progression of atherosclerosis. Elevated LDL-cholesterol concentrations have been suggested to induce endothelial dysfunction, but direct in vivo evidence for the relation is still lacking. Objective: We examined the hypothesis that a high-cholesterol, high-fat (HCHF) diet can directly cause endothelial dysfunction in vivo. Design: We measured inflammatory and endothelial dysfunctional markers in circulating blood and directly in endothelial cells, which were collected by femoral artery biopsies, in 10 baboons before and after a 7-wk HCHF dietary challenge. Results: We found that the HCHF diet induced a high inflammatory status, as indicated by increased concentrations of interleukin 6, tumor necrosis factor α (TNF-α), and monocyte chemoattractant protein 1. Although the concentrations of endothelial dysfunctional markers, such as soluble vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1, were not increased by the HCHF diet, membrane-bound VCAM-1 and membrane-bound E-selectin on endothelial cells were highly increased after 7 wk of the HCHF diet (P < 0.01). In contrast, the concentrations of endothelial nitric oxide synthase in endothelial cells were significantly reduced by the 7-wk HCHF diet (P < 0.01). Furthermore, the dietary challenge attenuated endothelial cell responses to TNF-α, lipopolysaccharide, native LDL cholesterol, and oxidized LDL-cholesterol stimulation. Conclusions: Our results show that an HCHF diet can directly induce inflammation and endothelial dysfunction. Prior in vivo exposure to an HCHF diet attenuates the in vitro responses of endothelial cells to atherogenic risk factors. This preconditioning phenomenon may have significant clinical relevance.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 751-759 |
| Number of pages | 9 |
| Journal | American Journal of Clinical Nutrition |
| Volume | 82 |
| Issue number | 4 |
| State | Published - 2005 |
| Externally published | Yes |
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Keywords
- Endothelium
- High-cholesterol
- High-fat diet
- Inflammation
- Nonhuman primates
ASJC Scopus subject areas
- Medicine (miscellaneous)
- Food Science
Cite this
Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet. / Shi, Qiang; Vandeberg, Jane F.; Jett, Catherine; Rice, Karen; Leland, Michelle M.; Talley, Leslie; Kushwaha, Rampratap S.; Rainwater, David L.; Vandeberg, John L.; Wang, Xing Li.
In: American Journal of Clinical Nutrition, Vol. 82, No. 4, 2005, p. 751-759.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Arterial endothelial dysfunction in baboons fed a high-cholesterol, high-fat diet
AU - Shi, Qiang
AU - Vandeberg, Jane F.
AU - Jett, Catherine
AU - Rice, Karen
AU - Leland, Michelle M.
AU - Talley, Leslie
AU - Kushwaha, Rampratap S.
AU - Rainwater, David L.
AU - Vandeberg, John L.
AU - Wang, Xing Li
PY - 2005
Y1 - 2005
N2 - Background: Endothelial dysfunction signals the initiation and progression of atherosclerosis. Elevated LDL-cholesterol concentrations have been suggested to induce endothelial dysfunction, but direct in vivo evidence for the relation is still lacking. Objective: We examined the hypothesis that a high-cholesterol, high-fat (HCHF) diet can directly cause endothelial dysfunction in vivo. Design: We measured inflammatory and endothelial dysfunctional markers in circulating blood and directly in endothelial cells, which were collected by femoral artery biopsies, in 10 baboons before and after a 7-wk HCHF dietary challenge. Results: We found that the HCHF diet induced a high inflammatory status, as indicated by increased concentrations of interleukin 6, tumor necrosis factor α (TNF-α), and monocyte chemoattractant protein 1. Although the concentrations of endothelial dysfunctional markers, such as soluble vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1, were not increased by the HCHF diet, membrane-bound VCAM-1 and membrane-bound E-selectin on endothelial cells were highly increased after 7 wk of the HCHF diet (P < 0.01). In contrast, the concentrations of endothelial nitric oxide synthase in endothelial cells were significantly reduced by the 7-wk HCHF diet (P < 0.01). Furthermore, the dietary challenge attenuated endothelial cell responses to TNF-α, lipopolysaccharide, native LDL cholesterol, and oxidized LDL-cholesterol stimulation. Conclusions: Our results show that an HCHF diet can directly induce inflammation and endothelial dysfunction. Prior in vivo exposure to an HCHF diet attenuates the in vitro responses of endothelial cells to atherogenic risk factors. This preconditioning phenomenon may have significant clinical relevance.
AB - Background: Endothelial dysfunction signals the initiation and progression of atherosclerosis. Elevated LDL-cholesterol concentrations have been suggested to induce endothelial dysfunction, but direct in vivo evidence for the relation is still lacking. Objective: We examined the hypothesis that a high-cholesterol, high-fat (HCHF) diet can directly cause endothelial dysfunction in vivo. Design: We measured inflammatory and endothelial dysfunctional markers in circulating blood and directly in endothelial cells, which were collected by femoral artery biopsies, in 10 baboons before and after a 7-wk HCHF dietary challenge. Results: We found that the HCHF diet induced a high inflammatory status, as indicated by increased concentrations of interleukin 6, tumor necrosis factor α (TNF-α), and monocyte chemoattractant protein 1. Although the concentrations of endothelial dysfunctional markers, such as soluble vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1, were not increased by the HCHF diet, membrane-bound VCAM-1 and membrane-bound E-selectin on endothelial cells were highly increased after 7 wk of the HCHF diet (P < 0.01). In contrast, the concentrations of endothelial nitric oxide synthase in endothelial cells were significantly reduced by the 7-wk HCHF diet (P < 0.01). Furthermore, the dietary challenge attenuated endothelial cell responses to TNF-α, lipopolysaccharide, native LDL cholesterol, and oxidized LDL-cholesterol stimulation. Conclusions: Our results show that an HCHF diet can directly induce inflammation and endothelial dysfunction. Prior in vivo exposure to an HCHF diet attenuates the in vitro responses of endothelial cells to atherogenic risk factors. This preconditioning phenomenon may have significant clinical relevance.
KW - Endothelium
KW - High-cholesterol
KW - High-fat diet
KW - Inflammation
KW - Nonhuman primates
UR - http://www.scopus.com/inward/record.url?scp=27744433469&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=27744433469&partnerID=8YFLogxK
M3 - Article
C2 - 16210703
AN - SCOPUS:27744433469
VL - 82
SP - 751
EP - 759
JO - American Journal of Clinical Nutrition
JF - American Journal of Clinical Nutrition
SN - 0002-9165
IS - 4
ER -