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Gend Med. 2011 Apr;8(2):150-5. doi: 10.1016/j.genm.2011.03.006.

High dietary fat promotes visceral obesity and impaired endothelial function in female mice with systemic lupus erythematosus.

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1
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216-4505, USA.

Abstract

BACKGROUND:

Inflammation contributes to metabolic and cardiovascular disease. Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disorder that predominantly affects young women. Cardiovascular disease is a major cause of mortality in patients with SLE. We recently reported that a model of SLE (female New Zealand Black/White F1 [NZBWF1] mice) developed characteristics of the metabolic syndrome.

OBJECTIVES:

In the present study, we tested the hypothesis that high dietary fat with SLE accelerated development of cardiovascular risk factors such as central obesity and vascular dysfunction.

METHODS:

Twenty-four-week-old female SLE mice (NZBWF1) were fed either a control diet (SLE, 10% kcal) or a high-fat (HF) diet (SLE + HF, 45% kcal) for a total of 14 weeks.

RESULTS:

Body weight was similar between SLE (42 [1] g, n = 5) and SLE + HF (45 [2] g, n = 6) mice, and weight gain was not different in the SLE + HF mice (+18.0 [3.0]%) compared with controls (+15.8 [3.6]%); food intake was not different (SLE, 2.2 [0.3] vs SLE + HF, 2.1 [0.2] g/24 hours). At the end of the experiment, 57% of the SLE + HF mice exhibited signs of albuminuria (>100 mg/dL) compared with only 20% of the control SLE mice. Endothelial-dependent relaxation in isolated carotid arteries was impaired in the SLE + HF group compared with that in the SLE group. Ovarian fat increased in SLE + HF mice (6.6 [0.5] g) compared with that in the control SLE mice (5.4 [0.1] g, P < 0.05), and liver weight decreased in SLE + HF (1.6 [0.1] g) mice compared with that in control mice (1.9 [0.1] g, P < 0.03).

CONCLUSIONS:

These data suggest that dietary fat accelerates renal injury and peripheral vascular dysfunction and promotes visceral obesity in a disease model with chronic inflammation.

PMID:
21536233
PMCID:
PMC3229028
DOI:
10.1016/j.genm.2011.03.006
[Indexed for MEDLINE]
Free PMC Article
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