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High fat feeding induces exaggerated endothelial dysfunction and insulin resistance in rats exposed to maternal separation (1085.7)
Author(s) -
Loria Analia,
Fox Brandon,
Pollock David,
Pollock Jennifer
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1085.7
Subject(s) - medicine , endocrinology , insulin resistance , angiotensin ii , phenylephrine , adiponectin , leptin , endothelial dysfunction , insulin , blood pressure , chemistry , obesity
We previously reported that adult male rats exposed to MatSep (3 hrs/day from day 2 to 14 of life) display normal baseline cardiovascular parameters but enhanced responses to angiotensin II (AngII) compared to controls (C, non‐MatSep littermates). We tested the hypothesis that a chronic HF diet (60% fat cal., 0.4 salt; 6 months) exaggerates metabolic and/or cardiovascular indices in MatSep rats. Plasma fasting glucose and insulin were higher in MatSep vs. C rats (p<0.05), showing a greater HOMA index in MatSep than C rats (1.0±0.1 vs. 1.7±0.1, p<0.05). Plasma adiponectin was lower in MatSep vs. C rats (19±2 vs. 28±2 ug/ml, p<0.05), although body weight and leptin were similar between groups. No differences in mean arterial pressure or heart rate were observed between MatSep and C rats (105±2 vs. 102±2mmHg; 326±6 vs. 317±3 bpm; n=6). Wire myography of thoracic aortae showed a greater vasoconstrictive response (%max constriction) to AngII (17±2 vs. 6±1, p<0.05) and phenylephrine (59±4 vs. 29±5, p<0.05) from MatSep rats. L‐NAME pre‐incubation revealed a loss of NO buffering capacity to AngII in MatSep aortae only (p<0.05). Impaired acetylcholine‐induced relaxation was greater in aortae from MatSep rats (49±6 vs. 27±3 % relax, p<0.05). These data reveal that MatSep followed by HF feeding induces a synergistic effect on disrupting vascular function and glucose homeostasis increasing the risk to cardiovascular disease. Grant Funding Source : HL111354 and PO1 HL69999