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Krzak, W. E., Gonyou, H. W., & Lawrence, L. M. (1991). Wood chewing by stabled horses: diurnal pattern and effects of exercise. J. Anim Sci., 69(3), 1053–1058.
Abstract: Nine yearling horses, stabled in individual stalls, were used in a trial to determine the diurnal pattern of wood chewing and the effects of exercise on this behavior. The trial was a Latin square design conducted over three 2-wk periods during which each horse was exposed to each of the three following treatments: 1) no exercise (NE), 2) exercise after the morning feeding (AM), and 3) exercise in the afternoon (PM). Horses were fed a complete pelleted feed in the morning and both pelleted feed and long-stemmed hay in the afternoon. Exercise consisted of 45 min on a mechanical walker followed by 45 min in a paddock with bare soil. Each stall was equipped with two untreated spruce boards during each period for wood chewing. Wood chewing was evaluated by videotaping each horse for 22 h during each period, determining the weight and volume of the boards before and after each period, and by visual appraisal of the boards. Intake of trace mineralized salt was also measured. Wood chewing occurred primarily between 2200 and 1200. All measures of wood chewing were correlated when totals for the entire 6 wk were analyzed. When analysis was performed on 2-wk values, videotape results were not correlated with volume or weight loss of boards. Horses chewed more when on the NE treatment (511 s/d) than when on AM or PM (57 and 136 s/d, respectively; P less than .05). Salt intake tended to be greater for NE than for the other treatments (P less than .10).(ABSTRACT TRUNCATED AT 250 WORDS)
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Nicol, C. J., Adachi, M., Akiyama, T. E., & Gonzalez, F. J. (2005). PPARgamma in endothelial cells influences high fat diet-induced hypertension. Am J Hypertens, 18(4 Pt 1), 549–556.
Abstract: BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful.
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