ABSTRACT
We recently showed that the antiobese efficacy of the AT1 receptor blocker telmisartan (TEL) is at least partially related to an Ang(1-7)-dependent mechanism. Ang(1-7) acts via Mas, thus raising the question of whether Mas-deficient (Mas-ko) mice are likewise predisposed to develop diet-induced obesity and, further, whether this can be prevented by TEL treatment. Mas-ko mice and FVB/N wild-type (wt) animals were treated with TEL (8 mg/kg/day) or vehicle while they were fed with high-fat diet (HFD) or chow. Mice were phenotyped regarding body weight, fat mass, insulin sensitivity, and leptin sensitivity. In response to HFD feeding, gain in body weight and impairment of leptin sensitivity were similar between wt and Mas-ko mice. TEL reduced body weight in both strains but effects were stronger in Mas-ko mice. TEL diminished fat mass and restored leptin sensitivity only in Mas-ko mice. Blood glucose was higher in wt than Mas-ko mice fed with HFD while not differing when they were fed with chow. Insulin challenge confirmed that wt mice became insulin resistant when fed with HFD while HFD feeding did not impair insulin sensitivity in Mas-ko mice. TEL had no further effect. Our findings on the influence of TEL on growth and metabolism in Mas-ko mice conflict with our previous findings in rats. We assume that the FVB/N background of the mice may partly explain these inconsistent data. Moreover, it also seems feasible that the MrgD receptor compensates for Mas deficiency.
Subject(s)
Angiotensin II Type 1 Receptor Blockers/pharmacology , Anti-Obesity Agents/pharmacology , Obesity/metabolism , Proto-Oncogene Proteins/deficiency , Receptor, Angiotensin, Type 1/metabolism , Receptors, G-Protein-Coupled/deficiency , Telmisartan/pharmacology , Animals , Body Weight/drug effects , Body Weight/genetics , Diet, High-Fat , Mice, Knockout , Obesity/drug therapy , Obesity/etiology , Proto-Oncogene Mas , Proto-Oncogene Proteins/genetics , Receptors, G-Protein-Coupled/geneticsABSTRACT
OBJECTIVE: To investigate the reliability (test-retest and inter-rater) and criterion-related validity of the modified sphygmomanometer test (MST) for the assessment of upper limb muscle strength in subjects with chronic stroke, and to determine whether the results are affected by the number of trials. PATIENTS AND METHODS: The strength of 11 upper limb muscle groups of 57 subjects with stroke was bilaterally assessed with portable dynamometers and the MST (measured in mmHg). To investigate whether the number of trials would affect the results, 1-way analysis of variance was applied. For the test-retest/inter-rater reliabilities and criterion-related validity of the MST, intra-class correlation coefficients (ICCs), Pearson's correlation coefficients, and coefficients of determination were calculated. RESULTS: Different numbers of trials provided similar values for all assessed muscles (0.01 ≤ F ≤ 0.18; 0.83 ≤ p ≤ 0.99) with adequate test-retest (0.83 ≤ ICC ≤ 0.97; p < 0.0001) and inter-rater reliabilities (0.79 ≤ ICC ≤ 0.97; p < 0.0001) and validity (0.61 ≤ r ≤ 0.95; p < 0.0001). The values obtained with the MST were good predictors of those obtained with portable dynamometers (0.60 ≤ r2 ≤ 0.86), except for pinch strength (0.39 ≤ r2 ≤ 0.54). CONCLUSION: The MST showed adequate measurement properties for the assessment of the strength of the upper limb muscles of subjects with chronic stroke. After familiarization a single trial provided adequate strength values.
