In addition to its role in the storage of fat, adipose tissue acts as an endocrine organ, and it contains a functional renin-angiotensin system (RAS). Angiotensin-converting enzyme (ACE) plays a key role in the RAS by converting angiotensin I to the bioactive peptide angiotensin II (Ang II). In the present study, the effect of targeting the RAS in body energy homeostasis and glucose tolerance was determined in homozygous mice in which the gene for ACE had been deleted (ACE ؊/؊ ) and compared with wild-type littermates. Compared with wild-type littermates, ACE ؊/؊ mice had lower body weight and a lower proportion of body fat, especially in the abdomen. ACE ؊/؊ mice had greater fed-state total energy expenditure (TEE) and resting energy expenditure (REE) than wild-type littermates. There were pronounced increases in gene expression of enzymes related to lipolysis and fatty acid oxidation (lipoprotein lipase, carnitine palmitoyl transferase, long-chain acetyl CoA dehydrogenase) in the liver of ACE ؊/؊ mice and also lower plasma leptin. In contrast, no differences were detected in daily food intake, activity, fed-state plasma lipids, or proportion of fat excreted in fecal matter. In conclusion, the reduction in ACE activity is associated with a decreased accumulation of body fat, especially in abdominal fat depots. The decreased body fat in ACE ؊/؊ mice is independent of food intake and appears to be due to a high energy expenditure related to increased metabolism of fatty acids in the liver, with the additional effect of increased glucose tolerance.fatty acid metabolism ͉ obesity ͉ ACE knockout mice ͉ glucose tolerance T he renin-angiotensin system (RAS) is important in both cardiovascular and body fluid homeostasis (1-3) and has recently been implicated in obesity and energy balance (see ref.4 for a review). All of the components of the RAS are present in adipose tissue and evidence suggests that this RAS is fully functional and can contribute to the accumulation of fat and to obesity (5-7). Recent studies showed that transgenic mice lacking the precursor peptide, angiotensinogen (AGT), have impaired weight gain and adipose tissue development (8), whereas mice with an overabundance of AGT in adipose tissue have markedly increased fat mass (9).Overexpression of genes associated with the RAS has been reported in human visceral adipose tissue in overweight subjects (10), and polymorphisms of the angiotensin-converting enzyme (ACE) gene have been linked to the incidence of obesity and alterations of body mass index (11,12). ACE plays a key role in the RAS in that it converts angiotensin I to the bioactive peptide angiotensin II (Ang II). Ang II has been identified as a trophic factor in the differentiation of preadipocytes to mature adipocytes (13). There is evidence that administration of ACE inhibitors reduces body weight gain in spontaneously hypertensive rats (14), obese Zucker rats (15), and humans (16). However, some studies have shown that the activity of the RAS is inversely related to the gain of body weight....
Interview group respondents were more likely to give top ranking responses to questions on service satisfaction and symptom control. Conclusions-Postal questionnaires are an acceptable alternative to interviews in retrospective post-bereavement surveys of care for the dying, at least in terms of response rate and response bias. However, the increased costs of interview surveys need to be balanced against the fact that postal questionnaires result in more missing data, and possibly less reliable answers to some questions. Caution is needed in combining results from the two data collection methods as interview respondents gave more positive answers to some questions.
Background-Addition of up to 15.0 g/d salt to the diet of chimpanzees caused large rises in blood pressure, which reversed when the added salt was removed. Effects of more modest alterations to sodium intakes in chimpanzees, akin to current efforts to lower sodium intakes in the human population, are unknown. Methods and Results-Sodium intakes were altered among 17 chimpanzees in Franceville, Gabon, and 110 chimpanzees in Bastrop, Tex. In Gabon, chimpanzees had a biscuit diet of constant nutrient composition except that the sodium content was changed episodically over 3 years from 75 to 35 to 120 mmol/d. In Bastrop, animals were divided into 2 groups; 1 group continued on the standard diet of 250 mmol/d sodium for 2 years, and sodium intake was halved for the other group. Lower sodium intake was associated with lower systolic, diastolic, and mean arterial blood pressures in Gabon (2-tailed PϽ0.001, unadjusted and adjusted for age, sex, and baseline weight) and Bastrop (PϽ0.01, unadjusted; Pϭ0.08 to 0.10, adjusted), with no threshold down to 35 mmol/d sodium. For systolic pressure, estimates were Ϫ12.7 mm Hg (95% confidence interval, Ϫ16.9 to Ϫ8.5, adjusted) per 100 mmol/d lower sodium in Gabon and Ϫ10.9 mm Hg (95% confidence interval, Ϫ18.9 to Ϫ2.9, unadjusted) and Ϫ5.7 mm Hg (95% confidence interval, Ϫ12.2 to 0.7, adjusted) for sodium intake lower by 122 mmol/d in Bastrop. Baseline systolic pressures higher by 10 mm Hg were associated with larger falls in systolic pressure by 4.3/2.9 mm Hg in Gabon/Bastrop per 100 mmol/d lower sodium. Conclusions-These findings from an essentially single-variable experiment in the species closest to Homo sapiens with high intakes of calcium and potassium support intensified public health efforts to lower sodium intake in the human population.
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