Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sucrose-fed rats, a model of metabolic syndrome, are characterized by insulin resistance, obesity, hypertension, and high plasma levels of triacylglycerols and angiotensin II (Ang II). However, whether tissue renin-angiotensin system (RAS) is altered in metabolic syndrome is unclear. To study this issue, food ad libitum and water (C) or 20% sucrose solution (SC) were given to adult male Wistar rats, for 30 days. Body weight (BW), blood pressure (BP), epididymal adipose tissue (EPI) mass, rate of in vivo fatty acid (FA) synthesis in EPI, circulating glucose, insulin, leptin, angiotensins I and II, triacylglycerols, and plasma renin (PRA) and angiotensin-converting enzyme (ACE) activities were evaluated. In kidneys and EPI, gene and protein expression of type 1 (AT(1)) and 2 (AT(2)) Ang II receptors, ACE, angiotensinogen (AGT) as well as protein expression of angiotensin-converting enzyme 2 (ACE2) were determined. In both tissues, Ang I, Ang II and Ang-(1-7) contents were also measured by HPLC. In SC rats higher BP, EPI mass, circulating triacylglycerols, insulin, leptin, PRA and, Ang II were found. In EPI, the rate of in vivo FA synthesis was associated with increased Ang-(1-7), protein expression of AT(1) and AT(2) receptors, ACE2, AGT, and gene expression of AGT although a reduction in ACE activity and in adipose Ang I and Ang II contents was observed. In kidneys, AT(1) and AT(2), ACE and AGT gene and protein expression as well as protein expression of ACE2 were unaltered while Ang II, Ang-(1-7) and ACE activity increased. These RAS component changes seem to be tissue specific and possibly are related to enhancement of FA synthesis, EPI mass and hypertension.
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PMID:High sucrose intake in rats is associated with increased ACE2 and angiotensin-(1-7) levels in the adipose tissue. 2034 75

The purpose is to consider the practical management of etiological work up in hypertension, beyond national or international recommendations, leading to consider the prior practice of hormonal assays or renal, renovascular or adrenal imaging. The ease of access to imaging, difficulties to meet the requirements to obtain reliable hormonal assays explain the use of first-line imaging in clinical practice. The renal and adrenal CT angiography provides diagnostic orientation without allowing a formal conclusion. Incidentaloma prevalence in the general population, increasing with age, underlines the limitations of a decision based only on imaging. The discovery of adrenal morphological abnormalities justifies the realization of hormonal assays to determine their causal relationship with hypertension. The aldosterone/PRA ratio, in standardized conditions, has the best diagnostic performance to screen for primary aldosteronism and is the pivotal test of the etiological diagnosis of hypertension. The identification of a subclinical Cushing should be considered in patients with adrenal morphological abnormalities, particularly in case of metabolic syndrome. The abdominal CTscan is initially recommended in the diagnosis of pheochromocytoma, but the recommende boichemical testing is urine metanephrines whose result will lead to search a pheochromocytoma or an extra-abdominal paraganglioma. Many drug interactions must be considered in order to interpret hormonal measurements and avoid erroneous diagnosis. Finally, a genetic context and the possibility of endocrine causes with normal abdominal CT scan should be considered: extra-abdominal paraganglioma, parathyroid adenoma and Cushing's disease with pituitary adenoma, requiring a multidisciplinary decision. The efficiency of imaging as first-line in the screening of secondary hypertension is relative and confrontation with hormone assays will be critical to the diagnostic and therapeutic management. In young women, hormonal measurements precede imaging in the etiological investigation of hypertension.
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PMID:[Hypertension etiological work up: Hormonological assessment always before imaging?] 2759 61