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Query: UMLS:C0948265 (metabolic syndrome)
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The clustering of cardiovascular risk factors was noted already a century ago, but it is only recently that a link between the CV risk cluster and insulin resistance has been postulated - a proposal which is not unanimously accepted. There is no doubt, however, that obesity per se impacts on renal function and the risk of chronic kidney disease (CKD). Particularly obesity early in life is an important predictor of CKD in adult life, but in adults as well a high body mass index (BMI) is an independent predictor of ESRD. The BMI threshold is lower in Asians. The link between obesity and CKD is not fully explained by the association between obesity and diabetes or hypertension respectively. Obesity is associated with increased glomerular filtration rate and renal blood flow, glomerulomegaly and in extreme cases focal segmental glomerulosclerosis. The causal role of obesity is underlined by the effect of weight loss on proteinuria and glomerular hyperfiltration. An even better predictor than BMI is visceral obesity (waist circumference). For kidney disease in the metabolic syndrome it is relevant that insulin resistance is linked to salt sensitivity and increased tubular reabsorption of sodium. Recent evidence points to adverse effects of aldosterone on podocytes, mediated by reactive oxygen species and resulting from hypothetical stimulants of aldosterone synthesis by visceral adipocytes.
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PMID:Metabolic syndrome and kidney disease. 1818 98

Kidney stones affect hypertensive patients disproportionately compared to normotensive individuals. On the other hand, some prospective data suggest that a history of nephrolithiasis was associated with a greater tendency to develop hypertension. Newer epidemiologic data also link obesity and diabetes, features of the metabolic syndrome, with nephrolithiasis. In this review, the association of hypertension, diabetes, and obesity with nephrolithiasis is reviewed, and possible pathogenic mechanisms are discussed. Patients with hypertension may have abnormalities of renal calcium metabolism, but data confirming this hypothesis are inconsistent. Higher body mass index and insulin resistance (i.e., the metabolic syndrome) may be etiologic in uric acid nephrolithiasis as increasing body weight is associated with decreasing urinary pH. The possibility that common pathophysiologic mechanisms underly these diseases is intriguing, and if better understood, could potentially lead to better therapies for stone prevention. Both hypertension and stones might be addressed through lifestyle modification to prevent weight gain. Adoption of a lower sodium diet with increased fruits and vegetables and low-fat dairy products, (for example, the dietary approaches to stop hypertension(DASH) diet), may be useful to prevent both stones and hypertension. In those patients in whom dietary modification and weight loss are ineffective, thiazide diuretics are likely to improve blood pressure control and decrease calciuria.
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PMID:The association of nephrolithiasis with hypertension and obesity: a review. 1821

A new guideline on metabolic syndrome (MS) in Japanese was introduced in 2005. The purpose of this study was to evaluate the prevalence and lifestyle characteristics of Japanese hypertensive patients with MS. Subjects were 290 patients (mean age: 64+/-11 years) who had been followed at our hospital. The waist circumference (WC) and body mass index (BMI) were assessed. Subjects who had BMI >or=25 kg/m(2) were defined as having BMI obesity, while abdominal obesity was defined as a WC >or=85 cm in men and >or=90 cm in women, respectively. Since all patients had hypertension, the definition of MS was made when the patient had abdominal obesity plus either dyslipidemia or glucose intolerance, or both. Among the subjects, 230 patients underwent 24-h home urine collection to measure urinary salt and potassium excretions. Dietary habits were also assessed by use of a questionnaire. Mean values of BMI and WC were 24.2+/-3.4 kg/m(2) and 87.1+/-9.6 cm, respectively. Among the total subject group, 39% patients were classified as having BMI obesity, 49% as having abdominal obesity, and 27% as having MS. BMI was significantly correlated with WC both in men (r=0.86; p<0.01) and in women (r=0.79; p<0.01). More men than women belonged to the BMI obesity (46% vs. 33%, p<0.05), abdominal obesity (63% vs. 39%, p<0.01) and MS (39% vs. 18%, p<0.01) groups. There were no significant differences in blood pressure between patients with and without MS, while patients with MS needed a greater number of antihypertensive drugs than those without MS. Mean urinary salt and potassium excretions were 8.9+/-3.8 g/day and 1.9+/-0.7 g/day, respectively. Urinary salt excretion of <6 g (100 mmol of sodium)/day was achieved in 20% of the subjects. Urinary salt excretion in the patients with MS was significantly higher than that in the patients without (10.1+/-4.2 vs. 8.5+/-3.6 g/day; p<0.01). Only 16% of the patients with MS achieved salt restriction (<6 g/day). The patients with MS had a significantly greater the chance to eat out than the patients without MS. They were also less aware of the need to increase their vegetable consumption. The results suggested that MS is prevalent in Japanese hypertensive patients. Patients with MS showed higher urinary salt excretion and needed more antihypertensive drugs to manage their blood pressure. Dietary counseling focusing not only on sodium restriction but also on the need to increase fruit and vegetable consumption seems to be important.
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PMID:Prevalence and lifestyle characteristics of hypertensive patients with metabolic syndrome followed at an outpatient clinic in fukuoka, Japan. 1825 May 57

We examined the role of epidermal growth factor (EGF) receptor in the pathogenesis of leptin-induced hypertension in the rat. Leptin, administered in increasing doses (0.1-0.5 mg/kg/day) for 10 days, increased phosphorylation levels of non-receptor tyrosine kinase, c-Src, EGF receptor and extracellular signal-regulated kinases (ERK) in aorta and kidney, which was accompanied by the increase in plasma concentration and urinary excretion of isoprostanes and H2O2. Blood pressure and renal Na+,K+-ATPase activity were higher, whereas urinary sodium excretion was lower in animals receiving leptin. The effects of leptin on renal Na+,K+-ATPase, natriuresis and blood pressure were abolished by NADPH oxidase inhibitor, apocynin, Src kinase inhibitor, PP2, EGF receptor inhibitor, AG1478, protein farnesyltransferase inhibitor, manumycin A, and ERK inhibitor, PD98059. In contrast, inhibitors of insulin-like growth factor-1 and platelet-derived growth factor receptors, AG1024 and AG1295, respectively, only slightly reduced ERK phosphorylation and had no effect on blood pressure in rats receiving leptin. These data indicate that: (1) experimental hyperleptinemia is associated with oxidative stress and c-Src-dependent transactivation of the EGF receptor, which stimulates ERK in vascular wall and the kidney, (2) overactivity of EGF receptor-ERK pathway contributes to leptin-induced hypertension by stimulating renal Na+,K+-ATPase and reducing sodium excretion, (3) inhibitors of c-Src, EGF receptor and ERK may be considered as a novel therapy for hypertension associated with hyperleptinemia, e.g. in patients with obesity and metabolic syndrome.
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PMID:Transactivation of epidermal growth factor receptor in vascular and renal systems in rats with experimental hyperleptinemia: role in leptin-induced hypertension. 1828 56

Objective was to assess dietary intake and physical activity in a Canadian population sample of male patients with HIV and metabolic abnormalities and to compare the data to Canadian recommendations. Sixty-five HIV-infected men with at least one feature associated with the metabolic syndrome (insulin resistance, dyslipidemia, central obesity, or lipodystrophy) were enrolled. Results from 7-day food records and activity logs were compared to the Dietary Reference Intakes and recommendations of Canada's Physical Activity Guide, respectively. Anthropometric data were also measured. Fifty-two percent of the subjects were overweight, another 15% were obese. However, energy intake (mean+/-SEM) (2153+/-99 kcal/d) was lower than the estimated requirement (2854+/-62 kcal/d; p<0.0001), and 84.5% of the patients reached the recommended minimum of 60 min of mild or 30 min of moderate daily exercise. Intake was adequate for protein, but high for fat and cholesterol in 40% of patients. No patient reached the recommendation for fiber. Intake from diet alone was suboptimal for most micronutrients. Prevalence was highest for low vitamin E (91% of patients) and magnesium (68%) intake, and high sodium intake (72%). In summary, a large proportion of HIV patients with metabolic abnormalities were overweight or obese. However, this was not associated with high energy intake, or reduced physical activity. High fat, low fiber and inadequate micronutrient intakes were prevalent.
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PMID:Dietary intake and physical activity in a Canadian population sample of male patients with HIV infection and metabolic abnormalities. 1828 80

Lifestyle and diet play important roles in the development of cardiovascular disease (CVD), which is the leading cause of death in Western countries. Metabolic syndrome, which is characterized by a group of metabolic risk factors, is associated with the subsequent development of type 2 diabetes and CVD. Epidemiological studies have documented that nutritional factors may affect the prevalence of the metabolic syndrome. Beyond weight control and reduction of total calories, the diet should be low in saturated fats, trans fats, cholesterol, sodium, and simple sugars. In addition, there should be ample intake of fruits, vegetables, whole grains, and monounsaturated fat; fish intake should be encouraged. These features are very reminiscent of the nutritional principles currently used to define the Mediterranean-style diet. This diet's high fiber content, n-3 fatty acids, and antioxidants, as well as phytochemicals from olive oil, legumes, whole grains, fruits, and vegetables, might be responsible for its beneficial effect on the health of metabolic syndrome patients. This may occur through the reduction of systemic vascular inflammation and endothelium dysfunction without having a drastic effect on body weight. The choice of healthy sources of carbohydrates, fat, and proteins, associated with regular physical activity and avoidance of smoking, is critical to fighting the war against chronic disease.
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PMID:Diet and the metabolic syndrome. 1837 Jul 98

The obesity pandemic is closely related to hypertension and metabolic syndrome. Visceral adipose tissue plays a key role in the metabolic and cardiovascular complications of being overweight. The pathophysiological link between visceral adiposity and cardiometabolic complications focuses on insulin sensitivity, sympathetic nervous system, renin-angiotensin-aldosterone system (RAAS) and, only recently, on cardiac natriuretic peptide system (CNPS). RAAS and CNPS are endogenous antagonistic systems on sodium balance, cardiovascular system, and metabolism. The circulating RAAS is dysregulated in obese patients, and adipose tissue has a full local renin-angiotensin system that is active at local and systemic level. Adipocyte biology and metabolism are influenced by local renin-angiotensin system, with angiotensin II acting as a 'growth factor' for adipocytes. CNPS induces natriuresis and diuresis, reduces blood pressure, and, moreover, has powerful lipolytic and lipomobilizing activity in humans but not in rodents. In obesity, lower plasmatic natriuretic peptides levels with increasing BMI, waist circumference, and metabolic syndrome have been documented. Thus, reduced CNPS effects coupled with increased RAAS activity have a central role in obesity and its deadly complications. We propose herein an integrated view of the dysregulation of these two antagonistic systems in human obesity complicated with hypertension, metabolic syndrome, and increased cardiovascular risk.
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PMID:Renin-angiotensin system, natriuretic peptides, obesity, metabolic syndrome, and hypertension: an integrated view in humans. 1926 35

Metabolic syndrome, which is caused by obesity, is now a global pandemic. Metabolic syndrome is an aggregation of hypertension, diabetes and dyslipidaemia. Insulin resistance is a key factor in the development of these components of metabolic syndrome. Concerning the mechanism for the development of hypertension in metabolic syndrome, the lack of insulin resistance in the kidney increases sodium reabsorption by hyperinsulinaemia, leading to sodium retention in the body, and resultant salt-sensitive hypertension. Moreover, hyperaldosteronism, which is caused by adipocyte-derived aldosterone-releasing factors, induces not only salt-sensitive hypertension, but also proteinuria in obese hypertensive rats. Salt loading markedly aggravates proteinuria and induces cardiac diastolic dysfunction in obese hypertensive rats, suggesting that salt and aldosterone exert unfavourable synergistic actions on the cardiovascular system, possibly through the overproduction of oxidative stress. In turn, reactive oxygen species (ROS), which are induced by adipokines such as tumour necrosis factor-alpha, non-esterified fatty acids, angiotensinogen etc., can activate the mineralocorticoid (MR) receptor, in an aldosterone-independent fashion. Therefore, aldosterone/MR activation plays a key role not only in the development of salt-sensitive hypertension, but also in cardiovascular injury in metabolic syndrome, possibly through its function as a feed-forward system.
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PMID:Aldosterone in salt-sensitive hypertension and metabolic syndrome. 1843 32

Increasing evidence suggests a role for prenatal environment in the onset of cardiovascular and metabolic disease in later life. In the rat, undernutrition in utero and a postnatal high-fat diet gives rise to a phenotype similar to the metabolic syndrome. As endothelial dysfunction is a feature of both CVD and the metabolic syndrome we investigated the impact of maternal undernutrition and/or postnatal high-fat on endothelial function. Virgin Wistar rats were mated and randomly assigned to groups to receive food either ad libitum (control) or at 30% of ad libitum intake throughout gestation. At postnatal day 250, a cohort from each group was challenged with a high-fat diet (D12451, 45% energy from fat; Research Diets, Inc., New Brunswick, NJ, USA) for the remainder of the study. At 1 year of age, small mesenteric arteries were dissected and mounted on a wire myograph and responses to phenylephrine, endothelin, acetylcholine, leptin and sodium nitroprusside assessed. Vasoconstriction to endothelin was significantly enhanced in all groups compared with controls (-log effective concentration equal to 50% of the maximal response (pEC50); P < 0.001). Endothelium-dependent vasodilatation to acetylcholine was significantly blunted in all groups compared with controls (% maximum response; P < 0.01), while dilatation to leptin and sodium nitroprusside was similar in all groups. These data demonstrate that both maternal undernutrition and postnatal high fat lead to vascular alterations and suggest that maternal undernutrition alone is at least as detrimental to offspring endothelial function as a long-term exposure to a high-fat diet in the offspring.
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PMID:Maternal undernutrition leads to endothelial dysfunction in adult male rat offspring independent of postnatal diet. 1849 97

Women with a history of preeclampsia are characterized by vascular dysfunction and an increased risk of cardiovascular disease. In the present study we investigated whether insulin sensitivity is decreased in women with previous preeclampsia and whether it is associated with endothelium-dependent and/or -independent vasodilation and/or features of metabolic syndrome. Twenty-eight nonobese women with previous severe preeclampsia and 20 women with a previous normotensive pregnancy were studied 5 to 6 years after the index pregnancy. Vasodilation was measured by venous occlusion plethysmography after intra-arterial infusions of sodium nitroprusside and acetylcholine and insulin sensitivity by the intravenous glucose tolerance test using the minimal model technique. The women were tested for lipid profile, inflammatory status and endothelial activation. Insulin sensitivity did not differ between the groups (P=0.24). Insulin sensitivity correlated positively to endothelium-dependent vasodilation only in the patient group in both low (beta=0.59; P=0.04) and high (beta=0.53; P=0.04) concentrations of acetylcholine and in a high concentration of sodium nitroprusside (beta=0.0007; P=0.006). In multivariate analysis, the waist/hip ratio (P=0.04) and serum triglycerides (P=0.04) had the most effect on insulin sensitivity in the patient group. Gestational weeks at the onset of preeclamptic hypertension (P=0.02) and proteinuria (P=0.02) associated positively with insulin sensitivity together with first-trimester body mass index (P=0.008) and maximum diastolic blood pressure during preeclampsia (P=0.005). The present study indicates a relation between insulin sensitivity with vascular dilatory function in women with previous preeclampsia. Furthermore, early onset preeclampsia correlates with impaired insulin sensitivity later in life.
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PMID:A relationship between insulin sensitivity and vasodilation in women with a history of preeclamptic pregnancy. 1857 72


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