Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0948265 (metabolic syndrome)
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Microalbuminuria is defined in principle as abnormally increased albumin excretion below the level that is characteristic for proteinuria. In diabetes, microalbuminuria is defined as having an excretion rate of 20 to 200 micrograms/min. This level of albuminuria predicts overt renal disease in both non-insulin-dependent diabetes mellitus and insulin-dependent diabetes mellitus patients, and it is also associated with increased mortality. In nondiabetic individuals, the albumin excretion rate is not normally distributed with a skewed upper distribution. Excretion rate is lower during daytime, even during rest, than overnight. The median values in several studies for daytime and overnight albumin excretion rates are approximately 4 and 3 micrograms/min, respectively, with the upper 90th percentile approximately 15 and 10 micrograms/min, respectively. Microalbuminuria in population studies is significantly, but weakly, correlated to blood pressure, triglycerides, and low high-density lipoprotein cholesterol, as well as plasma glucose and obesity. These parameters are elements of the so-called metabolic syndrome. New studies in insulin-dependent diabetes mellitus on the transition from normo- to microalbuminuria show that high normal excretion rate and poor metabolic control are associated with progression. In non-insulin-dependent diabetes mellitus, microalbuminuria is quite common (20% to 25% of patients) in both newly diagnosed patients and patients with established diabetes. In many studies, a prevalence of approximately 20% is found, and again microalbuminuria is associated with components of the metabolic syndrome, which includes poor metabolic control and blood pressure elevation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of microalbuminuria in diabetes and in the background population. 792 49

Most aspects of the nutritional therapy of diabetes mellitus apply equally to IDDM and NIDDM patients and are also appropriate for people with high risk of cardiovascular diseases. A restriction of energy, a reduction of saturated fatty acids as well as of alcoholic drinks and simple sugars are the most important measures. This modification of nutritional intake together with increased fibre consumption is not only appropriate to avoid hyperglycaemia in diabetic patients but has also its benefits in patients presenting with the metabolic syndrome (possible reduction of hyperinsulinaemia, hypertension and hyperlipoproteinaemia). Diabetic patients should have regular screening for microalbuminuria. At first signs of an early stage of nephropathy patients should be advised to restrict their protein intake. About 50% of daily energy intake should be derived from carbohydrates and fat intake should be no more than 35% of total energy (saturated fatty acids less than 10% of energy). Carbohydrate exchange units are usually not necessary in NIDDM patients. In addition diabetes specialty foods are not an essential part of the nutritional therapy. The success of the nutritional therapy in diabetic patients is substantially dependent upon qualified counselling and education of the patients by the physician (as far as possible with the assistance of a dietitian).
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PMID:[Nutritional therapy in diabetes mellitus]. 847 34

Marked changes in the plasma concentration of several non-glucose monosaccharides have been detected among patients++ with end-stage renal disease. To find changes specific to renal disease and not caused by a failing urinary excretion, we studied the plasma monosaccharide concentration in patients with early-stage glomerulonephritis whose renal function was normal or only mildly compromised. Plasma mannose, fructose and 1,5-anhydroglucitol (1,5-AG) concentrations were measured using gas chromatography/mass spectrometry and isotope-labelled sugar standard additions. The daily urinary protein excretion was positively correlated with the plasma cholesterol (r = 0.785), mannose (r = 0.550), triglyceride (r = 0.531 ) and fructose (r = 0.401) concentrations, while the correlation with 1,5-AG (r = -0.581) was inverse. The correlations were statistically significant. As previous studies have revealed a close positive correlation between the plasma mannose and glucose concentrations, we calculated the mannose/glucose concentration ratio to find out whether the increase in mannose concentration was or was not explained by ambient glucose. There was a strong correlation between the ratio and the urinary protein excretion (r = 0.704). It is inferred that the metabolic syndrome associated with glomerulonephritis and characterised by hyperlipidemia also involves a derangement in mannose and 1,5-AG metabolism.
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PMID:Proteinuria and plasma hexosugars in early-stage glomerulonephritis. 886 96

The high prevalence of atherosclerotic (macrovascular) complications in diabetes (1.5-6x higher than in non-diabetics) stimulated evaluation of new pathogenetic findings which could have an impact on prevention. In type 1 diabetics the development of nephropathy is a factor hastening the development of macroangiopathy. In type 2 diabetics on whom attention is concentrated at the moment interaction of various metabolic deviations is involved which include changes of lipoproteins (drop of HDL, changes in the size and composition of LDL), insulin resistance and glycosylation of proteins. There is an enhanced tendency to lipoprotein oxidation (LDL) which promote the development of cholesterol rich plaques in the arterial walls. Their rupture may cause occlusion and ensuing risks for life. Possibilities of prevention are not adequately made use of. This is due to a tendency to underrate the serious character of type 2 diabetes and also the high percentage of diabetics where the disease was diagnosed late. The metabolic syndrome which develops as a result of insulin resistance precedes for years manifestations of diabetes. Its detection makes it possible to screen subjects at risk, some of whom develop diabetes. At the same time it is also a pathogenetic factor of macrovascular complications. It leads to the cumulation of a number of risk conditions. More effective prevention can be implemented by intervention of all associated risk factors (smoking, hypertension), in the application of lifestyle provisions of energy reduction by promoting physical activity and by a rational diet (diabetes, obesity, hyperlipidaemia). The justification of pharmacotherapy for the high risk groups of diabetics with hyperlipidaemia is supported by results of recently published investigations where statins were used. For the sub-population of subjects at risk the perspective should be screening of risk factors, early diagnosis of diabetes, education, continuous primary care, comprehensive prevention using lifestyle provisions as well as advances in modern pharmacotherapy.
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PMID:[Prevention of atherosclerosis in diabetics]. 944 Oct 11

Concomitant arterial hypertension and metabolic disorders is a frequent finding raising the risk of micro- and macrovascular complications. While prevalence of stroke and myocardial infarction is going down in hypertensives, end-stage renal disease (ESRD) becomes a bigger problem especially in diabetic hypertensives. The metabolic abnormalities are linked to the hypertension by the sympathoadrenal system mediated by insulin resistance (IR); subjects with hyperinsulinemia and increased sympathetic activity tend to have higher blood pressure, typical dyslipidemia, reduced fibrinolytic activity and other risk factors (RF) called metabolic syndrome of IR. Albuminuria (AUR) is considered as an important RF for the development of nephropathy, ESRD, cardiovascular diseases. AUR is a marker of cardiovascular and total mortality in diabetic and/or non-diabetic hypertensives. AUR reflects the endothelial dysfunction not only in glomerulus but also in the other arteries. Tissue Renin-Angiotensin System plays a significant role in the pathogenesis of hypertension and metabolic disorders; it affects the arterial wall, kidneys and heart longitudinally. Life style is very essential in the treatment of hypertension and metabolic disorders: rational diet with reduced amount of salt and animal proteins, non-smoking and sufficient physical activity. Antihypertensive drugs without any metabolic side effects and with the renal protection are necessary for the patients with hypertension and metabolic disturbances. ACE-inhibitors and/or some of the Ca-antagonists seems to be valuable especially as combined therapy.
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PMID:[New approaches in the treatment of hypertension in metabolic diseases]. 972 74

Diabetes mellitus is very common in older persons. Changes in exercise habits, body habitus, leptin, amylin, tumor necrosis factor alpha, and nitric oxide all play a role in the pathogenesis of age-related insulin resistance. In older persons elevated glucose levels not only produce retinopathy, neuropathy, and nephropathy but also decrease quality of life, pain tolerance, cognition, and functional status and increase injurious falls, nocturia, incontinence, pressure ulcers, and orthostatic hypotension. The availability of multiple new therapies has enhanced the ability of physicians to improve glycemic control in older persons without unacceptable levels of hypoglycemia. Caregivers play an important role in the management of older diabetics. Depression increases mortality rate and hospital admissions in older diabetics. In many nursing homes the quality of diabetic care is marginal. A new causative theory of the metabolic syndrome involving cytokines and nitric oxide-the NO cytokine theory-is proposed.
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PMID:An overview of diabetes mellitus in older persons. 1033 29

A sub-study evaluated 698 younger (54.5 +/- 6.9 years) type 2 diabetics of the KID Study participants to establish the prevalence of diabetic complications and associated diseases and their correlation with body mass index (BMI), duration of disease and to C-peptide levels. Only 19.8% of the type 2 diabetics had a normal weight. In all weight subgroups, the average age of diabetes manifestation were around age 45. In 46.6% of all type 2 diabetics we could already demonstrate microangiopathic complications. Strikingly, 15.9% of the patients already had proliferative retinopathies and 12.6% had albuminuria of more than 1000 mg/dl. 74.7% of our type 2 diabetics presented with the well-known risk cluster of the metabolic syndrome: In every other patient, we found hypertension and/or hyperlipoproteinaemia. Accordingly, the prevalence of the macroangiopathic diabetic complications, coronary artery disease and peripheral vascular disease was 17.8%, which is high for a relatively young population with a mean age of 53.9 years and goes conform with recent literature (Lowel et al., 1999). An increase in BMI correlated significantly with deterioration of HbA1, a decrease in HDL cholesterol, an increase in triglycerides and with a higher prevalence of hypertension. The frequency of nephropathy increase significantly up to a BMI of 30-35 kg/m2. Retinopathies and polyneuropathies were associated with BMI but increased significantly with the duration of the diabetic state. In contrast to microangiopathic diabetic complications, there was already a high prevalence of nephropathy after a comparatively short duration of disease. The prevalence of hyperlipoproteinaemia and hypertension did not depend from the duration of diabetes. These concomitant diseases already were frequent early in the disease and did not increase with the duration of disease. However, there was a strong correlation between increasing hyperlipoproteinaemia and hypertension and higher C-peptide levels. We found no coincidence between C-peptide levels and microangiopathic diabetic complications.
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PMID:The KID Study VI: diabetic complications and associated diseases in younger type 2 diabetics still performing a profession. Prevalence and correlation with duration of diabetic state, BMI and C-peptide. 1059 94

Hypertension is twice as frequent in diabetic patients than in the general population. Its prevalence is higher in Type 2 than in Type 1 diabetes: in the former, the onset of hypertension often precedes the diagnosis of diabetes, whereas, in the latter it is strictly related to the presence of nephropathy. Sympathetic nerve overactivity is crucial in the pathogenesis of hypertension in diabetes. It can be related to the activation of the renin-angiotensin-aldosterone (RAA) system in Type 1 diabetic patients with chronic renal failure, or to a condition of insulin resistance/hyperinsulinemia in Type 2 patients with the metabolic syndrome. In patients with early autonomic neuropathy, vagal impairment can lead to a relative predominance of sympathetic activity in the sympatho-vagal balance. In these patients, the onset of hypertension is frequently preceded by reduced nocturnal dipping. Sympathetic overactivity stimulates RAA activity, promotes sodium reabsorption, and increases heart rate, stroke volume and peripheral vascular resistance, thus inducing hypertension and increasing cardiovascular risk. A number of drugs acting either directly or indirectly on sympathetic activity are available for the treatment of hypertension in diabetic subjects. Opinions on the potential advantages of the metabolic profile of some of these drugs are as yet conflicting.
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PMID:Sympathetic nervous system, diabetes, and hypertension. 1127 May 88

In Western society, the triad of hypertension, metabolic syndrome and obesity (which caries a high risk for renal disease) is increasing, as is the intake of caffeine. However, no information is available regarding the metabolic or renal consequences of caffeine consumption in this complex disease entity. The purpose of this study was to investigate the effects of chronic caffeine consumption on renal function and metabolic status in obese ZSF1 rats, an animal model of obesity, hypertension and the metabolic syndrome. Fifteen, 18-week-old male, obese ZSF1 rats were randomized to drink tap water (Cont, n = 8) or 0.1% solution of caffeine (Caff, n = 7) for 8 weeks. Metabolic and renal function measurements were performed at baseline and after 4 and 8 weeks of treatment. Caffeine treatment significantly (p < 0.05) reduced body weight, food, and fluid consumption and improved insulin sensitivity (fasting insulin 129.6+/-8.1 vs 97.5+/-3.6 microIU/mL; fed insulin 146.3+/-8.5 vs 110.6+/-3.4 microIU/mL; fasting glucose 138.7+/-13.4 vs 145+/-8.0 mg/dL; fed glucose 373+/-19.4 vs 283.3+/-19.6 mg/dL, Cont vs Caff, respectively). After 8 weeks of caffeine treatment, animals were less glycosuric as compared with control group. Area under glucose curves (AUC-glucose) in oral glucose tolerance test did not differ between the two groups (AUC- glucose: 592.5+/-42.7 vs 589.5+/-20.5 mg/dL x h, Cont vs Caff), whereas caffeine treatment significantly decreased AUC of insulin (AUC-insulin: 257.77+/-12.9 vs 198.0+/-5.9 microIU/mL x h, Cont vs. Caff, p<0.05). No differences were found with regard to plasma triglycerides and glycerol levels; however, caffeine significantly increased cholesterol levels after 4 and 8 weeks (2F-Anova, p<0.001). Moreover, caffeine significantly decreased creatinine clearance after 4 and 8 weeks (CrCl, Cont: 3.5+/-0.4, Caff: 2.2+/-0.2 L/kg/day, p<0.05) and increased protein/CrCl ratio (Cont: 323+/-30, Caff: 527+/-33 mg/L/day). Caffeine treatment for 8 weeks tended to increase plasma norepinephrine levels (p<0.06), but the two groups did not differ with regard to plasma renin activity, blood pressure, renal blood flow or and renal vascular resistance. The study indicates that caffeine improves insulin sensitivity but increases plasma cholesterol levels and impairs renal function in obesity with the metabolic syndrome and hypertension. Our results imply that the health consequences of chronic caffeine consumption may depend heavily on underlying pathophysiology process.
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PMID:Renal and metabolic effects of caffeine in obese (fa/fa(cp)), diabetic, hypertensive ZSF1 rats. 1141 48

A pandemic of obesity is contributing importantly to the prevalence of the metabolic syndrome characterized by hypertension, insulin resistance, and hyperlipidemia. In turn, the metabolic syndrome is contributing to vascular disease and the accelerating epidemic of chronic renal failure. Currently, pharmacological approaches to attenuate obesity and its cardiovascular/renal sequelae are limited. The purpose of this study was to determine the effects of 2-hydroxyestradiol, a metabolite of 17beta-estradiol with minimal estrogenic activity, on the development of obesity, the metabolic syndrome, and heart, vascular, and renal dysfunction in obese ZSF1 rats, a well-characterized genetic model of obesity and the metabolic syndrome with concomitant heart, vascular, and kidney disease. ZSF1 rats were treated, beginning at 12 weeks of age, for 26 weeks with vehicle or 2-hydroxyestradiol (10 microg/kg/h). At baseline and after 24 weeks of treatment, animals were placed in metabolic cages, and food intake, water intake, urine output, and urinary excretion of proteins and glucose were determined. Next, in fasting animals, plasma cholesterol was measured, an oral glucose tolerance test was conducted, and total glycated hemoglobin levels were determined. At the end of the study, animals were anesthetized and instrumented for assessment of heart performance, renal hemodynamics, and mesenteric vascular reactivity. 2-Hydroxyestradiol attenuated the development of obesity and improved endothelial function, decreased nephropathy, decreased the severity of diabetes, lowered arterial blood pressure, and reduced plasma cholesterol. 2-Hydroxyestradiol may be an important lead for the development of safe and effect drugs to attenuate obesity and its metabolic, vascular, and renal sequelae.
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PMID:2-Hydroxyestradiol attenuates the development of obesity, the metabolic syndrome, and vascular and renal dysfunction in obese ZSF1 rats. 1171 85


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