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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Jaeken's syndrome or the carbohydrate-deficient glycoprotein (CDG) syndrome, is a newly recognized metabolic syndrome with poor weight gain in children, and multisystematic abnormalities, mainly due to defective carbohydrate entities in many glycoproteins, leading to neurologic dysfunction. Using the standardized method of phenotype evaluation with computer assistance according to the Munich Dysmorphologic Database, two sisters with CDGs were examined to decide if this metabolic entity contains dysmorphic features characterising dysmorphic syndromes. Diagnosis was based on clinical symptomatology and transferrin isoforms which showed tetrasialotransferrin deficiency and increased disialotransferrin in serum. Dysmorphic studies can be helpful in recognition of this syndrome, now described for the first time in Poland.
Pediatr Pol 1996 Jul
PMID:[Jaeken's (CDG) syndrome in two sisters]. 880 67

The essential arterial hypertension is the second (after diabetes mellitus) cause of chronic renal failure which means a great social and economic burden to the society. It is well known that hypertension is a metabolic syndrome resulting in tissue injury. We tried to investigate the possible influence of some metabolic disturbances on renal function in nontreated essential hypertension. We have compared 25 patients with nontreated essential hypertension (11 women, 14 men) with 14 healthy volunteers (7 women, 7 men) matched for age. The patients' group was characterized by significantly higher urine excretion of NAG (N-acetyl-beta-D-glucosaminidase) (2.75 +/- 1.69 vs 1.82 +/- 1.46 p < 0.05) and a tendency to significantly higher urine fractional sodium excretion without significant difference in albumin excretion. These findings suggest that the tubular damage is present. We noticed the negative linear correlation between mean arterial pressure and (MAP) and NAG urine excretion in the group of hypertensive patients which may reflect the renal ischemia in tubulo-interstitial pathology. Our data suggests that in nontreated arterial hypertension the renal blood flow disturbances are the important cause of the deterioration of tubular function (which are earlier to glomerular damage).
Pol Arch Med Wewn 2000 Sep
PMID:[Does any relationship exist between metabolic disturbances and some markers of renal damage in patients with untreated essential hypertension?]. 1139 62

Insulin resistance is a key element of metabolic syndrome, which includes disturbances of glucose tolerance, obesity, hypertension, coronary heart disease dyslipidemia and many other defects. An important problem in scientific research is precise measurement of insulin sensitivity. The method considered "the gold standard" is glucose clamp, however, it is difficult to apply this method in large studies. Therefore, simple indices of insulin resistance are proposed. It remains unclear whether those indices are able to reflect changes occurring during insulin-sensitizing intervention. The aim of the present study was to assess the use of indirect indices for the changes in insulin sensitivity during exercise training and to compare those indices with results derived from clamp. Fourteen obese normoglycemic women participated in 12-week exercise training program, which included exercise performed on a bicycle ergometer, 5 days a week for 30 minutes. Insulin sensitivity (M/FFM value) before and after training was measured with hyperinsulinemic euglycemic clamp technique. Simple indices of insulin resistance were also assessed: fasting plasma insulin (INS), logarithm INS (log [INS]), homeostasis model assessment (HOMA), logarithm HOMA (log [HOMA]) and quantitative insulin sensitivity check index (QUICKI). Before training, all those indices were markedly related to M/FFM. After training, an increase in M/FFM was observed. None of the examined indices markedly changed after training. There was no correlations between changes of evaluated indices and in M/FFM during training, and no relationships of those parameters after training. Our study indicates that simple indices are not able to reflect changes occurring during insulin-sensitizing intervention.
Pol Arch Med Wewn 2003 May
PMID:[Assessment of insulin sensitivity during exercise training program in obese women. Comparison of simple indices with hyperinsulinemic euglycemic clamp technique]. 1476 77

This paper present definition, prevalence and inheritance of the metabolic syndrome. The dysmetabolic syndrome most likely results from interplay between several genes and affluent environment. The prevalence of the syndrome is also very age-dependent and higher in males than in females. In subjects with dysmetabolic syndrome the survival is reduced, particulary because of increased cardiovascular mortality. The dysmetabolic syndrome requires non-drug and drug treatment.
Pol Merkur Lekarski 2004 Apr
PMID:[Dysmetabolic syndrome]. 1551 40

There has been an increase in the incidence of obesity, which is a substantial component of metabolic syndrome. It is visceral obesity, which especially favours the occurrence of insulin resistance endothelial dysfunction and acceleration of atherogenesis. The influence of inflammation, neuro-humoral balance, genetic background and sleep apnoea on the metabolic syndrome development are discussed. Current opinions on the treatment of metabolic syndrome are shown.
Pol Merkur Lekarski 2004
PMID:[The metabolic syndrome--epidemic of XXI century]. 1560 65

Cardiovascular disease (CVD) is still the leading cause of mortality in general as well as in diabetic population. The metabolic syndrome is a cluster of risk factors for CVD. The life style plays a crucial role in the primary and secondary prevention of them. Discussion about optimal diet has been holding for years. The low-fat diet is commonly recommended as an antiatherogenic diet. This article reviews the current literature on the influence of diet on ingredients of metabolic syndrome.
Pol Merkur Lekarski 2005 Jul
PMID:[Does the optimal diet for the prevention of cardiovascular disease exist?]. 1619 43

We describe a case of 40-year-old male with giant obesity, with signs of metabolic syndrome, treated with low-calorie diet (700 kcal in 1-st year of treatment, 1200 kcal in 2-nd and 3-rd year of treatment), and supplementary pharmacotherapy with sibutramine. Patient initial weight was 170,9 kg, height 189 cm, BMI = 47,8 kg/m2. In summary weight loss in this patient was 52,9 kg, this is 30,9% of initial value. This case report shows that giant obesity with accompanying metabolic disorders and complications can be treated with combination of diet, physical activity and pharmacotherapy. The key factor of successful therapy is personal motivation of a patient.
Pol Arch Med Wewn 2005 Jun
PMID:[The influence of body mass reduction on metabolic disorders and complications in patient with morbid obesity. Three years observation]. 1645 48

Metabolic syndrome occurs in about 25% of the adult population in industrialised countries. The pathogenesis of this syndrome is associated with insulin resistance. There are growing evidence that proteins produced in adipose tissue can play a role in development of insulin resistance. One of them is adiponectin (APM1), that circulates in human plasma at high level (5-30 microg/ml). A reduction in APM1 expression is closely associated with insulin resistance in animal models and in studies in humans. APM1 correlates with typical features of metabolic syndrome: BMI, WHR, total cholesterol, HDL, LDL and triglyceride levels, glucose, insulin, degree of insulin resistance in hyperinsulinemic-euglycemic clamp, blood pressure, hyperuricemia. There are some hypotheses that in the future therapy with APM1 may play a role in reversing insulin resistance in many disorders.
Pol Merkur Lekarski 2005 Nov
PMID:[The role of adiponectin in pathogenesis of insulin resistance and metabolic syndrome]. 1649 21

Insulinresistance is a component of the metabolic syndrome and important pathogenetic factor of type 2 diabetes mellitus. There are evidences that activation of the renin-angiotensin system (RAS) can decrease insulin sensitivity of tissues. As I/D polymorphism of angiotensin converting enzyme (ACE) gene can influence the activity of RAS, it may also influence insulin resistance. Aim. To assess the relationship between the I/D polymorphism of ACE gene and degree of insulin resistance and intensity of metabolic syndrome in type 2 diabetic patients. Study group and methods. Examined group: 108 type 2 diabetic patients (38 women and 70 men), with mean duration of disease 9.07 +/- 6.68 years, mean age 59.98 +/- 9.10 years. Assessed parameters: body mass index (BMI), waist/hip ratio (WHR), arterial blood pressure. Laboratory tests: concentration of the glycosylated hemoglobin (HbA 1c), glucose, insulin, total cholesterol, HDL and LDL cholesterol, triglycerides, creatinine, uric acid. Insulin resistance was calculated by the HOMA rate. Criterion of insulin resistance was rate > or = 2.5. The diagnosis and assessment of intensity of metabolic syndrome was performed according to criteria of National Education Cholesterol Adult Treatment Program the Panel III. I/D ACE gene polymorphism was evaluated by polymerase chain reaction (PCR). Results. Groups with 11, ID and DD genotype were not different in age, BMI, WHR, duration of diabetes, the prevalence and duration of arterial hypertension, degree of metabolic control and insulinresistance assessed by HOMA rate and intensity of metabolic syndrome. DD genotype carriers had significant higher systolic and diastolic blood pressure (147.8 +/- 19.8 mmHg vs 138.2 +/- 16.5 mmHg, p = 0,02; 89.2 +/- 9.6 mmHg vs 81.7 +/- 8.6, p = 0,003, respectively) than II patients. Conclusion. In type 2 diabetic patients the I/D genotype of ACE gene is not associated with the increased insulin resistance assessed by HOMA rate and intensity of metabolic syndrome.
Pol Arch Med Wewn 2005 Dec
PMID:[I/D polymorphism of angiotensin I converting enzyme gene and insulin resistance and some parameters of metabolic syndrome in patients with type 2 diabetes]. 1678 86

The aim of this review is to present the up-to-date data about adiponectin and it's role in pathogenesis of cardiovascular disease. Adiponectin is a hormone derived from adipose tissue which regulates energy metabolism, and plays an important role in the pathogenesis of insulin resistance. Serum levels of adiponectin are reduced in obesity, hypertension, metabolic syndrome and type 2 diabetes. Moreover, plasma adiponectin concentration is inversely associated with LDL-cholesterol, TG and is positively related to HDL-cholesterol. Recent studies have indicated that adiponectin has antiinflammatory and antiatherogenic properties. Review of the data confirmed the hypothesis that adiponectin plays an important role in pathogenesis of cardiovascular disease.
Endokrynol Pol
PMID:[The role of adiponectin in pathogenesis of metabolic syndrome and cardiovascular disease]. 1725 36


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