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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The general practitioner man be confronted with the X syndrome, which includes central obesity, impaired glucose tolerance or type II diabetes mellitus, dyslipidemia and eventually hypertension. Insulinoresistance and hyperinsulinaemia contribute to the pathogenesis of these disorders. The syndrome X, which leads to important cardiovascular morbidity, needs appropriate treatment, which has to take into account the actions of drugs on glucose and lipid profiles. Syndrome X is rarely treated as a whole, but to treat separately each of its manifestations would be a mistake. The necessity of a global approach, a complete understanding of the familial environment and also the duration of the development of syndrome X justify the prominent part of the family doctor in the follow-up.
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PMID:[Syndrome X and general medicine]. 778 42

Syndrome X is a constellation of abnormalities; it appears to be strongly linked to insulin resistance and the risk of atherosclerosis. It consists of hypertension, glucose intolerance, obesity, dyslipidemia and, observed more recently, coagulation abnormalities. It is possible that treating blood pressure levels alone while ignoring or worsening other strongly associated risk factors has resulted in minimal effects on the incidence of coronary heart disease (CHD). Syndrome X has raised the awareness of these associated risk factors and has further led to the consideration of hypertension as a metabolic disease. The epidemiologic evidence in support of the link between insulin resistance and hypertension is reviewed, and the public health implications of these data are outlined.
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PMID:Reducing the incidence of coronary heart disease by managing hypertension: implications of syndrome X. 780 51

Obesity frequently clusters with hypertension, hyperlipidemia, non-insulin-dependent diabetes mellitus, and ischemic heart disease with hyperinsulinemia as syndrome X. Although central obesity has been recognized to have a strong genetic component, few candidate genes have been studied in this disorder. After a recently described association between the apolipoprotein-D (Apo-D) gene polymorphism and non-insulin-dependent diabetes mellitus by our group, we have now looked at a TaqI polymorphism of the Apo-D gene in two other components of syndrome X, namely obesity and hyperinsulinemia. Apo-D genotype differences were found between obese subjects (n = 57) and slim controls (n = 57; P = 0.006). Furthermore, in the obese group an association was found between the Apo-D genotype and fasting insulin (P < 0.001). Preliminary evidence, therefore, suggests that the TaqI Apo-D polymorphism can be used as a genetic marker for obesity and several components of syndrome X.
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PMID:Apolipoprotein-D polymorphism: a genetic marker for obesity and hyperinsulinemia. 791 35

The relationship of dyslipidemia, particularly hypercholesterolemia to coronary heart disease is now well established. Although ischemic heart disease and stroke share many of the same risk factors, the relationship of cholesterol to stroke remains controversial. The 6-year and 12-year follow-up of the MRFIT study showed that elevated cholesterol significantly increased the risk for fatal nonhemorrhagic stroke. Atkins found no evidence that lowering plasma cholesterol influenced the incidence of fatal or nonfatal stroke and regression analysis showed no statistical association between the magnitude of cholesterol reduction and the risk for fatal stroke. We cannot preclude the possibility that more effective cholesterol lowering over a longer period of time might be effective. Hypertension is the most powerful risk factor for stroke. The San Antonio Heart Study reported a clustering of cardiovascular risk factors in individuals who developed hypertension during an eight-year follow-up period (higher levels of BP, fasting TC and LDLC, TG, glucose and insulin, and BMI, less favourable fat deposition, and lower HDL). Insulin resistance may be the unifying factor that results in those phenomena, the so-called syndrome X. The important factor underlying syndrome X may be central or visceral obesity, suggesting that maintenance or attainment of ideal weight would be a powerful preventive factor against both CHD and nonhemorrhagic stroke. There is evidence from the Treatment of Mild Hypertension Study that nutritional/hygienic measures can reduce the syndrome X risk factors and hence the risk of coronary heart disease and stroke.
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PMID:Dyslipidemia and metabolic factors in the genesis of heart attack and stroke. 791 92

The potential associations between the factors making up the vascular multi-risk metabolic syndrome (VMMS) or syndrome X (hypertension, diabetes, lipidic disorders, hyperinsulinemia and obesity) are studied: a) in patients with recent cerebral infarct or acute myocardial infarct; b) in patients hospitalized for the management of their hypertension, diabetes or obesity; c) at two years of evolution since the initial diagnosis of hypertension, diabetes or obesity. The results confirm that the VMMS, either complete or incomplete, is detected starting from the clinical management of any of its components (hypertension, diabetes, obesity) or complications (cerebral or myocardial infarct). These results and the ones regarding the evolution at two years of the risk factors associations, allows a discussion of the physiopathologic reality of the VMMS as an entity or a causal association.
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PMID:[Detection and clinical course of metabolic multiple vascular risk syndrome]. 821 80

Urinary albumin excretion has been assessed in 585 newly-presenting Type 2 (non-insulin-dependent) diabetic patients (aged 53 (8) years, 67% male) at diagnosis with fasting plasma glucose 10.3 (3.2) mmol/l and over 3 years of dietary treatment. Urinary albumin at diagnosis, geometric mean (1 SD interval) corrected for dilution by regression on urine creatinine concentration of 10 mmol/l, was 17 (5-58) mg/l compared with 8 (3-18) mg/l in an age-matched non-diabetic reference population. Values greater than 50 mg/l were found in 17% of diabetic patients compared with 4% in the reference group. After diet therapy for 3 months, fasting plasma glucose decreased to 6.9 mmol/l and urinary albumin to 12 (4-31) mg/l (p < 0.0001). This suggests that increased urinary albumin excretion at diagnosis is in part functional, possibly secondary to glomerular hyperfiltration caused by hyperglycaemia and raised blood pressure. Over the next 3 years, mean fasting plasma glucose was 7.2 mmol/l, albumin excretion changed little, without significant increase either in patients with raised or normal albumin at diagnosis. Both at diagnosis and over 3 years, urinary albumin excretion was independently associated with fasting plasma glucose and triglyceride levels and with systolic blood pressure, but the combination of these factors only explained 10% of the total variance. This suggests the presence of additional pathological processes in patients with increased urinary albumin. Urinary albumin was not associated with other variables included in syndrome X, such as HDL cholesterol, fasting plasma insulin, obesity or central adiposity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:UK Prospective Diabetes Study (UKPDS). X. Urinary albumin excretion over 3 years in diet-treated type 2, (non-insulin-dependent) diabetic patients, and association with hypertension, hyperglycaemia and hypertriglyceridaemia. 824 50

The regional distribution of body fat has been identified as a significant risk factor for the development of noninsulin-dependent diabetes mellitus and cardiovascular disease (CVD). Several studies that have investigated the potential associations between topographic features of adipose tissue and indices reflecting carbohydrate and lipid metabolism have reported significant associations between abdominal fat deposition and metabolic complications. The development of computed tomography as a means to precisely measure the amount of subcutaneous and deep adipose tissue at any site of the body has shown that determination of the level of visceral adipose tissue is a critical measurement to perform in the assessment of the health hazards of obesity. Studies that we have conducted in premenopausal women have clearly shown that the level of visceral adipose tissue is the best correlate of lipoprotein ratios used to estimate the risk of CVD. We have also reported that a high level of visceral adipose tissue is associated with a deterioration of glucose tolerance and that the relationship between visceral fat deposition and glucose tolerance remains significant after controlling for the level of total-body fat. Because significant interrelationships were observed between abdominal visceral obesity, insulin resistance, and dyslipoproteinemias in obese women, it is suggested that visceral obesity is an important component of the insulin-resistance syndrome (syndrome X) that has been previously described. This cluster of morphological, hormonal, and metabolic alterations observed in abdominal obesity may have substantial implications for the treatment of this condition.
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PMID:Abdominal obesity as important component of insulin-resistance syndrome. 828 86

Mexican Americans appear to have a strong genetic predisposition to insulin resistance, android obesity, and type II diabetes, apparently as a function of Native American genetic heritage. Theoretical considerations suggest that insulin resistance may be a primary factor that plays a causative role in the induction of both obesity and diabetes. Measures which promote optimal insulin sensitivity--chromium picolinate, brewer's yeast, soluble fiber supplements, metformin, very-low-fat diet, exercise training--may have value for preventing, treating, or retarding the onset of obesity and diabetes, and merit clinical evaluation in this regard. Correction of insulin resistance may also lessen cardiovascular risk, in part by reducing LDL cholesterol and improving risk factors associated with Syndrome X. These comments are likely to be valid for other Native American groups at high risk for diabetes.
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PMID:Insulin resistance in Mexican Americans--a precursor to obesity and diabetes? 828 93

Using the molecular scanning technique of single-stranded conformational polymorphism (SSCP), we have examined the exons encoding the insulin receptor gene in 26 patients with syndromes of insulin resistance. We found 27 variant sequences, 4 of which were mutations that altered an amino acid. One patient with the Rabson-Mendenhall syndrome was homozygous for a mutation in the extracellular alpha-subunit (Ser to Leu323), one type A insulin-resistant patient was heterozygous for Pro to Leu1178, and another type A insulin-resistant patient was heterozygous for a mutation in the COOH-terminus of the receptor (Arg to Gln1351). The previously reported, and probably functionally insignificant, variant Val to Met985 was detected in one patient. No missense or nonsense insulin receptor mutations were found in any patients whose insulin resistance was associated with gross obesity, lipoatrophy, or acromegaloid features. No missense or nonsense mutations were found in subjects with polycystic ovary syndrome or Syndrome X. Putting these findings in the context of other work in this field, we conclude that subjects with leprechaunism or Rabson-Mendenhall syndrome have a high probability of having a missense or nonsense insulin receptor mutation. Nonobese, nondysmorphic, severely insulin-resistant females with hirsutism, acanthosis nigricans, and menstrual disturbance (type A phenotype) have an intermediate probability of having this type of insulin receptor mutation. Although insulin receptor mutations have been occasionally described in other phenotypes of insulin resistance, the frequency of point mutations in the exons of the insulin receptor gene in patients with those phenotypes appears to be low.
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PMID:Molecular scanning of the insulin receptor gene in syndromes of insulin resistance. 831 8

In western societies cardiovascular disease accounts for approximately one of every three deaths, and is a major contributor to chronic debiliation. During the last years our knowledge of factors that contribute to the development and progression of this disease has increased markedly. Elevated serum total cholesterol, hypertension and cigarette smoking are "traditional", well-known risk factors. In addition, low serum levels of high density lipoprotein (HDL) cholesterol predispose to development of disease, whereas in epidemiological studies the role of increased triglycerides is more controversial. During the last years derangements in several haemostatic components in persons who develop cardiovascular disease have been observed. Such alterations include increased plasma concentrations of fibrinogen, Factor VII coagulant activity and plasminogen activator inhibitor-1 (PAI-1). Furthermore, interactions between lipoproteins and haemostatic factors are gradually being disclosed. Serum triglycerides have been shown to correlate both to PAI-1 and to Factor VII. The lipoprotein (a), first described by Berg in 1963, also appears to be a link between lipoprotein metabolism and fibrinolytic function. In addition, linkages are observed between high triglycerides, low HDL cholesterol, reduced glucose tolerance, hyperinsulinemia, obesity, low physical activity, reduced fibrinolytic capacity and increased Factor VII. This clustering of risk factors has been suggested to be a coronary risk syndrome and has been called Reavens syndrome, syndrome X and insulin-resistance syndrome. A more descriptive name, athero-thrombogenic syndrome (ATS), has recently been suggested, thereby indicating that both atherosclerosis and thrombosis contribute to its development.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular risk factors: interactive effects of lipids, coagulation and fibrinolysis. 832 48


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