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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors revealed during dispensarization of pregnant women suffering from essential hypertension that the disease is relatively frequently associated with some metabolic disorders, i. e. obesity, gestational diabetes or impaired glucose tolerance. They draw attention to a similarity with Reaven's syndrome in non-pregnant women. The authors recommend to screen for diabetes all obese pregnant women and those with hypertension to detect an impaired glucose metabolism and prevent foetopathies in neonates of thus affected mothers. The authors consider obesity one of the subsidiary criteria in the differential diagnosis of essential hypertension and preeclampsia.
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PMID:[Gestational diabetes mellitus and disorders of glucose tolerance in pregnant women with essential hypertension]. 149 70

We have studied hypertension, obesity, diabetes and hypercholesterolaemia in those aged 45-79 years in the Cretan low risk population of Spili (n = 249; attendance 82%) to see if these conditions interacted in the same way as previously described for high risk populations. Hypertension, diabetes, obesity, and hypercholesterolaemia were found to be at least as prevalent in Spili as in Sweden. Furthermore, the previously described 'Metabolic Syndrome X', with insulin resistance and hyperinsulinaemia as a common denominator also seemed to exist in the Spili population where patients with these conditions had higher insulin and C-peptide levels than normals. Our finding should be viewed against the low prevalence of past myocardial infarction in Cretan men from Spili reported by us and confirming the results of the Seven Countries Study.
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PMID:Characteristics of the 'metabolic syndrome X' in a cardiovascular low risk population in Crete. 843 84

The author summarizes mechanisms by which insulin resistance and compensatory hyperinsulinism are manifested in the clinical picture. He divides the mechanisms into prereceptor, receptor and postreceptor mechanisms. The latter dominate in the population quantitatively and thus also by their impact because they create the so-called 5H syndrome (association of hyperinsulinism with hyperglycaemia (NIDDM), hyperlipoproteinaemia, hypertension, hirsutism and the polycystic ovary syndrome) or the so-called hormonal metabolic syndrome X, lethal tetrad, metabolic syndrome, syndrome of insulin resistance). The term syndrome X does not appear suitable as it is frequently mistaken for coronary X syndrome which probably is also conditioned by hyperinsulinism, for the hormonal metabolic X syndrome and probably also fot the "fragile X syndrome" in genetics. The 5H syndrome is caused by a postreceptor disorder of insulin efficiency for which so far the molecular basis and dominating organ site have not yet been defined adequately. Hyperinsulinism is conceived as an insulin resistance compensating phenomenon. In its development participates, however, in addition to compensatory hypersecretion also impaired insulin utilization (liver, muscles) and an impaired primary secretory response caused probably by a disorder of blood sugar control (glucokinase, GLUT 2). This is suggested by the frequently inadequate response of the blood sugar level, IRI and C-peptide during the oral glucose tolerance test (OGGT). A hyperinsulinaemic response may be encountered when the blood sugar curve is normal, flat, in impaired glucose tolerance and in diabetes. Thus OGGT alone is not suited for the early detection of the 5H syndrome unless concurrently the IRI and C-peptide response is recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical manifestations of the insulin resistance syndrome. The hormonal-metabolic syndrome X, the 5H syndrome and their etiopathogenesis]. 772 46

Carbohydrate and lipid metabolism was cross-sectionally assessed in 16 patients with endogenous hypercortisolism (endogenous Cushing syndrome). Five patients (31%) had fasting glucose levels over 6.6 mmol/l and a HbA1C over 7.5%. Six patients (38%) had diabetes mellitus based on an abnormal 75 g oral glucose tolerance test (OGTT) and two additional patients (13%) had impaired glucose tolerance based on an OGTT. Compared to obese individuals, patients with Cushing syndrome had an elevated glucose but no elevated insulin response to the OGTT. Regression analysis showed positive correlations between 24-h urinary free cortisol (UFC) and fasting blood glucose (P < 0.0005), UFC and OGTT glucose area under the curve (AUC) (P < 0.01), and UFC and HbA1C (P < 0.005). UFC levels were negatively correlated (P < 0.05) with OGTT insulin AUC and insulin/glucose ratios. Eleven (69%) patients required anti-hypertensive therapy for blood pressure control. Total cholesterol and triglycerides were elevated in patients with Cushing syndrome compared to obese controls, while LDL and HDL cholesterol, and Lp(a) were similar in the two groups. We conclude that impaired glucose tolerance and/or diabetes in patients with endogenous Cushing syndrome is due to the hyperglycemic effects of cortisol with relative insulinopenia. Thus, Cushing syndrome shares features with both the Metabolic Syndrome X and NIDDM, including impaired glucose uptake, hyperlipidemia and hypertension. However, in Cushing syndrome, a relative insulinopenia occurs, while in Metabolic Syndrome X and NIDDM, insulin excess is observed. In Cushing syndrome, as the hypercortisolemia exacerbates, insulinopenia becomes more paramount, suggesting that cortisol exerts a direct or indirect "toxic" effect on the beta-cell.
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PMID:Carbohydrate and lipid metabolism in endogenous hypercortisolism: shared features with metabolic syndrome X and NIDDM. 907 4

A relationship between Lewis (a-b-) phenotype and the metabolic syndrome X has been suggested. We studied the frequency of Lewis (a-b-) phenotype in subjects with non-insulin-dependent diabetes mellitus (NIDDM) as well as the relationship between Lewis phenotype and lipid concentration in NIDDM patients. Lewis red blood cell phenotyping was done in 207 NIDDM subjects and 345 non-diabetic control subjects by immuno-agglutination with anti-Lewis a and b monoclonal antibodies. Among NIDDM patients, the proportion with the Lewis (a-b-) phenotype was significantly increased (23.6% vs 14.3%, p = 0.01), and this phenotype was associated with higher levels of triglycerides (2.40 +/- 2.58 vs 1.97 +/- 1.25, p = 0.03). This study shows a relationship between NIDDM and Lewis (a-b-) phenotype. Hypertriglyceridaemia in Lewis-negative NIDDM could suggest an increased risk of ischaemic heart disease for these subjects.
Diabetes Metab 1997 Jun
PMID:Hypertriglyceridaemia and Lewis (A-B-) phenotype in non-insulin-dependent diabetic patients. 923 96

To investigate the metabolic and atherogenic effect of intra-abdominal fat accumulation, we examined correlation between variables of lipid and glucose and the fat distribution of abdominen by using computed tomography. Subjects were 292 of male and 161 of female who underwent coronary angiography. Intra-abdominal fat area was correlated with insulin concentration at 120 min in oral glucose tolerance tests and triglyceride level in male, on the other hand, in female were HDL-cholesterol level, apolipoprotein B, glucose area under curve and insulin concentration at 60 and 120 min. In an aspect of atherogenic effect of intra-abdominal fat, it was not atherogenic in isolated state in male, but atherogenic in diabetic female. Intra-abdominal fat was accompanied with hypertension and mid-band, which appeared between alpha and beta band in polyacrylamide diskgel electrophoresis. Cluster of intra-abdominal fat accumulation, hypertension and mid-band was atherogenic in male, in which insulin resistance play an important role in the coronary artery disease. On the contrary, intra-abdominal fat accumulation accompanied with exacerbation of glucose tolerance, hypertensive and high level of apolipoprotein B in female. We concluded that visceral fat accumulation was a generator of metabolic syndrome X in male and was a progression factor for diabetes, hypertensive and high apolipoprotein B level in female.
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PMID:Intra-abdominal fat, lipid metabolism and insulin resistance in coronary artery disease. 924 Jul 69

Non-insulin-dependent diabetes mellitus (NIDDM) is commonly associated with hypertriglyceridaemia, low serum HDL-cholesterol concentrations, hypertension, obesity and accelerated atherosclerosis (metabolic syndrome X). Since a similar dyslipidaemia occurs with the acute-phase response, we investigated whether elevated acute-phase/stress reactants (the innate immune system's response to environmental stress) and their major cytokine mediator (interleukin-6, IL-6) are associated with NIDDM and syndrome X, and may thus provide a unifying pathophysiological mechanism for these conditions. Two groups of Caucasian subjects with NIDDM were studied. Those with any 4 or 5 features of syndrome X (n = 19) were compared with a group with 0 or 1 feature of syndrome X (n = 25) but similar age, sex distribution, diabetes duration, glycaemic control and diabetes treatment. Healthy non-diabetic subjects of comparable age and sex acted as controls. Overnight urinary albumin excretion rate, a risk factor for cardiovascular disease, was also assayed in subjects to assess its relationship to the acute-phase response. Serum sialic acid was confirmed as a marker of the acute-phase response since serum concentrations were significantly related to established acute-phase proteins such as alpha-1 acid glycoprotein (r = 0.82, p < 0.0001). There was a significant graded increase of serum sialic acid, alpha-1 acid glycoprotein, IL-6 and urinary albumin excretion rate amongst the three groups, with the lowest levels in non-diabetic subjects, intermediate levels in NIDDM patients without syndrome X and highest levels in NIDDM patients with syndrome X. C-reactive protein and cortisol levels were also higher in syndrome X-positive compared to X-negative patients and serum amyloid A was higher in both diabetic groups than in the control group. We conclude that NIDDM is associated with an elevated acute-phase response, particularly in those with features of syndrome X. Abnormalities of the innate immune system may be a contributor to the hypertriglyceridaemia, low HDL cholesterol, hypertension, glucose intolerance, insulin resistance and accelerated atherosclerosis of NIDDM. Microalbuminuria may be a component of the acute-phase response.
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PMID:NIDDM as a disease of the innate immune system: association of acute-phase reactants and interleukin-6 with metabolic syndrome X. 2212 8

The relationships between metabolic disorders and cardiovascular diseases are very strong. Hypercholesterolaemia and diabetes mellitus, for instance, are well-known risk factors. The multifaceted metabolic syndrome or syndrome X, originally described by Reaven in 1988, comprises several abnormalities which are associated to insulin resistance and compensatory hyperinsulinaemia. Syndrome X results in an increased vascular risk by at least two mechanisms. On the one hand, it favours atherosclerosis and is associated to angiographic lesions, especially in the coronary arteries. On the other hand, it is associated to endothelial dysfunction which may contribute to myocardial ischaemia even in presence of angiographically normal arteries, a phenomenon named also syndrome X by the cardiologists. Thus, metabolic syndrome X and cardiological syndrome X are very close and syndrome X may be considered as a crossing between metabolic disorders and cardiovascular diseases.
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PMID:[Syndrome X, at the crossroads of metabolic and cardiovascular diseases]. 955 80

The present study was designed to develop an animal model of multiple risk factors, including obesity, hypertension, non-insulin-dependent diabetes mellitus, and hyperlipidemia. Hypothalamic obesity was induced by neonatal monosodium glutamate (MSG) treatment in spontaneously hypertensive rats (SHR). Female newborn SHR were treated intraperitoneally with 2 or 4 mg/kg body weight of MSG for 5 days. Obesity developed in SHR treated with 4 mg/kg of MSG but not in SHR treated with 2 mg/kg of MSG. Obese SHR had impaired glucose tolerance, hyperinsulinemia, and hypertriglyceridemia. However, the severity of hypertension was attenuated in obese SHR as compared with control SHR. The degree of obesity was closely related to the metabolic abnormalities, but inversely correlated with the blood pressure level. Macrovascular changes were investigated in obese SHR at 14 months of age. Intimal thickening was accelerated in the carotid artery of obese SHR as compared with that of nonobese SHR. Aortic contents of DNA and total cholesterol were significantly increased in obese SHR. SHR associated with MSG-induced obesity showed major manifestations of metabolic syndrome X. This animal model may be useful to study the clustering of risk factors for the development of macrovascular diseases.
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PMID:Obesity induced by neonatal monosodium glutamate treatment in spontaneously hypertensive rats: an animal model of multiple risk factors. 958 1

Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, alpha-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6. The dyslipidaemia common in Type II diabetes (hypertriglyceridaemia and low serum levels of HDL cholesterol) is also a feature of natural and experimental acute-phase reactions. We review evidence that a long-term cytokine-mediated acute-phase reaction occurs in Type II diabetes and is part of a wide-ranging innate immune response. Through the action of cytokines on the brain, liver, endothelium, adipose tissue and elsewhere, this process could be a major contributor to the biochemical and clinical features of metabolic syndrome X (glucose intolerance, dyslipidaemia, insulin resistance, hypertension, central obesity, accelerated atherosclerosis) but also provides a mechanism for many other abnormalities seen in Type II diabetes, including those in blood clotting, the reproductive system, metal ion metabolism, psychological behaviour and capillary permeability. In the short-term, the innate immune system restores homeostasis after environmental threats; we suggest that in Type II diabetes and impaired glucose tolerance long-term lifestyle and environmental stimulants, probably in those with an innately hypersensitive acute-phase response, produce disease instead of repair.
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PMID:Is type II diabetes mellitus a disease of the innate immune system? 1023 Jun 57


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