Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Augmented glucose utilisation or secretion of insulin-like-growth-factor II (IGF-II) are discussed as important pathogenetic factors in tumor-associated hypoglycemia (Doege-Potter Syndrome) with suppressed insulin and C-peptide levels. Primary malignant fibrous histiocytoma of the lung is an uncommon neoplasia and its association with hypoglycemia is rare and the causal relationship remains unclear. - We report a 57-year-old male with spontaneous hypoglycemia (1.67 mmol/l) due to a primary malignant fibrous histiocytoma of the lung, secreting IGF-II. Insulin (0.10 nmol/l; normal range 0.33-1.2) and C-peptide (3.0 mIU/l; 5-25) levels were suppressed in combination with low levels of growth hormone (<0.5 ng/ml; <7 ng/ml) and IGF-I (<66.0 ng/ml; 70-246). The elevated IGF-II level (787 ng/ml; 300-500) and decreased IGF-binding protein 3 (1.6 mg/l; 2-5) indicated a high free IGF-II activity. After surgery (resection of the right upper lobe), glucose (4.4 mmol/l), insulin (9.0 mIU/L) and C-peptide (0.84 nmol/l) levels returned to normal. Serum IGF-I (289 ng/ml) and the IGF-I/IGF-II ratio (<0.08 preoperative vs. 0.41 postoperative; >0.20) increased to the normal reference range. - In conclusion, malignant fibrous histiocytoma (MFH) is rarely described presenting as tumor-induced hypoglycemia. Doege-Potter Syndrome in MFH seems to be related to tumor-associated IGF-II production.
Exp Clin Endocrinol Diabetes 2000
PMID:Primary malignant fibrous histiocytoma of the lung: IGF-II producing tumor induces fasting hypoglycemia. 1114 28

The purpose of this study is to provide a contemporary qualitative and quantitative analysis of coronary angiograms from a large series of women enrolled in the Women's Ischemia Syndrome Evaluation (WISE) study who had suspected ischemic chest pain. Previous studies have suggested that women with chest pain have a lower prevalence of significant coronary artery disease (CAD) compared with men. Detailed analyses of angiographic findings relative to risk factors and outcomes are not available. All coronary angiograms were reviewed in a central core laboratory. Quantitative measurement of percent stenosis was used to assess the presence and severity of disease. Of the 323 women enrolled in the pilot phase, 34% had no detectable, 23% had measurable but minimal, and 43% had significant ( > 50% diameter stenosis) CAD. Of those with significant CAD, most had multivessel disease. Features suggesting complex plaque were identified in < 10%. Age, hypertension, diabetes mellitus, prior myocardial infarction (MI), current hormone replacement therapy, and unstable angina were all significant, independent predictors of presence of significant disease (p < 0.05). Subsequent hospitalization for a cardiac cause occurred more frequently in those women with minimal and significant disease compared with no disease (p = 0.001). The common findings of no and extensive CAD among symptomatic women at coronary angiography highlight the need for better clinical noninvasive evaluations for ischemia. Women with minimal CAD have intermediate rates of rehospitalization and cardiovascular events, and thus should not be considered low risk.
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PMID:Detailed angiographic analysis of women with suspected ischemic chest pain (pilot phase data from the NHLBI-sponsored Women's Ischemia Syndrome Evaluation [WISE] Study Angiographic Core Laboratory). 1130 81

This study in undertaken to evaluate the pattern of sensory conduction abnormalities in Guillain-Barre (GB) Syndrome. Thirty six patients with GB Syndrome following clinical and CSF examination were subjected to motor conduction studies of median, ulnar and paroneal nerves including F wave latencies and sensory conduction studies of median, ulnar and sural nerves bilaterally. Motor conduction abnormalities were seen in 32 out of 36 patients (83%) and were seen more frequently in the lower limbs than upper. Median sensory conduction was abnormal more frequently than ulnar (21 Vs 17 patients). Median sensory conduction was abnormal in 21, ulnar in 17 and sural in 10 patients. In all the patients having abnormal ulnar sensory conduction, median sensory conductions were also abnormal. The patients with abnormal sural conductions had abnormal median sensory conductions in all except one patient. A pattern of normal sural with abnormal median sensory conductions was present in 12 patients. Both sural and median sensory conductions were abnormal in 9 patients and both normal in 14 patients. One patient had abnormal sural conduction with normal median sensory conduction but he had underlying diabetes. A similar pattern was found in relation to ulnar and sural sensory conductions although it was less frequent and less specific. The discordance of sural and median sensory conduction is important in GB Syndrome. Normal sural conductions with abnormal median sensory conductions is suggestive of GB Syndrome in the presence of an appropriate clinical setting, but a reverse pattern should alert an underlying polyneuropathy.
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PMID:Pattern of sensory conduction in Guillain-Barre Syndrome. 1172 Dec 99

Atherosclerosis is a major vascular complication of diabetes and the primary cause of mortality in persons with this disease. Metabolic abnormalities related to the Insulin Resistance Syndrome or Metabolic Syndrome may importantly contribute to the increased risk of atherosclerosis associated with diabetes. Thiazolidinediones (TZDs) are oral insulin sensitizers in broad clinical use that enhance insulin-stimulated glucose uptake into skeletal muscle. TZDs can also improve cardiovascular risk factors and exert direct effects on vascular cells to potentially retard the atherosclerotic process. Direct vascular effects of TZDs likely result from their activity as ligands for the nuclear receptor, PPARgamma. All of the major cell types in the vasculature express PPARgamma, including intimal macrophages and vascular smooth muscle cells (VSMCs) in human atheroma. TZDs block VSMC growth by inducing cell cycle arrest in G1 through an inhibition of retinoblastoma protein phosphorylation. Migration of monocytes and VSMCs is also inhibited by TZDs, possibly through decreased matrix metalloproteinase production. Activation of PPARgamma by TZDs in macrophages induces ABCA1 transporter expression to promote reverse cholesterol transport. These antiatherogenic activities may also occur in vivo because TZDs have been shown to inhibit lesion formation in several animal models. Thus, TZD activation of PPARgamma may protect against atherosclerosis both by normalizing proatherogenic metabolic abnormalities of the insulin resistance/diabetes milieu and through an inhibition of vascular cell growth and movement.
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PMID:PPARgamma and atherosclerosis: effects on cell growth and movement. 1174 60

Caudal Regression Syndrome (CRS) is a rare fetal complication of diabetic pregnancy, which can result in long-term neurological, urologic, and orthopedic complications. Although the exact teratogenic mechanism is not known, hyperglycemia appears to play a crucial role as a teratogen, and therefore, stringent control of diabetes preconceptually and in early pregnancy is presumed to reduce the risk of occurrence. We report an unusual case of CRS affecting only one of a set of monozygotic twins, suggesting that as yet, unidentified factors other than hyperglycemia are included in its causation.
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PMID:Caudal Regression Syndrome in twin pregnancy with type II diabetes. 1189 27

To characterize a new insulin resistance syndrome in euglycemic midlife women and the relationship of its features (including hypertension and dyslipidemia), with hyperinsulinemia (AUC insulin > or = 100 microU/mL), retrospective cohort analysis was conducted in 278 consecutive women who presented to a Menopausal Health Program. Of 67 women with midlife weight gain "greater than 20 pounds since their twenties" and body mass indices (BMIs) between 25 and 32 kg/m(2), none of the subjects met criteria for Type 2 diabetes, 5 women had impaired glucose tolerance, and 36 women were hyperinsulinemic. Hyperinsulinemia was a highly statistically significant determinant of hypertension, dyslipidemia, and truncal obesity (Odds Ratios 10.6, 4.0, and 13.7; P values < or = 0.0001, < or = 0.007, and < or = 0.0001) in cross-tabulations. AUC insulin was the best predictor variable of hypertension and dyslipidemia in univariate and multivariate logistic regression models (univariate P values 0.0004 and 0.0088). After adjustment for BMI, age, and estrogen use, the final models, correctly classified, respectively, 74% and 69% of all cases in the dataset (model P values: < or = 0.0001 and < or = 0.0067) and AUC insulin had a log-linear (i.e., dose-dependent) relationship with hypertension and dyslipidemia, which suggests causality. We propose that the constellation of symptoms that includes midlife weight gain, "waist-gain," hypertension, dyslipidemia, and appetite dysregulation in euglycemic women with hyperinsulinemia be titled Syndrome W and suggest that the highly statistically significant relationship of hyperinsulinemia with the characteristic features are evidence of a causal role for insulin in its etiology. The identification of Syndrome W before the onset of overt impaired glucose tolerance, diabetes, or manifestations of coronary artery disease could have important clinical and public health implications for midlife women.
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PMID:Syndrome W: a new model of hyperinsulinemia, hypertension and midlife weight gain in healthy women with normal glucose tolerance. 1197 38

Observations on humans, on rats in vivo, and on isolated perfused rat livers indicate that insulin stimulates hepatic very-low-density lipoprotein (VLDL)-TAG secretion when the liver is chronically exposed to the hormone. They suggest that frequent stimulation of insulin secretion throughout the diurnal cycle may result in a chronic stimulation of VLDL secretion and increased delivery of acyl moieties to the periphery, particularly to muscle, the most important site of insulin-sensitive glucose disposal. If acyl groups are provided in excess of the oxidative needs of the tissue, this may lead to induction of insulin resistance, irrespective of whether obesity is established concomitantly. Dietary factors that stimulate hepatic VLDL secretion may have the same effect and contribute to the induction of a vicious spiral leading to the development of the full-blown Metabolic Syndrome and its pathological consequences, including type-2 diabetes, stroke, and cardiovascular disease.
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PMID:Insulin stimulation of hepatic triacylglycerol secretion in the insulin-replete state: implications for the etiology of peripheral insulin resistance. 1207 35

Metabolic Syndrome (MetS) has been defined as a clinical condition including impaired glucose tolerance or diabetes mellitus and/or insulin-resistance, associated with two or more of the following components: arterial hypertension, central obesity, dyslipidaemia, microalbuminuria. In a group of subjects with MetS we examined the macrohaemorheological profile, demonstrating a significant increase of blood, plasma and serum viscosity and a decrease of whole blood filterability. The results show that in these subjects a secondary hyperviscosity condition is present, but also that several significant correlations are present between the haemorheological variables and some aspects of MetS, especially those reflecting central obesity (waist to hip ratio) and insulin-resistance. The altered haemorheological profile likely contributes to explain the high cardiovascular risk present in MetS, but it may also participate, through its influence on haemodynamic pattern, in the pathogenesis of insulin-resistance.
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PMID:Haemorheological profile in metabolic Syndrome. 1212 29

Apoptosis is a physiological process of cell death that normally occurs when cells are damaged or no longer needed. One of its major roles is the maintenance of peripheral immune tolerance, by eliminating activated T and B cells beyond the course of an infection, and thus terminating immune responses. When apoptosis becomes dysfunctional, either being "too much" or "too little," a variety of different disease states may be triggered. For example, insufficient apoptosis of activated immune cells is the basis of the Canale Smith Syndrome /ALPS, whereas excessive apoptosis of ~ islet cells of the pancreas is involved in the pathogenesis of autoimmune diabetes mellitus. In this review, we explain the fundamental aspects and molecular mechanisms of apoptosis and their relevance to several important human autoimmune diseases.
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PMID:Apoptosis: a case where too much or too little can lead to autoimmunity. 1235 62

Hypertriglyceridaemia, diabetes, hypertension and obesity are the deadly quartet indicating a syndrome at high risk for cardiovascular disease for which, in 1998, WHO proposed the definition of Metabolic Syndrome, related to an elevated degree of insulin resistance. Treatment will often include behavioural changes that reduce body weight and increase physical activity A high-carbohydrate/low-fat diet with complex carbohydrates and mainly unsaturated fat is recommended. Replacing refined grain products and potatoes with minimally processed plant-based foods such as whole grains, fruit, and vegetables, and reducing the intake of high glycaemic load beverages may offer a simple strategy for reducing the incidence of coronary heart disease.
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PMID:Clinical, physiopathological and dietetic aspects of metabolic syndrome. 1240 57


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