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)

The antidiabetic and antioxidant effects of the herbal preparation ADD-199 were investigated in STZ-induced diabetic C(3)H mice and results were compared with two allopathic hypoglycaemic drugs, glibenclamide and metformin. Plasma glucose, insulin and lipids as well as liver glycogen, lipids and lipid peroxidation were measured following treatment for 8 weeks. The results indicated that plasma insulin levels in normal controls at termination were about 76 micromol/L compared to trace levels in untreated diabetic mice. Glibenclamide and ADD-199 increased insulin levels in diabetic mice up to 70% of levels in untreated non-diabetic mice whilst metformin had no effect. Basal plasma glucose levels in diabetic controls (18.8 mM) were reduced to 14.0 mM by 100 mg/kg ADD-199 in <2 weeks compared to 4 and 6 weeks for glibenclamide and metformin, respectively. This hypoglycaemic effect of ADD-199 appeared to be associated with the alkaloidal content of the extract. Treatment with ADD-199 or the hypoglycaemic agents reversed the observed elevation in plasma lipids but increased hepatic glycogen, triacylglycerol and cholesterol levels. Treatment also increased glucose uptake by isolated diaphragms and attenuated hepatic lipid peroxidation. These antihyperglycaemic and antioxidant actions of ADD-199 at a dose of 100mg/kg/day are comparable to those of the maximum daily therapeutic doses of glibenclamide (0.25 mg/kg) and metformin (50 mg/kg). These could explain the basis for use of this plant extract to manage diabetes mellitus (DM).
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PMID:The antidiabetic activity of the herbal preparation ADD-199 in mice: a comparative study with two oral hypoglycaemic drugs. 1565 71

Atherosclerosis, and the resulting coronary heart disease and stroke, is the most common cause of death in developed countries. Atherosclerosis is an inflammatory process that results in the development of complex lesions or plaques that protrude into the arterial lumen. Plaque rupture and thrombosis result in the acute clinical complications of myocardial infarction (MI) and stroke. Although certain risk factors (dyslipidemias, diabetes, hypertension) and humoral markers of plaque vulnerability (C-reactive protein, interleukin-6, 10 and 18, CD40L) have been identified, a highly sensitive and specific biomarker or protein profile, which could provide information on the stability/vulnerability of atherosclerotic lesions, remains to be identified. In this review, we report several proteomic approaches which have been applied to circulating or resident cells, atherosclerotic plaques or plasma, in the search for new proteins that could be used as cardiovascular biomarkers. First, an example using a differential proteomic approach (2-DE and MS) comparing the secretome from control mammary arteries and atherosclerotic plaques is displayed. Among the different proteins identified, we showed that low levels of HSP-27 could be a potential marker of atherosclerosis. Second, we have revised several studies performed in cells involved in the pathogenesis of atherosclerosis (foam cells and smooth muscle cells). Another approach consists of performing proteomic analysis on circulating cells or plasma, which will provide a global view of the whole body response to atherosclerotic aggression. Circulating cells can bear information reflecting directly an inflammatory or pro-coagulant state related to the pathology. As an illustration, we report that circulating monocytes and plasma in patients with acute coronary syndromes has disclosed that mature Cathepsin D is increased both in the plasma and monocytes of these patients. Finally, the problems of applying proteomic approach directly to plasma will be discussed. The purpose of this review is to provide the reader with an overview of different proteomic approaches that can be used to identify new biomarkers in vascular diseases.
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PMID:Quest for novel cardiovascular biomarkers by proteomic analysis. 1608 68

While selected pancreatic diseases may be best treated by total pancreatectomy (TP), the anticipated sequelae of pancreatic insufficiency make TP an undesirable alternative. Our aim was to determine if patients undergoing TP have a worse quality of life (QoL) than age- and gender-matched controls and poor long-term glycemic control. Ninety-nine patients undergoing TP from 1985 through 2002 were identified. The 34 survivors with no recurrent malignancy were surveyed with the Short Form-36 (SF-36), the Audit of Diabetes Dependent QoL (ADD QoL), the European Organization for Research and Treatment in Cancer Pancreas 26 (EORTC PAN 26), and our institutional questionnaire. Operative morbidity and mortality were 32% and 5%, respectively. Three late postoperative deaths (3%) were attributed to hypoglycemia. Of the 34 surviving patients, 27 (79%) agreed to participate at a mean of 7.5 years postoperatively. Seven patients had required 12 hospitalizations for poor glycemic control. Per the SF-36, two domains (role physical and general health) were decreased compared with an age- and gender-matched national population (P < .05). The ADD QoL demonstrated an overall decrease in QoL related specifically to the diabetes mellitus (P < .01), but comparison with insulin-dependent diabetics from other causes showed no significant difference in QoL. The EORTC PAN 26 instrument also showed measurable effects on QoL. Total pancreatectomy can be performed safely. QoL after TP is decreased compared with age- and gender-matched controls but not with diabetes from other causes; however, the changes are not overwhelming. TP should remain a viable option but in selected patients.
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PMID:Quality-of-life after total pancreatectomy: is it really that bad on long-term follow-up? 1626 76

Acute coronary syndromes (ACS) include unstable angina and non-ST elevation myocardial infarction (UA/NSTEMI) and ST-segment elevation myocardial infarction (STEMI). Acute coronary syndromes lead to important epidemiological and economical problems. In polish population an estimated incidence of ACS is 250 000 cases per year. 30-day mortality in UA/NSTEMI is approximately 3.5%, and 8.4% in STEMI. The atherosclerotic plaque instability with subsequent rupture and thrombus formation is a primary mechanism of ACS. Plaque destabilization is evoked by local and systemic inflammation. The primary risk factors in ACS are: age > 65 years, diabetes, peripheral artery disease, stroke, previous myocardial infarction and elevated levels of cardiac troponins. The guidelines for treatment of ACS are based on the results of large randomized clinical trials assessing the reduction of relevant clinical end-points (death, AMI, recurrent ischaemia). The goal of treatment of UA/NSTEMI is the stabilization of the plaque, prevention and reduction of myocardial ischaemia and AMI. Inefficient medical treatment and sustained symptoms are the indication for coronary angiography and percutaneous coronary intervention (PCI). The main goal of treatment in STEMI is quick regaining of the culprit vessel patency and maintaining of sufficient myocardial perfusion. It can be done by thrombolytic therapy or primary coronary angioplasty. In comparison to fibrynolysis PCI confers the lower risk of death and recurrent AMI. New regimens of pharmacological treatment (facilitated PCI) including the half-dose of fibrynolytic and GPIIbIIIa inhibitor prior to PCI are assessed to improve the efficiency of PCI.
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PMID:[Pathogenesis and treatment of acute coronary syndromes]. 1642 97

The incidence of diabetes is increasing in the general population because of increasing obesity, and is likely to result in a higher incidence of coronary artery disease. It was recently reported that diabetics (types I and II) dying suddenly from coronary artery disease have greater macrophage and T lymphocyte infiltration in atherosclerotic plaques, as well as larger necrotic cores compared with nondiabetics. The inflammatory cell infiltrates showed human leukocyte antigen-DR expression, which was greater in diabetics. The receptors for advanced glycosylation end-products expression, demonstrated by immunohistochemistry, was greater in diabetics than in nondiabetics in macrophages, smooth muscle cells and endothelial cells, and was associated with apoptosis of macrophages and smooth muscle cells, but not of endothelial cells. There is also a higher incidence of healed plaque ruptures and healed myocardial infarct in type II diabetics. Plaque burden is higher in diabetics than in nondiabetics; however, distal plaque burden was only significantly different in type II diabetics compared with nondiabetics. There was greater positive remodelling in diabetic coronary arteries than in nondiabetic ones, which correlated with the per cent necrotic core. Further studies are needed to better understand the mechanisms that govern greater inflammation and plaque burden in diabetics.
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PMID:Morphological characteristics of coronary atherosclerosis in diabetes mellitus. 1649 17

Plaque disruption and subsequent thrombus formation play a critical role in the clinical manifestations of atherothrombosis. Vulnerable lesions are characterized by the existence of core rich in lipid, macrophages and tissue factor (TF). Plaque disruption facilitates the interaction between flowing blood with the inner components (TF) of disrupted atherosclerotic lesions triggering the coagulation cascade. TF, thrombin, platelets, fibrin and inflammatory cells are involved in this process of acute thrombus formation. This pathologic process is significantly accelerated by several "cardiovascular risk factors" such as diabetes, smoking, dyslipemia, etc. We will review on the role of TF, plaque cell apoptosis and blood thrombogenicity acting as a thread of inflammatory and prothrombotic mediators. We will also review the role of activated platelets as source for pro-inflammatory cytokines and enunciation of thrombotic process. Overall, we will try to emphasize the most recent understanding of the concepts involved in the interaction between inflammation and coagulation within the setting of atherothrombotic disease.
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PMID:Links between inflammation and thrombogenicity in atherosclerosis. 1691 70

Plaque angiogenesis may be associated with the development of unstable and vulnerable plaques. Vascular endothelial growth factors (VEGFs) are potent angiogenic factors that can affect plaque neovascularization. Our objective was to determine the effect of diabetes on atherosclerosis and on the expression of angiogenesis-related genes in atherosclerotic lesions. Alloxan was used to induce diabetes in male Watanabe heritable hyperlipidemic (WHHL) rabbits that were sacrificed 2 and 6 months after the induction of diabetes. Nondiabetic WHHL rabbits served as controls. Blood glucose (Glc), serum-free fatty acids (FFA), and serum triglyceride levels were significantly higher in diabetic rabbits. Accelerated atherogenesis was observed in the diabetic WHHL rabbits together with increased intramyocellular lipids (IMCL), as determined by 1H-NMR spectroscopy. Atherosclerotic lesions in the diabetic rabbits had an increased content of macrophages and showed significant increases in immunostainings for vascular endothelial growth factor (VEGF)-A, VEGF-D, VEGF receptor-1, VEGF receptor-2, RAGE, and NF-kappaB. VEGF-A165 and VEGFR-2 mRNA levels were significantly increased in aortas of the diabetic rabbits, where a trend toward increased plaque vascularization was also observed. These results suggest that diabetes accelerates atherogenesis, up-regulates VEGF-A, VEGF-D, and VEGF receptor-2 expression, and increases NF-kappaB, RAGE, and inflammatory responses in atherosclerotic lesions in WHHL rabbits.
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PMID:VEGF-A, VEGF-D, VEGF receptor-1, VEGF receptor-2, NF-kappaB, and RAGE in atherosclerotic lesions of diabetic Watanabe heritable hyperlipidemic rabbits. 1693 42

Atherosclerosis is one of the most common causes of death in developed countries. Atherosclerosis is an inflammatory process that results in the development of complex lesions or plaques that protrude into the arterial lumen. Plaque rupture and thrombosis result in the acute clinical complications of myocardial infarction and stroke. Although certain risk factors (dyslipidemias, diabetes, hypertension) and humoral markers of plaque vulnerability (C-reactive protein, interleukin-6, -10 and -18, CD-40L) have been identified, a highly sensitive and specific biomarker or protein profile, which could provide information on the stability/vulnerability of atherosclerotic lesions, remains to be identified. Recently, we have described a novel strategy consisting in the proteomic analysis of proteins released by normal and atherosclerotic arterial walls in culture. This method enables harvesting of proteins that are only secreted by pathological or normal arterial walls. By focusing only on the secreted proteins found in the tissue culture media, there is an intended bias toward those molecules that would have a higher probability of later being found in plasma. Using this approach, we have shown that carotid atherosclerotic plaques cultured in vitro are able to secrete proteins, and also that a differential pattern of protein secretion of normal arteries vs pathological ones has been observed. In this chapter, the proteomic analysis of the human atheroma plaque secretome is described.
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PMID:Characterization of the human atheroma plaque secretome by proteomic analysis. 1717 85

Dirty electricity is a ubiquitous pollutant. It flows along wires and radiates from them and involves both extremely low frequency electromagnetic fields and radio frequency radiation. Until recently, dirty electricity has been largely ignored by the scientific community. Recent inventions of metering and filter equipment provide scientists with the tools to measure and reduce dirty electricity on electrical wires. Several case studies and anecdotal reports are presented. Graham/Stetzer (GS) filters have been installed in schools with sick building syndrome and both staff and students reported improved health and more energy. The number of students needing inhalers for asthma was reduced in one school and student behavior associated with ADD/ADHD improved in another school. Blood sugar levels for some diabetics respond to the amount of dirty electricity in their environment. Type 1 diabetics require less insulin and Type 2 diabetics have lower blood sugar levels in an electromagnetically clean environment. Individuals diagnosed with multiple sclerosis have better balance and fewer tremors. Those requiring a cane walked unassisted within a few days to weeks after GS filters were installed in their home. Several disorders, including asthma, ADD/ADHD, diabetes, multiple sclerosis, chronic fatigue, fibromyalgia, are increasing at an alarming rate, as is electromagnetic pollution in the form of dirty electricity, ground current, and radio frequency radiation from wireless devices. The connection between electromagnetic pollution and these disorders needs to be investigated and the percentage of people sensitive to this form of energy needs to be determined.
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PMID:Electromagnetic hypersensitivity: biological effects of dirty electricity with emphasis on diabetes and multiple sclerosis. 1717 85

The aim of this study was to determine if significant differences in plaque composition exist between the popliteal and tibial vessels in patients with severe peripheral arterial disease (PAD). Forty-four patients with PAD required either above-knee (n = 38), below-knee (n = 5), or through-knee (n = 1) amputation for pedal sepsis/gangrene. The 51 vessels (anterior tibial, n = 9; posterior tibial, n = 10; peroneal, n = 3; popliteal, n = 29) were obtained and underwent intravascular ultrasound (IVUS) evaluation ex vivo within 24 hr of amputation. Sequential IVUS data were obtained at known intervals throughout the vessel length and then analyzed with radiofrequency techniques for quantification of plaque composition, plaque volume, and total vessel volume. Plaque composition was categorized as fibrous, fibro-fatty, necrotic core, and dense calcium. Clinical data were obtained via review of electronic records at the time of amputation. Two-sided t-tests were performed to compare components within each plaque. Results are expressed as mean percentage +/- standard error of the mean. Tibial vessels had more dense calcium within these plaques than popliteal arteries (33.8 +/- 5.6% vs. 10.6 +/- 1.9%, p < 0.001). Consequently, distal vessels had less fibro-fatty and fibrous plaque than popliteal arteries (7.7 +/- 1.4% vs. 13.1 +/- 1.2%, p < 0.005; 42.4 +/- 4.7% vs. 61.4 +/- 2.2%, p < 0.001, respectively). Necrotic core plaque composition was found to be similar when comparing tibial versus popliteal arteries (16.1% vs. 14.9%, p = nonsignificant). Clinical factors including diabetes, hyperlipidemia, and chronic renal insufficiency were not associated with plaque composition differences using a univariate analysis. As we progress distally in the arterial tree of patients with PAD, calcium plaque content increases with decreasing burden of fibro-fatty plaque. Clinical and demographic factors, with the exception of smoking, were not found to be associated with atherosclerotic plaque composition.
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PMID:Arterial calcification increases in distal arteries in patients with peripheral arterial disease. 1864 Aug 12


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