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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this article we have focused on the evolving pattern of nutritional management of the person with diabetes. Before the advent of insulin in 1922, it was sufficient to identify a meal plan that would keep people alive until they could be rescued from mortality due to diabetic ketoacidosis (the major killer of the era) by pharmacologic means. Now, the life expectancy of people with diabetes is close to that of the general population and focus has turned to combating the new threats of macrovascular disease and kidney failure. Over recent years the susceptibility of NIDDM patients to macrovascular events has been established and the twofold increase in risk of a heart attack in diabetic men is outshadowed by the four- to fivefold risk in diabetic women and the 13- to 17-fold greater risk in diabetics under the age of 30 years compared with their nondiabetic counterparts. The mechanism behind the susceptibility to macrovascular disease has generated a veritable plethora of investigations focusing on the atherogenic profile of diabetic dyslipidemia. Hyperinsulinemia, insulin resistance, and overtreatment of the diabetic with insulin have been claimed as contributors to the development of premature atherosclerosis. The hallmark of the diabetic dyslipidemia is the tendency to elevated VLDL triglyceride levels and the closely linked reduction in HDL cholesterol. Although there is some controversy on the relationship between triglyceride levels and the incidence of CAD, there is no doubt that HDL is an independent risk factor. It can now be safely said that elevated triglycerides are a risk factor in women and that in men elevated triglycerides constitute a risk factor if accompanied by a reduced HDL level. For these reasons, any approach to nutritional management of the diabetic must attempt not only to normalize glycemia but to make every effort to reduce the atherogenic profile. In the accompanying algorithm (Fig. 4), we consider the risk factors conducive to a reduction in life expectancy and offer a meal plan that is appropriate for the individual with diabetes. For the 80% of NIDDM patients who are obese, a diet with a reduction of 500 to 1000 kcal is in order and this may be achieved by a periodic VLCD. We examined carefully the controversy related to yo-yo dieting and support the notion that its effects in humans are not all that harmful. Ingestion of simple sugars in the high carbohydrate diet has negative effects both on carbohydrate and lipid metabolism.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The good, the bad, and the ugly in diabetic diets. 131 32

The software driving the Cerec CAD/CAM system has recently been updated. In this study, the marginal accuracy of computer-machined porcelain inlays was determined using the original and the updated software. Two types of MOD cavities in Frasaco resin teeth were prepared with either sharp or rounded box corners. The distance of the occlusal and proximal marginal interface was determined using a measuring microscope. The mean occlusal interfacial distance was 52 microns for both programs. Only the box corners showed a significantly larger space, of which the mean value was approximately 200 microns. The updated version improved the marginal accuracy at the box corners. Further reduction of the interfacial distance was accomplished by rounding the sharp box corners.
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PMID:Marginal accuracy of CAD/CAM inlays made with the original and the updated software. 162 22

Based on the data reviewed, it is necessary to conclude that diabetes is associated with profound changes in HDL metabolism. However, once we go beyond this simple generalization, it is apparent that the relationship between diabetes and HDL metabolism is not a simple one. A good deal of the complication evolves from the fact that IDDM and NIDDM seem to affect HDL metabolism quite differently, with the only apparent similarity the fact that plasma HDL-cholesterol concentration can be low in untreated patients with either IDDM or NIDDM. Thus, in patients with IDDM the primary event seems to be related to the insulin-deficient state, which results in a decrease in HDL turnover rate and resultant decline in plasma HDL-cholesterol concentration. In contrast, HDL turnover appears to be accelerated, not reduced in patients with NIDDM, and the low plasma HDL-cholesterol concentration is a consequence of the increased turnover rate. In addition, patients with NIDDM are not absolutely insulin deficient, and available evidence suggests that the higher the plasma insulin level, the lower the plasma HDL-cholesterol concentration in these patients. The differences noted above in the effect of IDDM and NIDDM on HDL metabolism are of great interest, and, unfortunately, not very well understood. There is, however, one additional difference, which may be of paramount clinical importance. For reasons not totally clear, plasma HDL-cholesterol concentrations in patients with IDDM treated with insulin are not lower than normal, and even tend to be higher than these values in a nondiabetic population. Possibly as a result of this phenomenon, there is no evidence that changes in plasma HDL-cholesterol concentration play a role in the development of macrovascular complications in IDDM. Although it is apparent from the considerations discussed in this review that a great deal more needs to be learned about the effect of insulin deficiency on HDL metabolism, changes in HDL metabolism do not appear to be clinically important in patients with IDDM. Unfortunately, this does not appear to be the situation in patients with NIDDM. Plasma HDL-cholesterol concentrations are lower than normal in patients with NIDDM, and this finding seems to be related to increased morbidity and mortality from CAD. Furthermore, there is no form of anti-diabetic treatment, irrespective of how effective it has been in achieving glycemic control, that has been shown to substantially increase plasma HDL-cholesterol level. Indeed, it has been difficult to demonstrate a consistent effect of any therapeutic approach on plasma HDL-cholesterol concentration.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:HDL metabolism in diabetes. 330 Dec 37

In order to evaluate whether Lp(a), a lipoprotein that is potentially thrombogenic and atherogenic, is a potential risk factor for CAD in non-insulin-dependent diabetes (NIDDM), we compared the Lp(a) and its distribution in 145 NIDDM patients with that in 94 healthy control subjects. Furthermore, we studied the effect of insulin treatment on serum Lp(a) in 108 patients with NIDDM. Male and female NIDDM patients had similar Lp(a) concentrations to healthy controls (median value 167 mg L-1, range 15-1550 mg L-1 vs. 157 mg L-1, range 15-919 mg L-1, NS and 92, range 15-1190 mg L-1 vs. 103 mg L-1, range 15-842 mg L-1, NS). Also, the cumulative distribution of Lp(a) did not differ between the NIDDM patients and healthy subjects. Insulin treatment increased Lp(a) in diabetics with a Lp(a) concentration of less than 300 mg L-1, but this effect was not related to the concomitant improvement in metabolic control (mean change (+/- SEM) of HbA1c from 9.80 +/- 0.15 to 8.00 +/- 0.12; P < 0.001). In subjects with elevated Lp(a) concentrations (> 300 mg L-1) the Lp(a) concentration was unaffected by insulin, despite a similar improvement in glycaemic control. These results suggest that insulin may modulate the concentration of Lp(a).
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PMID:Effect of insulin treatment on serum lipoprotein(a) in non-insulin-dependent diabetes. 778 67

This in vitro study compared the marginal adaptation of CAD/CAM and laboratory-made ceramic inlays before, during and after loading. Six MOD inlay preparations of standardized design with one cervical margin in dentine and the other in enamel were prepared for each inlay type: CAD/CAM fabricated MGC-glass ceramic inlays, CAD/CAM fabricated feldspathic porcelain inlays, laboratory-made glass ceramic inlays and laboratory-made feldspathic porcelain inlays. Appropriate luting composite materials were used. The restored teeth were subjected to occlusal loading, thermal cycling, toothbrush-toothpaste abrasion and chemical degradation in vitro. Marginal adaptation was quantitated along the entire length of the cavosurface margin and along selected sections of the margin using SEM, following in vitro testing corresponding to 0, 0.5, 1.0, 2.7 and 5.0 years of clinical service. In addition, marginal fit of the cemented inlays was evaluated in the SEM. The initial marginal adaptation in enamel was excellent in all groups. After in vitro testing, significant marginal discrepancies were found in all groups. A high percentage of marginal openings was recorded, notably in the cervical portions of the margins in both enamel and dentine.
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PMID:Marginal adaptation and fit of adhesive ceramic inlays. 842 82

Coronary angiographic profile of 75 patients (63 males and 12 females) with noninsulin dependent diabetes mellitus (NIDDM) and CAD was compared with 75 nondiabetic patients (63 males and 12 females) with CAD. No difference was present between the mean age (56.2 +/- 7.4 vs 56.1 +/- 7.7 years; p = NS), presenting complaints (67 unstable angina and 8 stable angina with positive TMT in both the groups) and other coronary risk factors between the two groups. Severity and diffuseness of coronary artery involvement was assessed by a coronary artery score (CAS) using the segmental distribution method for coronary artery lesions. Diabetic patients with CAD had a higher CAS (18.7 +/- 10.3) as compared to the nondiabetic patients with CAD (12.7 +/- 9.6) (p < 0.01). Diabetic patients with CAD had a higher number of TVD [43 (57.3%) vs 31 (41.3%); p < 0.01] while the DVD and SVD was not significantly different. As compared to the nondiabetic group, diabetics had a higher total number of coronary artery lesions (300 vs 200; p < 0.001), a higher lesion per patient ratio (4.0 lesions/patient vs 2.6 lesions/patient; p < 0.001), a higher number of concentric lesions, [151 (50.3%) vs 90 (45%); p < 0.01] and a higher number of multiple irregularity lesions, [36 (21%) vs 27 (9%); p < 0.05]. The diffuse involvement of vessels was not significantly different between the two groups in LAD (12.1% vs 5.3%; p = NS), LCx (14.2% vs 5.8%; p = NS) and RCA (10.5% vs 5.0%; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Angiographic severity and morphological spectrum of coronary artery disease in non insulin dependent diabetes mellitus. 855 76

There are contrasting data about the relationship between obesity and macrovascular complications in type 2 diabetes mellitus, and it is not known if risk factors for coronary artery disease are different in normal weight and overweight or obese patients. All 2113 patients with type 2 diabetes mellitus referring to the Diabetic Clinic of Asti were studied. Patients were divided into tertiles of body mass index, according to their sex (BMI < 26.9; >/= 26.9 and < 31.4; >/= 31.4 kg/m(2) for females and BMI < 25.7; >/= 25.7 and < 28.8; >/= 28.8 kg/m(2) for males). Age, BMI, duration of diabetes, blood pressure, HbA(1c) total cholesterol, HDL-cholesterol, LDL-cholesterol, and prevalence of insulin treatment and hypertension were higher in females, whereas exercise, alcohol intake, smoking habits and prevalence of dyslipidemia were higher in males. An increase in BMI was associated with an increase in HbA(1c), number of cigarettes/day, blood pressure, triglycerides, C-peptide, prevalence of hypertension and dyslipidemia, and with a decrease in age, duration of diabetes and HDL-cholesterol values. In spite of an apparently worse cardiovascular risk profile, females showed a 50% lower prevalence of CAD than males and the prevalence of CAD was not significantly different in obese compared to other BMI categories. Multiple logistic regression showed that risk factors for CAD were different in males and females and similar in the lower tertiles of BMI, while different in the highest. In obese females, risk factors for CAD were age, reduced HDL-cholesterol and increased HbA(1c) levels; in males they were years of smoking and duration of diabetes. These data suggest that in type 2 diabetes, risk factors for CAD are different in the two sexes and in patients with the highest BMI compared to the normal and overweight subjects; blood glucose control and duration of diabetes seem more important than conventional cardiovascular risk factors in obese patients.
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PMID:Sex- and BMI-related differences in risk factors for coronary artery disease in patients with type 2 diabetes mellitus. 1066 19

The aim of the present cross-sectional angiographic study was to examine if there is a relationship between the severity of CAD and postprandial lipemia in patients with type 2 diabetes mellitus. Special emphasis was directed to determining the contribution of apolipoprotein B-48 (apoB-48)-containing and B-100 (apoB-100)-containing triglyceride-rich particles to the magnitude of postprandial lipemia and degree of CAD. The role of apolipoprotein E (apoE) phenotype as a modulator of postprandial lipemia was also evaluated. The severity of CAD was determined by a quantitative coronary angiography and the subjects were classified into two groups based on the presence (severe CAD) or absence (mild CAD) of at least 50% stenosis in a major coronary vessel. The study population consisted of 43 subjects (31 men and 12 women) with fair glycemic control and comparable fasting lipids and body mass index. Postprandial responses of TG, apoB-48 and apoB-100 in lipoprotein subfractions (chylomicrons, VLDL1, VLDL2 and IDL) were determined after a fat load. Type 2 diabetic patients exhibited the classical dyslipidemia of the insulin resistance syndrome and delayed clearance of both hepatic and intestinal particles. Fasting or postprandial lipid or lipoprotein measurements, including apoB-48 and apoB-100 concentrations, did not differ between the groups. The presence or absence of apoE-4 allele did not significantly influence postprandial lipemia. The severity of the most significant coronary stenosis in angiography correlated with plasma and with chylomicron area under curve (AUC) for TG (n=27) and chylomicron AUC for apoB-48 (n=20). The strongest correlate of maximal stenosis was area under incremental curve (AUIC) for apoB-100 in IDL fraction (r=0.548, P=0. 012, n=20). In conclusion, postprandial apoB-48 and apoB-100 metabolism in triglyceride rich lipoproteins is distorted in type 2 diabetic patients, even in those with only mild CAD. The data suggest that postprandial change in small remnant particle numbers may contribute to the severity of CAD in type 2 diabetes.
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PMID:Postprandial metabolism of apolipoprotein B-48- and B-100-containing particles in type 2 diabetes mellitus: relations to angiographically verified severity of coronary artery disease. 1078 48

The authors report a case of hypoglycemia in a subject with NIDDM and CAD. The clinical syndrome, which was diagnosed as an induced form for a long time, was found to be spontaneous and caused by metastasised kidney neoplasm. This led to considerable problems of differentiated diagnosis owing to the concomitance of diabetes and vascular pathology. An adequate assessment of the clinical findings and the instrumental and biohumoral tests would have enabled a more rapid diagnosis, thus allowing a correct therapeutic approach to be adopted.
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PMID:[Diabetes mellitus and spontaneous hypoglycemia. Report of a clinical case with extrainsular neoplasm]. 1103 35

Up to 80% of diabetic patients die of macrovascular complications, including CAD, stroke, and peripheral vascular disease. Because of the growing numbers of diabetic patients and the increased mortality after their first cardiovascular event, it is critical to identify and treat risk factors early and aggressively in these patients. Numerous studies in patients with type 2 diabetes have shown the benefits of aggressive treatment of blood pressure and lipids to levels that 10 years ago would have seemed abnormally low. The downward changes in "normal" limits can be frustrating to primary care physicians, but advances in treatment are redefining "normal" levels required to avoid complications in this high-risk population.
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PMID:Reducing cardiovascular risk in diabetes. Which factors to modify first? 1131 67


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