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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherosclerotic changes have not been demonstrated directly in asymptomatic hyperglycaemic non-diabetic subjects, although high mortality due to coronary heart disease has been reported. We measured arterial wall thickness non-invasively, in order to directly demonstrate atherosclerosis of the carotid arteries of hyperglycaemic non-diabetic subjects and to evaluate its risk factors. The thicknesses of the intimal plus medial complex (IMT) of the carotid arteries of 112 asymptomatic hyperglycaemic non-diabetic subjects (aged 22-81, 95 males and 17 females) were compared with those of 55 healthy male subjects and 211 non-insulin-dependent NIDDM male diabetic patients. The subjects were subgrouped into impaired glucose-tolerant (IGT) subjects who had a 2-h glycaemic level of more than 7.8 mmol/l, and non-IGT subjects whose 2-h glycaemic levels were within 6.7-7.7 mmol/l. Non-IGT and IGT subjects showed significantly greater IMTs than age-matched healthy males and showed no significant differences compared to age-matched NIDDM patients. Multivariate analysis demonstrated that the risk factors for IMT of non-IGT and IGT subjects were age and systolic blood pressure. According to data on the accumulation of atherogenic risks (hypertension, dyslipidaemia, and smoking), IMT increased linearly in non-IGT and IGT subjects. However, non-IGT and IGT subjects without hyperlipidaemia, hypertension, or smoking risk still had significantly greater IMT than age-matched normal males (1.019 +/- 0.063 vs 0.770 +/- 0.111 mm, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Asymptomatic hyperglycaemia is associated with increased intimal plus medial thickness of the carotid artery. 748 42

Many models of diabetes dyslipidemia are available. Animals with chemically-induced diabetes have been used to study insulin-dependent diabetes. Hypercholesterolemia in streptozotocin-induced diabetes in rats results from increased intestinal absorption and synthesis of cholesterol. Lipoproteins from diabetic rats are oxidized and demonstrate cytotoxicity, a feature which can be prevented by insulin or antioxidant treatment. Diabetic rabbits fed a cholesterol-rich diet do not develop atherosclerotic lesions because accumulated VLDL are apo E-depleted, too large and do not enter into the arterial wall. Models for non-insulin-dependent diabetes (NIDDM) are obtained through selective breeding or dietary conditions. The obese Zucker rat (fa/fa) is characterized by hyperphagy, hyperglycaemia, hyperinsulinemia, insulin-resistance, hypertriglyceridemia and hypercholesteolemia. It responds to dietary, hormonal and drug treatments, but does not develop atherosclerosis spontaneously. It is used as a model for obesity, NIDDM and type IV hyperlipidemia. The JCR:LA cp rat bears the corpulent gene and develops similar characteristics to those of the Zucker rat. However, insulin-resistance is more severe in homozygous males (cp/cp), and cardiovascular lesions are observed. Their appearance is reduced by treatments which decrease hyperinsulinemia and insulin resistance but not by lowering lipid levels alone. The sand rats (Psammomys obesus) develop obesity and NIDDM when fed a laboratory diet. When cholesterol and anti-thyroid drug are added to the diet, they develop cardiovascular lesions. This species constitutes a new model for studying atherosclerosis-related diabetes.
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PMID:Dyslipidemia and diabetes: animal models. 762 69

Insulin resistance and hyperinsulinemia are characteristic features not only of obesity and NIDDM, but are associated with the development of hypertension, hyperlipidemia, and atherosclerosis. DeFronzo et al has used the analogy that insulin resistance can be viewed as a large iceberg submerged just below the water. The physician recognizes only the tips of the iceberg--obesity, diabetes, hypertension, hypertriglyceridemia and low-HDL cholesterol, and atherosclerosis--which protrude above the surface, while the complete insulin-resistance syndrome may be missed. With the recognition that insulin resistance consists of a cluster of nutritional causes and biochemical abnormalities, it is important for the various subspecialties to work together closely to define the mechanism(s) responsible for the defects in insulin-mediated glucose metabolism and to discover effective strategies for prevention and treatment.
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PMID:Diabesity: the deadly pentad disease. 785 Dec 30

We studied risk factors and the relationship of lacunes to diabetes mellitus, age, hypertension, hyperlipidemia, atherosclerosis and also to intellectual impairment, comparing brain MRI (magnetic resonance imaging) findings to the multiple risk factors and the results of a cube-handdrawing test. Brain MRI was performed using a Shimazu SMT-150, 1.5 Tesla, in 118 asymptomatic NIDDM and 39 asymptomatic nondiabetic patients. In diabetics, 65 had lacunes and the incidence of lacunes was significantly higher in diabetics with coronary insufficiency by ECG and hypertension, but not significantly different in those with or without the other risk factors. Cube hand-drawing is a good indication of space cognition ability supported by the wide association areas of the brain. Drawing was tested in 41 diabetics and 39 nondiabetics. Correlation of lacunes to deformity in drawing and age was high in both diabetics and nondiabetics. Multiple lacunes were closely related to intellectual impairment.
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PMID:Asymptomatic lacunes and their relationship to intellectual disturbances. 791 15

In order to identify previously undiagnosed cases of non-insulin dependent diabetes (NIDDM) in general practice, we measured non-fasting blood-glucose in all risk patients (n = 1,790) between 35-69 years old belonging to 29 general practices in Kolding. Patients at risk for NIDDM were defined as those suffering from one or more of the following: overweight, arterial hypertension, coronary heart disease, hyperlipidaemia, stroke, gout, cataract, Dupuytren's contracture, peripheral atherosclerosis or recurrent urinary- or skin-infections. A positive result, defined as a non-fasting blood-glucose of > or = 8.0 mmol/l using the same stix-lot-nr. on Refloflux S machines, was found in 86 individuals. These were then followed up with two fasting blood-glucose measurements carried out in a central laboratory, whereby 34 patients with NIDDM were identified. The newly-diagnosed NIDDM patients mostly suffered from diseases related to the insulin resistance syndrome, and we thus recommend measurement of non-fasting blood-glucose as a screening procedure in such patients. When carrying out measurements in general practice, it is important to know the precision and accuracy of the apparatus used.
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PMID:[Selective screening for non-insulin-dependent diabetes mellitus. A study among 35-69 year-old patients at risk in general practice in Kolding]. 801 51

We studied the prevalence of non-insulin dependent diabetes (NIDDM) and hyperlipemia in older than 15 years old population in the city of San Luis Potosi and in a rural area 50 km north of this city. They are located in the state of San Luis Potosi in the central plateau of Mexico. A total of 1136 subjects were surveyed (645 males, 491 females). Weight and height were measured and the body mass index (BMI) calculated in all subjects. After a fasting capillary sample was obtained, 75 g of glucose were given and a second sample was taken 120 minutes later. The WHO recommendations for diagnosis of DM were used. The overall prevalence of DM was 10.0%: the lowest rate was for individuals in the rural area (0.9%) which contrasts with the 11% seen in the urban population (p 0.0001). In the urban subjects, the highest rates were observed in the very low income group (27.7%) whereas the low income group had a rate of 6.2%; the prevalence was 7.0, 7.7 and 18.2% in the medium, high medium and high socioeconomic groups. The prevalence was influenced by age, BMI, sex (males = 6.8% females = 14.3%) and socioeconomic status; hypercholesterolemia (> 200 mg/dL) was found in 16%. In conclusion, we have documented high rates of NIDDM in a mexican urban population with very high levels in the very poor which contrasts with the rural population.
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PMID:[Prevalences of diabetes, glucose intolerance, hyperlipemia and risk factors as a function of socioeconomic level]. 807 61

Lipoprotein composition was determined using ultracentrifugation in 20 non-insulin-dependent (NIDDM) diabetic patients on diet only (D), 20 NIDDM patients on diet and sulfonylurea therapy (T), and 20 nondiabetic control subjects (C), all of whom had total plasma cholesterol concentrations < 6.5 mmol/L and total plasma triglyceride concentrations < 3.0 mmol/L. Although the groups were well matched for age, body mass index, total triglyceride levels, and total cholesterol concentrations, there were significant compositional abnormalities in the low-density lipoprotein (LDL) fractions of diabetic subjects. The LDL total lipid to apolipoprotein B weight ratio (representing the density distributions of LDL particles) was reduced in both diabetic groups: 3.75 +/- 0.3, 3.50 +/- 0.28, and 3.54 +/- 0.22 in C, D, and T groups, respectively (mean +/- SD; P < .05). This was associated with a significant shift in the hydrated density distributions of LDL in the diabetic groups, with the average peak densities being 1.0320 g/mL (in C), 1.0365 g/mL (in D), and 1.0380 g/mL (in T) (P < .05). The LDL particles were also smaller in the NIDDM patients: 21.1 +/- 0.7, 20.4 +/- 0.5, and 20.6 +/- 0.5 nm in C, D, and T groups, respectively (P < .05). When the NIDDM groups were analyzed together, the LDL peak density was found to correlate with both insulin resistance (measured by a modified Harano technique; r = 0.37, P < .015) and total triglyceride concentrations (r = 0.40, P < .01). The results show that diabetic patients have small, dense LDL particles, which may be related to insulin resistance, and that these occur with minimal elevations of total triglyceride concentrations. These potentially atherogenic changes may contribute to the increased coronary heart disease in diabetic patients with mild hyperlipidemia.
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PMID:Lipoprotein compositional abnormalities and insulin resistance in type II diabetic patients with mild hyperlipidemia. 831 6

A proband with chylomicronemia, pancreatitis, and non-insulin-dependent diabetes (NIDDM) bears two different mutations in exon 3 of the lipoprotein lipase (LPL) gene: a missense mutation, 75Arg-->Ser, inherited through the paternal line and a truncation, 73Tyr-->Ter, through the maternal line. NIDDM appeared to be independently segregating. The R75S mutant was studied in extracts and media from transfected COS-1 cells. Detectable amounts of catalytically competent R75S LPL suggested destabilization of the active homodimer as with exon 5 mutants (Hata et al. 1992. J. Biol. Chem. 267:20132-20139). Hydrolysis of a short-chain fatty acid ester indicated that R75S does not directly affect activation of LPL by apoC-II. Subjects with NIDDM and wild-type LPL, and nondiabetic middle-aged carriers of the 73Tyr-->Ter truncation had moderate hypertriglyceridemia (260-521 mg/dl) and reduced high density lipoprotein cholesterol. A maternal aunt with NIDDM carried the truncation. Her phenotype (triglycerides of 5,300 mg/dl, eruptive xanthomatosis, and recurrent pancreatitis) was as severe as that in homozygotes or compound heterozygotes. We conclude: (a) diabetic carriers of dysfunctional LPL alleles are at risk for severe lipemia; and (b) the physiologic defects in NIDDM may be additive or synergistic with heterozygous LPL deficiency.
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PMID:Mutations in exon 3 of the lipoprotein lipase gene segregating in a family with hypertriglyceridemia, pancreatitis, and non-insulin-dependent diabetes. 832 86

Non-insulin-dependent diabetes (NIDDM) is a common multimetabolic disorder with potential (and potentially severe) long-term complications affecting large and small blood vessels. Where microvascular complications (retinopathy, nephropathy and neuropathy) are concerned, the Diabetes Control and Complications Trial (DCCT), as well as much circumstantial evidence, suggests that hyperglycaemia is the main aetiological factor and this is likely to apply in NIDDM as well as IDDM. Unfortunately, achieving normoglycaemia in NIDDM is not easy and it is unclear whether insulin has advantages over oral hypoglycaemic agents or vice versa. Turning to macrovascular disease, it is unclear which of the many potentially atherogenic abnormalities-hypertension, hyperinsulinaemia, hyperlipidaemia, etc-are most important. A further problem is that macrovascular disease is already well developed in many patients when NIDDM is diagnosed and we do not know whether secondary prevention is effective. Nevertheless, it is sensible to try to reverse the atherogenic milieu and this should be done in the first instance by lifestyle modification rather than drugs. Even if we cannot manipulate the biochemistry to prevent small or large vessel complications, much can still be done; proactive foot care can prevent ulceration, timely laser treatment can prevent visual loss and thrombolytic therapy is relatively more effective in diabetic patients with myocardial infarction than in their non-diabetic peers. Finally, patients with NIDDM need intensive education and each needs an individualised treatment plan and goals.
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PMID:Targets of therapy for NIDDM. 852 19

Insulin resistance appears to be central to obesity, NIDDM, hyperlipidemia, and cardiovascular disease. While obese women with abdominal (android) fat distribution are more insulin resistant than those with peripheral (gynecoid) obesity, in nonobese women, the relationship between abdominal fat and insulin resistance is unknown. By measuring regional adiposity with dual-energy X-ray absorptiometry and insulin sensitivity by euglycemic-hyperinsulinemic clamp in 22 healthy women, with a mean +/- SE body BMI of 26.7 +/- 0.9 kg/m2 and differing risk factors for NIDDM, we found a strong negative relationship between central abdominal (intra-abdominal plus abdominal subcutaneous) fat and whole-body insulin sensitivity (r = -0.89, P < 0.0001) and nonoxidative glucose disposal (r = -0.77, P < 0.001), independent of total adiposity, family history of NIDDM, and past gestational diabetes. There was a large variation in insulin sensitivity, with a similar variation in central fat, even in those whose BMI was <25 kg/m2. Abdominal fat had a significantly stronger relationship with insulin sensitivity than peripheral nonabdominal fat (r2 = 0.79 vs. 0.44), and higher levels were associated with increased fasting nonesterified fatty acids, lipid oxidation, and hepatic glucose output. Because 79% of the variance in insulin sensitivity in this heterogeneous population was accounted for by central fat, abdominal adiposity appears to be a strong marker and may be a major determinant of insulin resistance in women.
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PMID:Abdominal fat and insulin resistance in normal and overweight women: Direct measurements reveal a strong relationship in subjects at both low and high risk of NIDDM. 862 Oct 15


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