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Showing papers by "K. G. M. M. Alberti published in 1994"


Journal ArticleDOI
TL;DR: Management of NIDDM requires, of the doctor and the diabetes health care team, comprehensive knowledge and time, and two-way collaboration with the diabetic person, as well as smoking, infections, drug interactions and the side-effects of therapy.
Abstract: NIDDM is common. It may begin without symptoms. Prevalence increases with age, obesity, dyslipoproteinaemia and a positive family history of diabetes. It is strongly associated with cardiovascular disease and hypertension. It is vital to consider not only glucose metabolism but also other parts of the metabolic syndrome (obesity, hypertension, lipid disorders, cardiovascular diseases) as well as smoking, infections, drug interactions and the side-effects of therapy. Management of NIDDM requires, of the doctor and the diabetes health care team, comprehensive knowledge and time, and two-way collaboration with the diabetic person. The impact of NIDDM on quality of life, long-term complications and mortality should be considered. Self-monitoring is important both in management and in education; it improves the quality and safety of therapy. Objectives and priorities of treatment must be tailored to the individual; particular care must be taken to avoid overtreatment in the elderly. General Goals for People with Diabetes.

108 citations


Journal ArticleDOI
TL;DR: Isoform mobility, the number of isoform bands expressed, and the presence of CAD were the three most important independent predictors of Lp(a) concentration (descending order).
Abstract: Lipoprotein(a) [Lp(a)] concentration and apolipoprotein(a) [apo(a)] isoforms (identified by sodium dodecyl sulfate-polyacrylamide gel electrophoresis [SDS-PAGE] and Western blotting) were determined in a group of 508 asymptomatic Caucasian members of the community and in 318 Caucasian patients with angiographically defined coronary artery disease (CAD). Conventional risk factors for CAD were also measured. Lp(a) concentration was almost twice as high in subjects with CAD (geometric mean, 152 mg/L [geometric SD, 10 to 1398 mg/L]) as in asymptomatic control subjects (geometric mean, 84 mg/L [geometric SD, 21 to 334 mg/L]). Asymptomatic women had higher concentrations of Lp(a) than asymptomatic men. Patients with CAD were older and were more likely to have smoked and to have a first-degree relative with premature CAD (< 55 years of age), and a higher proportion were male. Patients with CAD had higher concentrations of Lp(a) independently of the number of isoform bands expressed. When apo(a) isoforms were allocated to 1 of 10 classes on the basis of their molecular size (Rf versus apoB in SDS-PAGE), patients with CAD did not express an excess of low-molecular-mass (higher concentration) isoforms but did express a higher proportion of double-band phenotypes with fewer "null" phenotypes. The relationship between the two isoform bands in a double-band phenotype was the same in both populations. Isoform mobility was defined as a continuous variable equal to the mobility of a single isoform band (single-band phenotypes) or the mean of the two isoforms in a double-band phenotype. Two variables, isoform mobility and the number of isoform bands expressed, were used to summarize the large range of isoform patterns (at least 45) that could be identified. Isoform mobility, the number of isoform bands expressed, and the presence of CAD were the three most important independent predictors of Lp(a) concentration (descending order). Only sex and LDL cholesterol were additional independent predictors of Lp(a) concentration in step-wise regression models including a wide range of demographic factors and lipid and glycemic risk factors. We conclude that Lp(a) concentration is associated with CAD independently of the isoform pattern expressed. The apo(a) gene locus exerts a strong control over circulating Lp(a) concentration, and a better understanding of the control of expression of the apo(a) gene will be essential to understand the relationship between Lp(a) and CAD.

49 citations


Journal ArticleDOI
TL;DR: Circulating insulin levels in themselves have been reported to influence the counter‐regulatory hormone response to hypoglycaemia in man and the effect of insulin on a specific aspect of this response was examined during euglycaemia by stimulating the pituitary‐adrenal axis with human corticotrophin‐releasing hormone.
Abstract: Summary OBJECTIVE Circulating insulin levels in themselves have been reported to influence the counter-regulatory hormone response to hypoglycaemia in man. The effect of insulin on a specific aspect of this response was examined during euglycaemia by stimulating the pituitary-adrenal axis with human corticotrophin-releasing hormone (CRH). SUBJECTS Eight healthy males. DESIGN Following an overnight fast, insulin was infused at 15 (low) and 60 (high) mU/kg/h from 0900 h for 180 minutes on separate occasions in random order. On each occasion, blood glucose was clamped at euglycaemia, and 1 μ/kg/kg (i.v. bolus) human CRH was administered at 120 minutes. MEASUREMENTS Circulating hormone concentrations were determined by radioimmunoassay. Peak Cortisol and ACTH responses were compared for the two study conditions. RESULTS Mean serum insulin levels were threefold higher during the high compared with the low insulin infusion (mean difference 320 pmol/l, 95% confidence interval (CI) 150-490, P<0001). Blood glucose levels during the clamps were comparable (mean difference 0 15 mmol/l, 95% CI 0-0.63). Plasma Cortisol levels increased following CRH, although the peak concentration was significantly lower during the high insulin infusion (mean difference 36 nmol/l, CI 0-110, P< 0.02). However, peak ACTH levels were comparable for the two insulin levels (mean difference 8 ng/l (1.8 pmol/l), CI 0-50). CONCLUSIONS The peak Cortisol response to CRH was diminished at the higher circulating insulin levels. This was not dependent upon concurrent hypoglycaemia and did not appear to be mediated at the level of the pituitary gland.

15 citations


Journal ArticleDOI
TL;DR: The group treated with metoprolol showed a significant rise in fasting insulin after 6 months with no change in PAI-1, suggesting that the previously described link between these two may not be causal.
Abstract: This double-blind, randomized parallel group study investigated the effect of 6 months β-adrenoceptor antagonist therapy with either metoprolol (β1-selective without intrinsic sympathomimetic activity [ISA]) or epanolol (β1-selective with ISA) on markers of endogenous fibrinolysis in 20 patients with chronic stable angina receiving concurrent treatment with nifedipine.

10 citations


Journal ArticleDOI
K Azad1, S Court1, J M Parkin1, M F Laker1, K. G. M. M. Alberti1 
TL;DR: Triglycerides rose and HDL cholesterol fell following feeding and inconsistent effects were seen on apoA-I and apoB, the distribution of all data was consistent with Gaussian apart from triglycerides which was log normal.
Abstract: Serum total cholesterol, high-density lipoprotein (HDL) cholesterol, triglyceride, apolipoprotein (apo) A-I and apoB concentrations were estimated and low-density lipoprotein (LDL) cholesterol levels were calculated in 132 children aged 11.4-17.3 years. The effect of feeding was investigated by estimating postprandial values and also by studying the effects of a test meal. The distribution of all data was consistent with Gaussian apart from triglycerides which was log normal. Overall fasting values were [mean (standard deviation; SD)] cholesterol 4.5 (0.8) mmol/L, HDL cholesterol 1.5 (0.4) mmol/L, LDL cholesterol 2.6 (0.8) mmol/L, apoA-I 1.5 (0.3) g/L, apoB 1.0 (0.4) g/L and triglycerides 0.76 (0.38-1.51) mmol/L, the values for triglycerides being mean (95% confidence intervals). Girls had higher triglycerides than boys [0.82 (0.43-1.54) versus 0.70 (0.36-1.33)] and different effects of age on lipids were found, HDL cholesterol being negatively correlated with age in boys (r = -0.37; P < 0.001), but not in girls, and apoA-I being negatively correlated with age in boys (r = -0.31; P = 0.006), but positively correlated with age in girls (r = 0.32; P = 0.008). Triglycerides rose and HDL cholesterol fell following feeding and inconsistent effects were seen on apoA-I and apoB.

7 citations