Diabete & metabolisme最新文献

Glomerular hyperfiltration is a candidate marker for diabetic nephropathy in insulin-dependent diabetic patients since it can reflect elevated glomerular capillary pressure, a cause of glomerulosclerosis. We studied the potential contribution of several dietary components to glomerular hyperfiltration during a cross-sectional study of 110 consecutive normotensive, non-proteinuric insulin-dependent patients with respect to glomerular filtration rate (GFR) and food intake. GFR was measured using the 51Cr-EDTA plasma disappearance technique. Glomerular hyperfiltration was defined as GFR > 137 ml.min-1 1.73 m-2 (mean +2 SD of age-matched healthy controls). Food intake was recorded with a computer-assisted programme. Thirteen patients displaying glomerular hyperfiltration ingested more protein (1.60 +/- 37 vs 1.38 +/- 0.34 g.kg-1 body weight.day-1; p = 0.032) and more fat (1.70 +/- 0.54 vs 1.39 +/- 0.44 g.kg-1 body weight.day-1; p = 0.022) than other subjects, although their total energy intakes were similar. Univariate regression analysis showed that GFR was positively related to both protein (r = 0.28; p = 0.003) and fat (r = 0.25; p = 0.007) intakes and negatively related to age (r = -0.29; p = 0.002). Stepwise multivariate regression analysis indicated 2 independent determinants for GFR: age (F = 15.26) and fat intake (F = 13.15). Excess fat intake may contribute to glomerular hyperfiltration in insulin-dependent diabetes.

This review examines the association between retroviruses and diabetes in the mouse model, the role of retroviruses in the pathogenesis of Type 1 diabetes and the mechanisms by which retroviruses can induce an autoimmune reaction. Three putative mechanisms are considered: the expression of retroviral protein(s) on the beta-cell surface as the first step in immune response against beta cells; the homology of a retroviral product with a self antigen inducing a cross-reacting autoimmune response (molecular mimicry); and a retroviral product showing homology with interleukin-2 and inducing T-cell activation against beta-cell antigens and loss of tolerance. These findings are discussed for their possible implications in the pathogenesis of human Type 1 diabetes.

The aim of the present study was to assess the possible modifications in the parameters of red cell aggregation and blood and plasma viscosity in 92 diabetic patients compared to 82 non diabetic control subjects. Based on the presence of microalbuminuria (> 30 mg/24 h) and/or retinopathy each group of diabetic patients was divided into two subgroups. This study shows increased red cell aggregation and blood viscosity among diabetic patients with microangiopathy. There was a very good correlation between fibrinogen level and the different rheological measurements. The results of this study confirm the importance of the blood rheology abnormalities observable in diabetes. These disorders increase peripheral vascular resistances and ischemia and therefore worsen diabetic nephropathy and retinopathy.

This is the second a series of three articles which reviews the identification of risk factors of a disease, here: diabetes or complications of diabetes. In the first of the series [1], we gave the definition of a risk factor, along with measures of its force-relative risk and odds ratio, followed by the epidemiological definitions of the diseases: diabetes, coronary heart disease and hypertension. Risk factors were further discussed and we completed the discussion by some observations on the bias which can arise from a study or from its analysis, which can lead the researcher to the wrong conclusion. In this second article we define the three types of epidemiological studies which are used to determine whether factors are associated with a disease: observational or cross-sectional studies, cohort studies and casecohort studies. Examples are provided of each of these study types; their advantages and disadvantages are discussed. The final paper will provide some examples of the identification of risk factors from the literature. The first example involves diabetes and pancreatic cancer, the second birth weight and non-insulin dependent diabetes. Having found an association between a risk factor and diabetes, we will discuss whether it can be considered to be a risk factor, and if so whether it is likely to be a cause of the disease.

The efficacy of the new intestinal alpha-glucosidase inhibitor, miglitol, and glibenclamide were compared in a 6-month double-blind controlled protocol involving 100 non-insulin dependent diabetic patients under diet alone. HbA1c levels (initially between 7 and 11%) were reduced (p < 0.05): -0.78 +/- 0.21% after miglitol and -1.18 +/- 0.20% after glibenclamide. The difference between the two treatments was not significant, although glibenclamide appeared to be more active than miglitol at 8 (p = 0.002) and 16 weeks (p = 0.01) but not at 24 weeks. Fasting glycaemia decreased after miglitol (8.7 +/- 0.3 vs 9.6 +/- 0.3 mmol/l, p = 0.005) and after glibenclamide (8.0 +/- 0.3 vs 9.1 +/- 0.3, p = 0.007). After miglitol, a decrease was noted after breakfast (p < 0.001) and lunch (p < 0.001). The same was true for glibenclamide (p = 0.004 and p < 0.001 respectively). A significant reduction in glucose incremental area during a standard meal test was noted at the end of miglitol (p = 0.008) or glibenclamide treatment (p = 0.04). Subgroups of nonresponders to both treatments were identified (10/49 with miglitol, 9/47 with glibenclamide). Side effects were recorded in 10 patients treated with miglitol (flatulence and meteorism, diarrhoea, 1 discontinued therapy) and in 10 treated with glibenclamide (asthenia, sensation of hunger). This study indicates that miglitol is suitable for initial application in diet-resistant Type 2 diabetic patients, providing, a persistent effect and acceptable side effects.

Lipoprotein abnormalities [mainly high levels of very-low-density lipoprotein triglycerides (TG) and low levels of high-density lipoprotein cholesterol] increase the risk of cardiovascular disease in Type 2 diabetic patients. Moreover, only fasting TG and central obesity appear to independently predict mortality from CAD in glucose-intolerant and diabetic subjects. It is noteworthy that fasting lipid levels in these patients are often relatively unaffected, and that plasma TG may remain < 2 g/l, the cutoff point currently considered to define moderate hypertriglyceridemia. Our study of postprandial lipaemia shows that lipid intolerance (a greater increase of postprandial TG and a slower return towards basal levels) was almost always present in these patients, enabling us to detect atherogenic changes in plasma lipoproteins. Preliminary results indicate that fenofibrate treatment in Type 2 diabetes under optimised metabolic control improves not only fasting lipid levels but also postprandial lipaemia and associated abnormalities in lipoprotein levels and composition.

Numerous studies show increasing evidences that a low post-prandial triglyceride metabolic capacity is likely to favour cardio-vascular disease, particularly coronary and cerebro-vascular atherosclerosis. Because of high fasting triglycerides, low HDL and high LDL3 lipid profile, abdominal obesity and insulin-resistance, Type 2 diabetic patients are candidates to altered post-prandial lipemia. However many practical and methodological difficulties remain concerning the nature, lipid quantity and composition of the lipid load, the choice of accurate markers of liver derived lipoproteins, pointing out the urgent need for a standardization procedure.