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Resting energy expenditure (REE) is believed to be increased in type 2 diabetes, an increase that is associated with deteriorating glucose tolerance during its development. Meanwhile, insulin resistance, a state linked to obesity and observed in all type 2 diabetic patients, is associated with reduced REE. Our aim was to compare REE in obese patients with and without diabetes. REE, body composition (total body water, density, percentage fat and fat-free mass: 3-compartment model) and metabolic control were assessed in fifty obese Caucasian patients with diabetes (glycated haemoglobin level 7.6 (SD 1.5) %) and fifty obese patients who were non-diabetic. Despite being more overweight and younger, obese non-diabetic patients had an absolute REE (7.73 (SD 1.44) v. 8.12 (SD 1.37) MJ; P=0.17) and percentage fat-free mass similar to those of obese diabetic patients. Even when adjusted for differences in body composition, REE remained similar in both groups. Furthermore, REE (absolute and adjusted) was unaffected by both glucose level and control (glycated haemoglobin), with fat-free mass being the only determinant of REE. We conclude that REE is not necessarily increased by the presence of diabetes in obese people.

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Insulin use is common in type 2 diabetes and is frequently accompanied by weight gain, the composition of which is poorly understood. The present study evaluates insulin-induced body composition changes. Body weight and composition of thirty-two type 2 diabetic patients undergoing their first 12 months of insulin therapy were compared with those observed in thirty-two type 2 diabetic patients previously treated on insulin (minimum 1 year). Body composition was determined by simultaneous body water spaces (bioelectrical impedance analysis) and body density measurements. After 6 months, glycosylated Hb (HbA1c) significantly improved in the newly treated group (P<0.0001), but remained stable in those treated previously. HbA1c did not differ between 6 and 12 months in the two groups. Body weight significantly (P=0.04) changed over 12 months in those newly treated only (+2.8 kg), essentially comprising fat-free mass (P=0.044). Fat mass remained unchanged (P=0.85) as did total body water, while extracellular: total body water ratio tended to increase in those newly treated (P=0.059). Weight changes correlated with HbA1c changes (R2 0.134, P=0.002) in the initial 6 months only. Insulin therapy leads to weight gain (2.8 kg), predominantly fat-free mass, over 12 months. After 6 months, newly treated patients continued gaining weight despite an unchanged HbA1c, suggesting the potential anabolic role of insulin in subsequent gains. Therefore, in the initial 6 months, weight gain can be attributed to a 'glucose control-related effect' and further gain appears to be due to a 'non-glucose control-related' effect of insulin treatment.

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OBJECTIVE: Insulin is used commonly in Type 2 diabetes and is often accompanied by weight gain. The composition of this weight gain is poorly understood. Predominant increases in fat mass could increase cardiovascular risks. The aim of the study was to evaluate insulin-induced body composition changes. RESEARCH DESIGN AND METHODS: Body weight and composition of 35 Type 2 diabetic patients during their first 6 months of insulin therapy was compared with those in 34 Type 2 diabetic individuals treated with insulin for at least 1 year prior to commencing the study. Body composition was determined by the simultaneous measurement of body water spaces and body density. RESULTS: Over 6 months, glycaemic control improved in the new treatment group only (HbA(1c): 7.26 +/- 0.81 vs. 9.66 +/- 1.60%; P < 0.0001), remaining stable in the previously treated group (7.67 +/- 1.25 vs. 7.76 +/- 1.26%; P = NS). Weight significantly increased over time in the newly treated group (+1.7 kg; P = 0.04), but not in the previously treated group (-0.3 kg). It comprised of both fat (+0.85 kg) and fat-free mass (+0.55 kg). Total body water remained unchanged. Using bioelectrical impedance analysis, the gain in fat mass was +2.2 kg; P = 0.048. CONCLUSIONS: Over 6 months, insulin therapy leads to a weight gain of 1.7 kg because of an increase in both fat and fat-free mass. When body composition is determined by bioelectrical impedance analysis, the results are biased by fluctuations in hydration.

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The position statement about diabetic retinopathy postulates that at least 3-5 years of duration of diabetes are needed for the retinopathy to occur, and initial retinal examination should be performed within 3-5 years after the initial diagnosis. We report here the case of a 18 year-old type 1 diabetic woman with a proliferative retinopathy discovered 2 years after the onset of a clinical diabetes. The hypothesis of a Latent Autoimmun Diabetes in Adults (LADA) could not be excluded and we propose, particularly in this context, to detect a diabetic retinopathy at the onset of diabetes.

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UNLABELLED: THEORY AND REALITY: Diabetes mellitus is known to be associated with excess cardiovascular risk. Prescription of antiplatelet agents such as acetylsalicylic acid would thus appear to be warranted. That is the theory, but the reality is much different. A review of the literature provides evidence on the use of acetylsalicylic acid for primary and secondary preventive care, but conclusions are often extrapolated from studies conducted in the general population. EVIDENCE OF A BENEFICIAL EFFECT IN DIABETICS: The HOT study, conducted in hypertensive patients) demonstrated that acetylsalicylic acid at the dose of 75 mg a day, reduced the rate of major cardiovascular events by 15% (p = 0.03) and of myocardial infarction by 36% (p = 0.02) with no effect on stroke. In diabetic patients (n = 1500), the benefit was even more pronounced. RISKS: The risk of bleeding must be balanced against the beneficial cardiovascular effect. Diabetic retinopathy is not aggravated by aspirin. The data reported in the literature do not however enable any evidenced-based decision on dosing for the diabetic population with numerous cardiovascular risks.

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Coronary Risk Profile (CRP), assessed according to the Framingham equation takes the presence of diabetes into account, but not the glycaemic control or the body overweight. We have performed an observational survey to study the respective roles of changes in body weight or glycaemic control on calculated CRP, in a given subject, by an effect on several items of the CRP equation (systolic blood pressure, total and HDL cholesterol) which can be modified by blood glucose or weight. We have studied the CRP of 179 type 1 and 208 type 2 diabetes patients, admitted in the department of diabetology of the Angers Hospital, twice (interval < 3 years; 1.6 +/- 0.8 yr). The patients yielded no coronary heart disease, their age ranged from 30 to 74 yr (mean +/- SD: 53 +/- 13), they were not on antihypertensive or lipid lowering medication. Glycaemic control was assessed by glyco-haemoglobin (HbA1c), systolic blood pressure (SBP) was measured with an automatic device (Dinamap). Total and HDL cholesterol were determined by an enzymatic method, in fasting patients. Only age at first examination was taken into account to compute CRP. Initially, SBP was 131 +/- 17 mmHg, total and HDL cholesterol were 2.20 +/- 0.47 et 0.56 +/- 0.20 g/L, respectively. SBP was positively correlated with body weight (Rho = 0.310; p < 0.0001), but not with HbA1c. Median 5 yr CRP was 5% (range: < 1%-25%). Between both admissions, mean change in body weight, HbA1c and 5 yr CRP was +1.0 kg (range: -27 à +29), -0.2% (range: -4.5 à +7.6) et -0.01% (range: -10 à +13) respectively. Change in CRP between both admissions was associated with change in HbA1c (Rho = 0.109; p = 0.0315) but not in body weight (Rho = 0.072; p = 0.1588). This result was explained by the effect of the change in HbA1c on total cholesterol (Rho = 0.151; p = 0.003), (no effect on SBP or HDL cholesterol: Rho = 0.008 and Rho = 0.019; NS, respectively). These results suggest that, in diabetic patients, changes in glycaemic control affect their CRP by an effect on total cholesterol, but the changes in body weight do not affect their CRP.

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UNLABELLED: Hypertension and non-insulin-dependent diabetes mellitus (NIDDM) are two major risk factors for end-stage renal failure. The value of microalbuminuria (urinary albumin excretion [UAE]: 30-300 mg/24 h) as an indicator of the glomerular filtration rate (GFR) is not known in these patients. METHODS: The relationships between microalbuminuria and GFR in subjects with NIDDM and hypertension were studied cross-sectionally (Study I) and longitudinally (Study II). RESULTS: In study I, 205 NIDDM subjects with hypertension (151 with normoalbuminuria [UAE < 30 mg/24 h] and 54 with microalbuminuria) were studied. The GFR of subjects with normoalbuminuria (97 +/- 30 ml/min) (mean +/- SD), and microalbuminuria (97 +/- 27 ml/min; NS) were similar. Study II examined 51 of the subjects with normoalbuminuria and 21 with microalbuminuria 22 months (range 13-57) later. The GFR of subjects with microalbuminuria (-10 +/- 19 ml/min) declined more than in those with normoalbuminuria (+4 +/- 17 ml/min; Student's t-test: p = 0.0022). The predictive value of microalbuminuria for a drop in GFR was independent of the antihypertensive treatment used, the follow-up time, or changes in UAE. The only variable linked to GFR loss in subjects with microalbuminuria was an increase in diastolic blood pressure (p = 0.0298). CONCLUSION: Microalbuminuria is a risk factor for a drop in GRF in NIDDM subjects with hypertension, and a reduction in blood pressure is the only effective way to prevent a loss of GFR in subjects with microalbuminuria.

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BACKGROUND: Microalbuminuria, a marker of early renal damage, predicts mortality in non-diabetic subjects. The loss of circadian blood pressure regulation is associated with the severity of essential hypertension and has been reported in hypertension due to renal disease. We therefore looked for a possible link between microalbuminuria and the smaller decrease in nocturnal blood pressure that occurs in essential hypertension.METHODS: The 24 h ambulatory blood pressure of 52 subjects with essential hypertension was measured and their urine tested for microalbuminuria (urinary albumin excretion of 30-300 mg/24 h). RESULTS: The subjects with (n = 10) and without (n = 42) microalbuminuria were comparable in clinical characteristics, antihypertensive treatments and serum creatinine. They had significantly different night-time systolic, diastolic and mean blood pressure decreases on ambulatory blood pressure monitoring. Two-factor analysis of variance showed that the day-night blood pressure decrease was linked to microalbuminuria status. The day-night blood pressure change of subjects with microalbuminuria differed from that of subjects without microalbuminuria independently from the daytime blood pressure level. CONCLUSION: Subjects with essential hypertension and microalbuminuria show a loss of nocturnal blood pressure decline. Whether microalbuminuria indicates a subtype of essential hypertension due to renal disease or severe hypertension with early renal damage remains to be clarified.

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The aim of this study was to evaluate the circadian blood pressure variations in subjects with or without microalbuminuria (Urinary Albumin Excretion (UAE) between 30 and 300 mg/24 h. Forty-nine non-insulin dependent diabetic subjects with essential arterial hypertension and without proteinuria (UAE < 300 mg/24 h) were consecutively recruited. Systolic (SBP) and Diastolic Blood Pressure (DBP) have been measured using a SpaceLabs 90207 ambulatory blood pressure monitor, every 15 minutes during daytime (7:00 a.m. to 22:00 p.m.) and every 30 minutes during nighttime (22:00 p.m. 7:00 a.m.). UAE has been measured by nephelometry on three 24 h urine collections. The group with microalbuminuria (n = 16) was not different from the group with normoalbuminuria (n = 33) for age, sex ratio, body mass index, known diabetes duration, proportion of anti-hypertensive treatment, serum creatinine and HbA1c. Daytime blood pressures (SBP/DBP: 144 +/- 15/83 +/- 8 vs 137 +/- 13/84 +/- 9 mmHg) and nighttime DBP (75 +/- 7 vs 74 +/- 9 mmHg) were comparable between both groups. In contrast, the nighttime SBP was higher in subjects with microalbuminuria than in those without (139 +/- 17 vs 129 +/- 17 mmHg; p = 0.016). If dippers are the subjects with a nocturnal blood pressure reduction (SBP and/or DBP) below 4%, there is a relationship between "non dippler" subjects and those with microalbuminuria (Chi-squared test = 5.67; p = 0.017). In conclusion, hypertensive non-insulin dependent diabetic subjects with microalbuminuria have a loss of nocturnal blood pressure decrease.

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