Interest of cystatin C in screening diabetic patients for early impairment of renal function.

We compared cystatin C, creatinine, and the Cockroft formula for assessment of early renal failure, defined as a (51)Cr-EDTA clearance < 80 mL/min, in 89 diabetic patients with various degrees of renal impairment (glomerular filtration rate [GFR], 11.4 to 196.5 mL/min). The relationships between cystatin C, creatinine, and (51)Cr-EDTA clearance were linearized by plotting the reciprocals of the values, and correlation coefficients were determined. Sensitivity and specificity for the diagnosis of early renal failure were calculated from receiver operating characteristic (ROC) curves. Over the whole population, cystatin C was as well correlated with GFR (r =.74) as was creatinine (r =.67) or the Cockroft formula (r =.88). Moreover, its diagnostic accuracy was comparable to that of the 2 other parameters. Its sensitivity (86.8%) was better than that of creatinine (77.4%) for screening GFR < 80 mL/min, although the Cockroft formula was more sensitive (96.2%). The study of albuminuric diabetics (n = 63) led to similar conclusions, except for a poor sensitivity of cystatin C. In the 36 patients whose plasma creatinine was < 1 mg/dL, 10 (27.7%) had GFR < 80 mL/min. The correlation of creatinine with GFR, its diagnostic accuracy, and sensitivity were significantly lower than those of cystatin C. In this population of patients with normal creatinine levels, the correlation coefficient of cystatin C, its sensitivity, and its diagnostic accuracy were comparable to those of the Cockroft formula. A moderate reduction in GFR may be present in diabetic patients with low creatinine levels. Although Cockroft formula remains the most reliable and the less expensive tool for the evaluation of renal function, cystatin C is a more reliable criterion for screening and assessment than creatinine and represents a useful alternative to the Cockcroft-Gault formula.

Splanchnic tissues play a crucial role in uremic glucose intolerance.

OBJECTIVE: Determine the mechanism of glucose intolerance in chronically uremic subjects. DESIGN: Comparison of doubly labeled oral glucose tolerance tests. SUBJECTS: Seven nondialyzed chronically uremic subjects (creatinine, 420 +/- 104 micromol/L) and 7 healthy subjects, matched for age and body mass index. INTERVENTION: Plasma glucose was labeled by an infusion of dideuterated glucose started 120 minutes before ingestion of 1 g/kg of naturally 13C-enriched corn starch glucose. Glucose levels and oxidation were monitored for 330 minutes after glucose ingestion. RESULTS: Uremic subjects had normal fasting plasma glucose levels and impaired glucose tolerance with high plasma insulin (P <.001 versus controls). Glucose tolerance was impaired because of an increased total rate of appearance of glucose (cumulated on 330 minutes: uremic, 1,231 +/- 42 mg/kg/330 min, controls, 1,031 +/- 64; P <.05). Peripheral glucose uptake was increased (P <.05) because of an increased nonoxidative disposal (P =.051). CONCLUSIONS: Although peripheral glucose uptake resisted the stimulatory effect of the high insulin levels, glucose tolerance was impaired through splanchnic metabolic disturbances: reduced splanchnic glucose uptake and increased endogenous glucose production. The respective contribution of these abnormalities remains to be determined.

[Diet and physical activity in type 2 diabetes prevention]. / Diététique et activité physique dans la prévention et le traitement du diabète de type 2.

As diabetes is directly influenced by the way of life, a control of diet and physical activity may help in a prevention of the disease. Three recent studies have demonstrated this beneficial effect. Reduction caloric intake, controlling body weight and limitation of saturated fat absorption have proved their benefit effect in predisposed population; in the same way physical activity is effective in weight control and improvement insulino-resistance. So prevention of type 2 diabetes may be effective. A delay in the appearance of the disease may be quite useful in decreasing the importance of complications by decreasing time exposure to high blood glucose level.

Effects of subthalamic nucleus deep brain stimulation and levodopa on energy production rate and substrate oxidation in Parkinson's disease.

Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9.7 (SEM 7.1) kg after surgery, whereas patients on pharmacologic treatment lost 3.8 (SEM 10.0) kg since diagnosis. In STN-DBS-treated patients, REE (-16.5 %; P<0.001), lipid oxidation (-27 %; P<0.05) and protein oxidation (-46 %; P<0.05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0.05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (-8.3 %; P<0.05) and glucose oxidation (-37 %; P<0.01) with a slight hyperglycaemic effect (after levodopa challenge: 5.6 (SEM 0.8) v. before levodopa challenge: 5.3 (SEM 0.6) mmol/l; P<0.01). Switching 'on' STN-DBS acutely reduced REE (-17.5 %; P<0.01) and lipid oxidation (-24 %; P<0.001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5.4 (SEM 1.4) v. 5.5 (SEM 1.3) mmol/l; P<0.01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.

Mechanism of increased plasma glucose levels after oral glucose ingestion in normal-weight middle-aged subjects.

BACKGROUND/AIMS: To determine the decline in glucose tolerance in normal-weight middle-aged subjects, we performed a cross-sectional study using double-labelled oral glucose tolerance tests in 8 middle-aged (46.3 +/- 0.9 years) and in 8 young (23.6 +/- 0.5) subjects with similar normal body weight. METHODS: Plasma glucose was labelled by an infusion of dideuterated glucose started 120 min before ingestion of 1 g/kg of naturally (13)C-enriched corn starch glucose. Glucose levels, substrate oxidation (indirect calorimetry) and exogenous glucose oxidation ((13)C enrichment of expired CO(2)) were monitored for 330 min. RESULTS: In the middle-aged subjects, the appearance of exogenous glucose was reduced (723 +/- 52 mg/kg/330 min) compared to young subjects (864 +/- 38; p < 0.05), and systemic glucose production was normal. Plasma glucose levels were increased due to a reduced glucose disappearance rate (middle aged: 1,046 +/- 61 mg/kg/330 min vs. young 1,242 +/- 67; p < 0.05), concerning both oxidative and non-oxidative disposal. This reduction was no longer apparent when the results were normalized for fat-free mass. Insulin levels were similar in young and middle-aged subjects. CONCLUSION: In normal-weight middle-aged individuals, glucose intolerance is mainly due to the reduction in the mass of fat-free glucose-utilizing tissues. The higher plasma glucose levels enable normal glucose supply to peripheral tissues, and increase splanchnic glucose uptake.