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Biomedical subjects

R Roussel

Publications and source records attributed to R Roussel.

8 recordsLinked to original sources
PubMed2005

Increased plasma adiponectin concentrations are associated with microangiopathy in type 1 diabetic subjects.

AIMS/HYPOTHESIS: Insulin resistance is related to an increased risk of diabetic retinopathy and nephropathy in type 1 diabetes. Patients with insulin resistance and/or macrovascular disease have abnormally low levels of adiponectin. The aim of this study was to investigate the relationships between adiponectin and renal and retinal diabetic complications in type 1 diabetic patients. METHODS: In this 6-year prospective follow-up observational study, we evaluated the severity of retinopathy at baseline and determined the incident risk of microalbuminuria in 126 normoalbuminuric patients with type 1 diabetes. Each patient was age- and sex-matched to two non-diabetic control subjects. RESULTS: Plasma adiponectin concentrations were significantly higher in diabetic subjects than in control subjects (p < 0.0001). The adiponectin concentration was significantly higher in patients with severe diabetic retinopathy than in those without (39.1+/-14.0 vs 29.0+/-13.0 microg/ml, p = 0.0005). The 18 patients who developed persistent microalbuminuria had higher adiponectin concentrations than the other patients (35.8+/-14.5 vs 30.6+/-13.7 microg/ml). Increased adiponectin concentrations were independently associated with the occurrence of microalbuminuria (p = 0.0158) after adjustment for baseline urinary albumin concentration (p = 0.004), sex (p = 0.0054), blood pressure (NS) and metabolic control (NS). CONCLUSIONS/INTERPRETATION: The elevated adiponectin concentrations observed in subjects with microvascular disease may indicate an altered regulation of this adipocytokine in patients with complications associated with type 1 diabetes.

Adiponectin↗
PubMed2000

Semiselective POCE NMR spectroscopy.

A new scheme is proposed to edit separately glutamate C(3) and C(4) resonances of (1)H bound to (13)C, in order to resolve these two signals which overlap at intermediate magnetic fields (1.5 T-3 T), commonly available for human brain studies. The two edited spectra are obtained by combining the individual acquisitions from a four-scan measurement in two different ways. The four acquisitions correspond to the two steps of the classical POCE scheme combined with another two-scan module, where the relative phases of the C(3) and C(4) (1)H resonances are manipulated using zero quantum and double quantum coherence pathways. This new technique exhibits the same sensitivity as POCE and allows the (13)C labeling of C(3) and C(4) glutamate from [1-(13)C]glucose to be monitored separately in the rat brain at 3 T.

Animals↗
PubMed1998

13C/31P NMR studies of glucose transport in human skeletal muscle.

The muscle intracellular (IC) free glucose concentration and the rate of muscle glycogen synthesis were measured by using in vivo 13C and 31P NMR spectroscopy in normal volunteers under hyperinsulinemic ( approximately 300 pM) clamp conditions at the following three plasma glucose levels: euglycemia ( approximately 6 mM), mild ( approximately 10 mM), and high ( approximately 16 mM) hyperglycemia. In keeping with biopsy studies, muscle IC free glucose concentration at euglycemia (-0.03 +/- 0.03 mmol/kg of muscle, mean +/- SEM, n = 10) was not statistically different from zero. A small but statistically significant amount of IC free glucose was observed during mild and high hyperglycemia: 0.15 +/- 0.08 (n = 5) and 0.43 +/- 0.20 mmol/kg of muscle (n = 5), respectively. Muscle glycogen synthesis rate, in mmol per kg of muscle per min, was 111 +/- 11 at euglycemia (n = 10), 263 +/- 29 during mild hyperglycemia (n = 5), and 338 +/- 42 during high hyperglycemia (n = 5), these three rates being significantly different from each other. As previous in vitro and in vivo studies, these rates suggest a Km (concentration at which unidirectional glucose transport reaches half-maximal rate) of the muscle glucose transport system in the 15-25 mM range under hyperinsulinemic conditions. The low concentrations of muscle IC free glucose observed under hyperinsulinemic conditions were interpreted, with this estimate and in the framework of metabolic control theory, as glucose transport being the predominant step controlling muscle glucose flux not only at euglycemia but also during hyperglycemia.

Biological Transport↗
PubMed1998

Effect of arsenite on induction of CYP1A and CYP2H in primary cultures of chick hepatocytes.

In earlier studies, treatment with sodium arsenite was shown to decrease total hepatic CYP in rats. A concomitant increase in heme oxygenase, the rate-limiting step in heme degradation to biliverdin, was considered responsible for the decrease in CYP. Here we investigated the effect of sodium arsenite on induction of CYP2H, CYP1A, and heme oxygenase in primary cultures of chicken embryo hepatocytes. When added simultaneously with inducer, arsenite inhibited phenobarbital-mediated increases in CYP2H and 3-methylcholanthrene-mediated increases in CYP1A, as measured enzymatically and immunochemically. Near maximal decreases were observed in these forms of CYP at a concentration of 2.5 microM sodium arsenite. The concentration-dependent decreases in CYP2H and CYP1A by sodium arsenite were concomitant with increases in heme oxygenase. Sodium arsenite was not toxic at concentrations as high as 10 microM, as indicated by protein synthesis and the reduction of MTT by intact cells. Sodium arsenite had no effect on induction of CYP2H1 mRNA, suggesting that the decreases in this form of CYP occurred post-transcriptionally. Treatment of cells with tin mesoporphyrin (SnMeso), an inhibitor of heme oxygenase, resulted in inhibition of arsenite-induced heme oxygenase. However, SnMeso did not alter the effect of arsenite to prevent phenobarbital-mediated increases in CYP2H protein. SnMeso alone inhibited phenobarbital-mediated increases in CYP2H. Inclusion of 2 or 5 microM exogenous heme with arsenite did not prevent the arsenite-mediated decrease in CYP2H. Combined treatment with heme and phenobarbital induced heme oxygenase to the same extent as treatment with heme, arsenite, and phenobarbital. However, CYP2H activity was decreased only when the treatment included arsenite. These results suggest that elevated levels of heme oxygenase alone are not responsible for arsenite-mediated decreases in CYP2H.

Animals↗
PubMed1997

Evidence for 100% 13C NMR visibility of glucose in human skeletal muscle.

The accuracy of the measurement of total muscle glucose by in vivo 13C NMR spectroscopy was tested in five normal volunteers during a euglycemic [1-13C]glucose infusion. The NMR visible concentration calibrated using an external reference was compared with that calculated from plasma glucose concentration, assuming that glucose remained extracellular. The NMR measurement always provided higher values than the calculation from plasma glucose: 0.51 +/- 0.035 (mean +/- SE) versus 0.38 +/- 0.005 mmol/liter of muscle on average. This systematic difference was interpreted as reflecting the presence of muscle glucose-6-phosphate, co-resonating with free glucose. Thus, glucose appeared to be virtually 100% NMR visible in human skeletal muscle.

Adult↗
PubMed1997

Pharmacokinetic study of alpha1-antitrypsin infusion in alpha1-antitrypsin deficiency.

OBJECTIVES: To ascertain how long 120 mg/kg alpha1-antitrypsin concentrate (alpha1-AT-C), administered I.V. every 2 weeks, can maintain alpha1-antitrypsin (alpha1-AT) serum levels above 70 to 80 mg/dL. Secondary objectives were to summarize the nature, severity, and relationship of a plasma-derived alpha1-AT-C infusion to any side effects. METHODS: This was an open-label uncontrolled pharmacokinetic study. Alpha1-AT-C was administered I.V. every 2 weeks for 10 infusions in 23 patients with PIZ alpha1-AT deficiency. Serum alpha1-AT levels and neutralizing elastase activity were measured preinfusion, postinfusion, and at nadir. During two infusion periods, daily serum alpha1-AT and neutralizing elastase activities were measured on the seventh to 14th days. Five patients received BAL assays for alpha1-AT and neutralizing elastase activity. Adverse events were recorded in a patient diary and by a nurse at each infusion visit. RESULTS: The 120-mg/kg dose of alpha1-AT-C could not maintain nadir serum protective levels above 70 or 80 mg/dL for the entire 14-day dosing interval in most patients. None of the patients had alpha1-AT levels above 80 mg/dL for all 14 days. The serum alpha1-AT and neutralizing elastase levels correlated suggesting functional activity. The BAL alpha1-AT and neutralizing elastase activities were low and did not correlate with serum levels. CONCLUSION: Alpha1-AT-C at 120 mg/kg administered every 2 weeks did not maintain nadir serum alpha1-AT levels above 70 to 80 mg/dL for a 14-day dosing interval. Higher doses every 2 weeks or decreased interval between infusions may be required.

Adult↗
PubMed1996

In vivo NMR evidence for moderate glucose accumulation in human skeletal muscle during hyperglycemia.

Although the absence of intracellular (IC) free glucose is direct evidence of glucose transport being the rate-limiting step for muscle glucose disposal at euglycemia, the scarcity of data in humans during hyperglycemia precludes any definitive conclusion. In the present study, 13C and 31P in vivo nuclear magnetic resonance (NMR) data from two separate groups of subjects were combined to measure IC free glucose in the human skeletal muscle. When these noninvasive tools were used with an infusion of [1-13C]glucose, a steady-state concentration of 1.2 +/- 0.2 mmol IC glucose/l IC water was observed at the end of a 2-h hyperglycemic clamp with somatostatin infusion, during which glycemia was maintained at approximately 22 mmol/l and insulinemia at approximately 5 mU/l. Despite this moderate glucose accumulation, the persistence of a large transmembrane glucose gradient suggests that the posttransport steps do not play a significant role in the control of muscle glucose disposal in these specific conditions, relevant to insulinopenic diabetic patients.

Adult↗