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P Thiéblot

Publications and source records attributed to P Thiéblot.

At least 19 recordsLinked to original sources
PubMed2002

Divergence in plasmatic and urinary isoprostane levels in type 2 diabetes.

BACKGROUND: Oxidative stress is currently suggested as a mechanism underlying diabetes. The present study was designed to evaluate isoprostane levels in plasma and in urine in type 2 diabetic patients, and to compare them to other currently used biomarkers of oxidative stress. METHODS: The work was performed in a control group (n = 10) and in a type 2 diabetic group (n = 10). Besides the traditional biochemical parameters, we evaluated the plasma and urine levels of isoprostanes and malondialdehyde (MDA) as markers of oxidative stress. RESULTS: We found increased plasma and urine MDA in the diabetic patients and almost significantly decreased plasma vitamin E. Urinary isoprostane levels in diabetic patients were increased but they presented a strong tendency to a decrease in plasma isoprostanes. It is therefore suggested that, in the studied diabetic patients, although the production of isoprostanes in the body was increased (as other plasma oxidative stress biomarkers were altered) it did not lead to an increase in plasma isoprostane levels. It could be hypothesised that this results from an increased elimination of this metabolite and therefore an increased excretion in urine. CONCLUSION: Our results showed that the measurement of same oxidative stress biomarker, isoprostane, in two different biologic fluids, plasma and urine, led to divergent results and emphasised the importance to measure a biomarker both in the circulation fluid (plasma) and in the elimination fluid (urine), to have a general idea of what is occurring in the organism.

Aged↗
PubMed1998

[Epidemiologic characteristics of 336 thyroid cancers observed in the Auvergne region].

Patients treated and followed for thyroid cancer by a multidisciplinary group were studied between 1989 and 1993, 336 patients living in the French region Auvergne underwent total or partial thyroidectomy for thyroid carcinoma. The sex ratio was 4.3 and the median age was 52 (14-57) and 49 (17-83) in females and males respectively. Papillary carcinoma was the most common form: 76.5 of all thyroid tumors. The incidence of occult thyroid cancer was 17.4%; tumor size was smaller than for intranodular cancer (p < 0.00001). Tumor size at diagnosis of patients who died was higher than in patient who survived (p < 0.0001) and changed with histological type. It decreased between 1989 and 1993 (p < 0.01). 73% of the patients were asymptomatic before surgery, 23% described a rapid growth of their nodule. Clinically, 43.9% of the patients had a single nodule, 83% of these nodules were suspect because of their hardness. Median follow-up was 2.8 years. 279 patients are living and well, 28 were lost to follow-up and 39 died. There were 30 (8.93%) deaths due to thyroid carcinoma. In our study, significant prognostic factors for death were age at diagnosis (p < 0.0001), histological type (p < 0.0001) and nodular size (p < 0.01).

Adolescent↗
PubMed1997

Glucocorticoids do not regulate the expression of proteolytic genes in skeletal muscle from Cushing's syndrome patients.

Glucocorticoids signal enhanced proteolysis in various instances of muscle atrophy and increased gene expression of components of the lysosomal, Ca(2+)-dependent, and/or ubiquitin-proteasome proteolytic pathways in both rat skeletal muscle and myotubes. Cushing's syndrome is characterized by chronic excessive glucocorticoid production, which results in muscle wasting. We report here no change in messenger RNA levels for cathepsin D (a lysosomal proteinase), m-calpain (a Ca(2+)-activated proteinase), ubiquitin, 14-kDa ubiquitin-activating enzyme E2, and 20S proteasome subunits (i.e. critical components of the ubiquitin-proteasome proteolytic process) in skeletal muscle from such patients. Thus, in striking contrast with animal studies, glucocorticoids did not regulate the expression of muscle proteolytic genes in Cushing's syndrome. In humans, messenger RNA levels, for at least ubiquitin and proteasome subunits, are elevated in acute situations of muscle wasting, such as head trauma or sepsis. Because Cushing's syndrome is a chronic catabolic condition, we suggest that the lack of regulation of proteolytic genes in such patients may represent an adaptive regulatory mechanisms, preventing sustained increased protein breakdown and avoiding rapid muscle wasting.

Adult↗
PubMed1995

Response of leucine metabolism to hyperinsulinemia under amino acid replacement in experimental hyperthyroidism.

We investigated the responsiveness of protein metabolism to insulin as a mediator of the protein catabolic response to hyperthyroidism in humans. Six healthy volunteers were studied in a postabsorptive state before and after oral intake of thyroid hormones (2 micrograms.kg-1.day-1 L-thyroxine for 6 wk along with 1 microgram.kg-1.day-1 triiodothyronine for the last 2 wk). Insulin was infused at 7.14 nmol.kg-1.min-1 for 140 min under euglycemic and eukalemic clamps. An appropriate amino acid infusion was used to blunt insulin-induced hypoaminoacidemia. Leucine kinetics were assessed using a primed continuous infusion of L-[1-13C]leucine. Hyperthyroidism induced a significant increase (P < 0.05) in leucine endogenous appearance rate (a reflection of proteolysis; 2.15 +/- 0.06 vs. 1.76 +/- 0.03 mumol.kg-1.min-1 in the control state), oxidation (0.54 +/- 0.04 vs. 0.47 +/- 0.07), and nonoxidative disposal (a reflection of protein synthesis; 1.80 +/- 0.06 vs. 1.45 +/- 0.06). Insulin lowered proteolysis. Further hyperthyroidism improved the ability of insulin to inhibit proteolysis, whether considered as an absolute decrease (-0.57 +/- 0.02 vs. -0.45 +/- 0.05 mumol.kg-1.min-1, P < 0.05) or related to insulinemia [1.59 +/- 0.11 vs. 1.01 +/- 0.08 mumol leucine.kg-1.min-1/(nmol insulin/l), P < 0.05]. Insulin also moderately (but significantly P < 0.05) lowered protein synthesis in both control and hyperthyroid states. These changes in insulin action may provide a mechanism to save body protein during hyperthyroidism.

Adult↗
PubMed1994

Effect of hyperinsulinemia and hyperaminoacidemia on muscle and liver protein synthesis in lactating goats.

The experiment was carried out to clarify the roles of insulin and amino acids on protein synthesis in fed lactating goats (30 days postpartum). Protein synthesis in the liver and various skeletal muscles was assessed after an intravenous injection of a large dose of unlabeled valine containing a tracer dose of L-[2,3,4-3H]valine. The animals were divided into three groups. Group I was infused with insulin (1.7 mumol/min) for 2.5 h under glucose, potassium, and amino acid replacement. Group A was infused with an amino acid mixture to create stable hyperaminoacidemia for 2.5 h. Group C animals were controls. The fractional synthesis rates (FSR) were 31.5 +/- 2.2, 6.5 +/- 0.4, 4.3 +/- 0.8, 4.0 +/- 1.2, 3.9 +/- 1.2, and 3.6 +/- 0.4%/day (SD) in liver, masseter, diaphragm, anconeus, semitendinosus, and longissimus dorsi, respectively, for group C. Neither hyperinsulinemia in group I nor hyperaminoacidemia in group A had not affected by hyperinsulinemia but was stimulated by hyperaminoacidemia (+30%, P < 0.05). In contrast to previous experiments in which a labeled amino acid was constantly infused, this study revealed a stimulating effect of amino acids on protein synthesis in the liver but not in skeletal muscles. As previously observed in studies with the constant-infusion method, insulin had no effect on protein synthesis.

Amino Acids↗
PubMed1993

Familial HDL deficiency due to marked hypercatabolism of normal apoA-I.

In this article, we describe a 46-year-old man with severe high-density lipoprotein (HDL) deficiency and his kindred. In the proband, HDL cholesterol and apolipoprotein (apo) A-I levels were 5 and 4.5 mg/dL, respectively. Xanthomata, xanthelasma, arcus corneae, and hepatosplenomegaly were not present. The proband had coronary artery disease, but it was impossible to state whether the HDL deficiency cosegregated with premature coronary artery disease in this kindred. Pedigree analysis was suggestive of a codominant familial disease. Polymerase chain reaction amplification of the apoA-I gene of the proband, followed by subcloning and sequencing, did not reveal any mutation in either the coding regions or intron-exon junctions. A kinetic study using deuterated leucine to endogenously label apoA-I was performed to elucidate the metabolic basis of the apoA-I deficiency. We demonstrated marked hypercatabolism of apoA-I in the proband, with a fractional catabolic rate more than 10 times faster than normal; the plasma residence time of apoA-I in the proband was only 0.38 day compared with 4.10 days in a control subject. The apoA-I production rate was also substantially decreased in the proband. The association of a normal apoA-I gene sequence with marked hypercatabolism of apoA-I is similar to that described in Tangier disease. However, except for the presence of mild, diffuse, corneal deposits, this patient had no evidence of the reticuloendothelial cholesterol deposition characteristic of Tangier disease. This study establishes that a form of severe hypoalphalipoproteinemia distinct from Tangier disease can be caused by marked hypercatabolism of a normal A-I apolipoprotein.

Apolipoprotein A-I↗
PubMed1992

[Epidemiology of goiter in Auvergne].

An epidemiological study about goiter, related to the French national survey concerning school children aged 10-16, was carried out in region Auvergne. The prevalence of goiter was 12.52%, including 2.8% patients with WHO stages I and II, thus being slightly below national average (16.7%). Iodine urinary excretion was 62.9 +/- 34.3 micrograms per gram creatinine (French mean value 85.0), although sometimes major variation was noted in the same area. Later, two studies were performed in adults, in two places of Haute-Loire and Puy-de-Dôme, respectively Arsac-en-Velay and Besse-en-Chandesse. Both places were selected because of high frequency of goiter in children. Prevalence in adults was 16.1% in Arsac-en-Velay including 12.5% stages I and II, and 8.9% in Besse-en-Chandesse including 5.9% stages I and II. Mean iodine urinary excretion was respectively 59.78 micrograms/gram creatinine and 43.45 micrograms/liter. Thus, these surveys confirm a significant prevalence of goiter in Region Auvergne, with endemic places, and a generally low iodine urinary excretion.

Adolescent↗