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Biomedical subjects

B Charbonnel

Publications and source records attributed to B Charbonnel.

At least 19 recordsLinked to original sources
PubMed1992

[Oral and dietary treatments of type 2 diabetes].

Non insulin-dependent diabetes mellitus requires a metabolic and vascular treatment in order to prevent macroangiopathy. Personal diet management, which is similar in diabetic and non diabetic comparable patients, is the basis of therapy. Any significant result cannot be expected without its observance. Sulfonylurea and biguanide drugs can enhance diet action and must be prescribed secondarily according to the level of hyperglycaemia. Blood pressure and lipid control is as important as glycaemic normalization. Early diet management of obese people should be the best approach to prevent type II diabetes.

Administration, Oral↗
PubMed1992

Effects of a combination of bedtime intermediate-acting insulin and glibenclamide in type 2 (non-insulin-dependent) diabetic patients with secondary failure to respond to oral hypoglycaemic agents.

The effect of a subcutaneous injection of an intermediate-acting insulin at bedtime combined with glibenclamide has been evaluated in 16 non-insulin-diabetic patients with secondary failure to respond to oral agents. The patients showed poor metabolic control (HbA1 greater than 11%) after two months on diet and glibenclamide treatment (15 mg.day-1). For 3 months the glibenclamide was continued together with an injection of an intermediate-acting insulin at bedtime in order to maintain fasting blood glucose under 120 mg.dl-1. A significant reduction in fasting blood glucose and HbA1 (15.50 vs 10.35%) and fructosamine (2.03 vs 1.69 mmol.l-1) was observed (230 to 141 mg.dl-1) at a mean insulin dose of 0.28 U.kg-1. The peak blood glucose after a standard test meal was also significantly improved (290 vs 203 mg.dl-1). Two months after the bedtime insulin injection had been withdrawn, only one patient was still being treated with oral agents alone. Except for another patient who dropped out, all the others had to be treated again with insulin because their fasting blood glucose exceeded 180 mg.dl-1. It is concluded that a single subcutaneous injection of an intermediate-acting insulin at bedtime combined with glibenclamide improved fasting and post-meal blood glucose concentrations in non-insulin-dependent patients resistant to diet and oral hypoglycaemic treatment. Almost all of the patients relapsed after insulin was withdrawn.

Administration, Oral↗
PubMed1991

Acute insulin response to intravenous glucose, glucagon and arginine in some subjects at risk for type 1 (insulin-dependent) diabetes mellitus.

The relationships between first-phase insulin secretion to i.v. glucagon and i.v. arginine were studied in 19 healthy adult volunteers (Group I) and in 21 subjects at risk for Type 1 (insulin-dependent) diabetes mellitus with either a "normal" (n = 11; Group IIa) or a "low" insulin response to i.v. glucose (n = 10; Group IIb). Groups I and IIa displayed similar insulin responses to the three secretagogues. In contrast, Group IIb demonstrated lower insulin responses to both glucagon and arginine than control subjects (p less than 0.007 and p less than 0.04 respectively) or than "normo-responders" to glucose (p less than 0.007 and p less than 0.04 respectively). In Group IIb however, arginine-stimulated insulin release was increased compared to the response to glucose (p less than 0.006), while glucagon and glucose led to non-statistically different responses. Five "low-responders" developed Type 1 diabetes. As a group, they displayed lower responses to glucagon and to arginine than subjects who up to now have not developed the disease (p less than 0.05 and p less than 0.0003 respectively). In the subjects who progressed to diabetes, the responses to glucose and glucagon were similarly blunted. In the "low-responders" who have not developed the disease, no statistical difference could be detected between mean responses to glucagon and glucose, but four out of these five subjects had a glucagon-stimulated response within the control range and higher than their corresponding response to glucose. Arginine led to a higher stimulation than glucose, in subgroups that either progressed to diabetes (p less than 0.006) or did not (p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Effect of nifedipine on glucose potentiation of the acute insulin response to arginine in non-insulin-dependent diabetics.

The effect of 7-days of nifedipine treatment on insulin secretion has been analyzed in hypertensive patients with non-insulin-dependent mellitus (NIDDM). Pancreatic beta-cell function was assessed as insulin release following stimulation with arginine after potentiation by hyperglycaemia. Two groups of 5 patients with NIDDM (fasting blood glucose 139.2 mg.dl-1), on the same controlled diet, were compared; one was treated with nifedipine 30 mg per d and the other was the control. The mean blood pressure in the nifedipine group decreased (110 vs 102 mm Hg). Fasting blood glucose and basal plasma insulin were not affected by nifedipine. The acute insulin response (AIR) to 5 g arginine after potentiation by hyperglycaemia (clamped at 240 and 350 mg/dl for 30 min) was significantly (P less than 0.05) decreased, as well as the potentiation slope (line relating AIR and plasma glucose level) in those patients, and were unchanged in the control group. Thus, nifedipine may impair insulin secretion at high glucose levels in patients with NiDDM.

Aged↗
PubMed1991

Suppression of corpus luteum function by the gonadotropin-releasing hormone antagonist Nal-Glu: effect of the dose and timing of human chorionic gonadotropin administration.

OBJECTIVE: To assess the effect of gonadotropin-releasing hormone antagonist Nal-Glu administration in the luteal phase and the potential rescue by exogenous human chorionic gonadotropin (hCG) of corpus luteum (CL) after antagonist treatment. DESIGN: We studied the dose of Nal-Glu required for luteolysis and subsequently we coadministered low doses of hCG for 3 consecutive days either simultaneously to Nal-Glu administration (n = 5), or 48 (n = 5), or 72 hours (n = 5) later. Six additional participants received pharmacological doses of hCG 48 hours after the luteolytic dose of Nal-Glu. SETTING: Participants were studied in Clinique Endocrinologique, Nantes, and in Service d'Endocrinologie, Hôpital Bicêtre, Le Kremlin Bicetre, France. PARTICIPANTS: Twenty-nine normal young women (ages 20 to 35) were studied. INTERVENTIONS: None. MAIN OUTCOME MEASURE: Measurements of follicle-stimulating hormone, luteinizing hormone (LH), estradiol, Progesterone (P) levels were performed by radioimmunoassay before, during, and after the various treatment regimens. RESULTS: Complete luteolysis occurred in women who received 10 mg of Nal-Glu daily on days 4 and 5 after the LH surge. The coadministration of Nal-Glu and hCG overrode the effect of the antagonist (P = 48.8 +/- 22.5 versus 60.8 +/- 3.1 nmol/L in controls treated with hCG alone [NS]). When hCG treatment was started 48 hours after Nal-Glu, a partial luteolysis occurred (P = 33.8 +/- 10.9 versus 117 +/- 12.9 nmol/L, P less than 0.01). When hCG was started 72 hours after Nal-Glu, a complete luteolysis occurred (P = 5.8 +/- 2.05 versus 36.2 +/- 0.6 nmol/L, P less than 0.01). Higher doses of hCG (1,500 or 5,000 IU) administered 72 hours after Nal-Glu resulted in a significant rescue of CL function (P = 37.7 +/- 4.8 and P = 43.8 +/- 22.2 versus 74.5 +/- 19.8 and 130.2 +/- 14.3 nmol/L, P less than 0.05), respectively. CONCLUSIONS: These results confirm the LH dependence of CL function. The suppression of CL LH support for 72 hours induced a compromise of the CL nonreversible by low doses of hCG mimicking early pregnancy but reversible with pharmacological doses.

Adult↗
PubMed1991

Comparative continuous-indirect-calorimetry study of two carbohydrates with different glycemic indices.

Six healthy young men were studied by indirect calorimetry for 6 h after eating a meal composed of glucose or manioc starch (equivalent to 50 g dextrose). Blood was drawn every 30 min for 6 h to measure plasma glucose, free fatty acid (FFA), and insulin concentrations. The glycemic index of the starch was 57%. Plasma insulin and glucose concentrations were significantly higher from 150 to 210 min and FFA concentrations remained significantly lower from 210 to 360 min after starch than after glucose. Carbohydrate oxidation rose from a similar initial concentration for glucose and starch, to a constant concentration until 200 min before becoming significantly higher for the starch load until the end of the test. Total glucose oxidation was significantly higher with starch. Total fat oxidation did not differ after the two loads. A negative correlation was found between glucose oxidation and plasma FFA concentrations. Use of low-glycemic-index carbohydrates increases carbohydrate oxidation because of lower plasma FFA concentrations and fat oxidation.

Absorption↗
PubMed1991

Plasma vitamin A and E in type 1 (insulin-dependent) and type 2 (non-insulin-dependent) adult diabetic patients.

Vitamin A and E status was studied in 35 type 1 (insulin-dependent) and 35 type 2 (non-insulin-dependent) diabetic patients and in 30 control subjects. Vitamin A blood concentration was significantly decreased in type 1 and increased in type 2 diabetic patients as compared to control subjects. No correlation was found between vitamin A blood concentration and blood glucose control as evaluated with HbA1c. Blood Vitamin E concentrations were significantly increased in both groups of diabetic patients and were statistically correlated with blood cholesterol, apoprotein B and triglycerides, but not with HbA1c.

Adolescent↗
PubMed1979

[Plasma hormonal pattern of the late diabetic pregnancy (author's transl)].

Plasma estradiol, estriol, progesterone, H.C.S. and cortisol were measured (RIA methods) every two days, in 20 diabetic pregnancies (classes B, C or D of White), between the 33th week and the delivery, and were compared with normal pregnancies. Estriol was always normal, and progesterone values were at the upper limit of the normal range; estradiol, H.C.S. and cortisol were normal or elevated, with mean values significantly higher than controls. E2 and/or progesterone dramatically decreased in 5 cases before birth, just as the urinary measurements. In this study, the insulin requirements were not correlated with these plasma hormone values. Besides pathogenic hypothesis )glycemic control of H.C.S. and cortisol--abnormalities of metabolic pathways of estrogens ?), this work informs the inferred hormonal deficiency in diabetic placenta. Also, it is unable to determine the practical usefulness of these plasma measurements in the management of diabetic pregnancy.

Adult↗