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L Boine

Publications and source records attributed to L Boine.

5 recordsLinked to original sources
PubMed1991

Benfluorex and blood glucose control in non insulin-dependent diabetic patients.

Benfluorex has been reported to decrease blood glucose in different dismetabolic conditions, particularly in noninsulin-dependent diabetic (NIDD) patients, but the mechanism of this effect is poorly known. We evaluate fasting glucose production (3H-glucose infusion) and B-cell secretion (phi 1, phi 2 and glucose utilization SI) (minimal model technique) in 7 mild, diet treated, NIDDM patients after 6-week administration of benfluorex (450 mg/day) and placebo, in random sequence and double blind design. Body weight, HbA1c, plasma glucose profile, fasting plasma insulin, lactate, pyruvate, beta-OH-butyrate, total cholesterol, HDL-cholesterol and triglycerides were also measured at the end of each treatment. Mean values of body weight (71 +/- 4 vs 69 +/- 4 kg, p less than 0.01), HbA1c (8.3 +/- 0.2 vs 7.7 +/- 0.2%, p less than 0.01), fasting plasma glucose (137.0 +/- 6.5 vs 121.4 +/- 5.6 mg/dl, p less than 0.01), lactate (1.82 +/- 0.13 vs 1.22 +/- 0.11 mmol/l, p less than 0.0025) pyruvate (0.164 +/- 0.011 vs 0.095 +/- 0.010 mmol/l, p less than 0.0005), and beta-OH-butyrate (0.91 +/- 0.06 vs 0.66 +/- 0.04 mmol/l, p less than 0.005) were significantly lower after benfluorex than after placebo. phi 1, phi 2 and SI values were not significantly different in the two treatments. Fasting glucose production was significantly lower after benfluorex than after placebo: 2.46 +/- 1.57 vs 1.84 +/- 0.85 mg/kg.min, p less than 0.02. These results demonstrate that 6-week treatment with benfluorex produces a significant blood glucose lowering effect in mild NIDDM patients, mainly by decreasing glucose production.

Blood Glucose↗
PubMed1988

Insulin binding to monocytes and in vivo peripheral insulin sensitivity are normal in Graves' disease.

Insulin resistance in hyperthyroidism seems to depend on increased glucose production rather than on decreased glucose utilization. A decreased insulin binding on different target cells has been reported in patients in whom an in vivo evaluation of peripheral insulin sensitivity was lacking. In 20 patients with Graves' disease (6 males, 14 females), aged 40.0 +/- 2.0 yr, BMI 23.7 +/- 0.7, and in 20 well-matched controls we performed the following tests: 75 g o.G.T.T., euglycemic-hyperinsulinemic clamp at 50 microU/ml combined with D-[3-3H] glucose infusion in tracer amounts, in vitro insulin binding on circulating monocytes. Fasting plasma glucose values were similar in the two groups, whereas plasma insulin values were significantly higher in hyperthyroids (21.4 +/- 2.5 vs 10.6 +/- 0.6 microU/ml, p less than 0.01). The values of peripheral glucose utilization (5.61 +/- 0.24 vs 6.01 +/- 0.22 mg/kg-min) and of total specific insulin binding (4.07 +/- 0.20 vs 4.39 +/- 0.23% bound to 10(7) cells/ml) were not significantly different in the two groups. These results indicate that in vitro and in vivo data, when recorded in the same patients, are concordant to confirm a normal peripheral tissue sensitivity to insulin in Graves' disease.

Adult↗
PubMed1988

Insulin resistance in Graves' disease: a quantitative in-vivo evaluation.

Hyperthyroidism is considered to be an insulin-resistant state, but a quantitative evaluation of some action of insulin is still lacking. We performed euglycaemic clamp at about 350 and 7000 pmol l-1 plasma insulin concentration in combination with the 3H-glucose infusion in 12 patients with Graves' disease and in 12 matched controls. Fasting plasma insulin (126 +/- 6.5 vs. 77.5 +/- 5.7 pmol l-1; P less than 0.001), C-peptide (502 +/- 36 vs. 363 +/- 41 pmol l-1; P less than 0.001) and glucagon (47 +/- 3.3 vs. 33.3 +/- 3 pmol l-1; P less than 0.01) were significantly higher in hyperthyroids than in euthyroids. Basal hepatic glucose production was significantly higher in hyperthyroids than in euthyroids (18.3 +/- 1.4 vs. 9.2 +/- 0.5 mumol l-1; P less than 0.0001), and its suppression during physiological hyperinsulinaemia was only 50% in hyperthyroids. Glucose utilization and suppression of lipolysis were normally stimulated by insulin. All parameters altered during hyperthyroidism were normalized during methimazole-induced euthyroidism. We conclude that insulin resistance involves mainly glucose rather than lipid and is selective at the hepatic level.

Adult↗