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Biomedical subjects

P Brunetti

Publications and source records attributed to P Brunetti.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

Long-term therapy with addition of pioglitazone to metformin compared with the addition of gliclazide to metformin in patients with type 2 diabetes: a randomized, comparative study.

BACKGROUND: This 52-week, randomized, double-blind study compared the efficacy and safety of metformin plus pioglitazone with the established combination of metformin plus gliclazide in type 2 diabetes mellitus. METHODS: Patients with poorly controlled type 2 diabetes (HbA1c > or = 7.5% to < or =11.0%) received either pioglitazone 15 mg o.d. (titrated up to 45 mg; n = 317) or gliclazide 80 mg o.d. (titrated up to 320 mg; n = 313) and metformin at the pre-study dose. HbA1c, fasting plasma glucose (FPG), insulin, lipids and the urinary albumin/creatinine ratio were measured. RESULTS: There were no significant differences in HbA1c (1% decrease in both groups) and FPG between groups. There was a decrease in fasting insulin in the pioglitazone group compared to an increase in the gliclazide group (p < 0.001). There were significantly greater improvements in triglycerides and HDL-cholesterol in the metformin plus pioglitazone group compared to the metformin plus gliclazide group (p < 0.001). Mean LDL-cholesterol decreased with metformin plus gliclazide and increased with metformin plus pioglitazone (p < 0.001); however, this increase was considerably less marked than that in HDL-cholesterol. The mean urinary albumin/creatinine ratio was reduced by 10% in the metformin plus pioglitazone group compared to an increase of 6% in the metformin plus gliclazide group (p = 0.027). The incidence of adverse events was comparable between groups and both combinations were well tolerated. CONCLUSIONS: Compared to the established combination of metformin plus gliclazide, this study indicates potential benefits of addition of pioglitazone to metformin in terms of improvements in microalbuminuria and specific abnormalities associated with diabetic dyslipidemia.

Diabetes Mellitus, Type 2↗
PubMedDate not supplied

Glucose intolerance in uremia (A- and B-cell function during conservative and dialytic management.

Glucose tolerance and insulin and glucagon secretion were investigated in two groups of uremic patients, respectively on conservative and hemodialytic treatment. For this purpose, a glucose infusion was performed in the fasting state. Glucose intolerance was observed in uremic patients; hemodialysis improved, but did not normalize the glucose disposal. In uremic patients both on conservative and dialytic treatment plasma insulin and glucagon levels were higher than in the control group; the pattern of glucagon suppression was well maintained. The data obtained suggest that glucose intolerance in uremia is related mainly to peripheral insulin resistance and is not due to hyperglucagonemia.

Adult↗
PubMedDate not supplied

Urinary excretion and plasma levels of norepinephrine and epinephrine during diabetic ketoacidosis.

Sympathetic activity was determined in 13 ketoacidotic diabetics by evaluation of plasma and urinary catecholamines, before and in the course of medical management. Patients were divided into two groups. Group A (severe ketoacidosis, n = 5) and Group B (moderate ketoacidosis, = 8), depending on plasma glucose, pH and plasma bicarbonate levels. The results showed an enhanced sympathetic activity in all patients before treatment, with significant decrease during therapy. In Group A plasma catecholamines were higher than in Group B, both before and in the course of therapy. A significant correlation was found between basal plasma catecholamines and initial plasma glucose, plasma bicarbonate, hours of therapy and insulin dosage required to obtain plasma glucose levels below 150 mg/100 ml .These results, suggesting a close correlation between glycometabolic control and adrenergic activity, emphasize the role of the sympathetic nervous system as a powerful contrainsular factor in the pathogenesis and metabolic derangement of diabetic ketoacidosis.

Adolescent↗
PubMedDate not supplied

Low dose metformin in the treatment of type II non-insulin-dependent diabetes: clinical and metabolic evaluations.

Low doses of metformin (500 mg twice daily) were administered to 20 diabetic patients, combined with the original sulfonylurea treatment which had become ineffective even at full dosage. After 1 and 5 weeks, the effects of the drug on glycemic control, blood intermediate metabolites and monocyte insulin receptors were monitored. Metformin clearly improved glycemic control by reducing both fasting blood glucose from 189.88 +/- 21.11 mg/dl to 131.12 +/- 16.02 mg/dl after 1 week and to 130.11 +/- 13.29 mg/dl after 5 weeks (p less than 0.025 both after 1 and 5 weeks); the diurnal blood glucose average fell from 235.33 +/- 24.11 mg/dl to 174.66 +/- 23.45 mg/dl (p less than 0.0025) after 1 week and to 177.65 +/- 21.71 mg/dl (p less than 0.0005) after 5 weeks. Consequently both blood glycosylated hemoglobin (p = n.s. after 1 week, p less than 0.025 after 5 weeks) and serum fructosamine (p less than 0.0025 after both 1 and 5 weeks) also decreased after metformin treatment. No change in plasma insulin and C-peptide levels was reported and no modification in diurnal rhythms of blood lactate, pyruvate, alanine glycerol and beta-OH-butyrate was detected at any time during metformin treatment. All the changes documented in the binding values were already complete at the end of the first week; insulin binding to monocytes increased slightly but significantly (p less than 0.05) and the number of receptors per cell rose (p less than 0.05) but could not be correlated to any index of glycemic control. These data suggest that the antidiabetic action of metformin is neither related to its lactate-increasing activity nor does it depend upon its inducing an increase in insulin binding values. This metformin-related hypoglycemic effect might be the result, at least in part, of a reduced oxidative phosphorylation without inhibition of hepatic gluconeogenesis and/or of decreased hepatic glucose output. Moreover, our data are also consistent with the hypothesis that metformin might affect insulin action at a post-receptor level.

3-Hydroxybutyric Acid↗
PubMedDate not supplied

Red cell 2,3-DPG levels in diabetic vasculopathy.

RBC 2,3-DPG resulted statistically increased versus normal subjects in 22 insulin-dependent diabetics affected by arterial vasculopathy and in 19 vasculopathic non-diabetic patients. RBC 2,3-DPG, on the other hand, did not differ from the normal mean in 16 insulin-dependent diabetics without vascular involvement. The increase of RBC 2,3-DPG represents principally a consequence of the vasculopathy.

Diabetes Mellitus, Type 1↗
PubMedDate not supplied

Glucagon and carbohydrate disorder in a totally pancreatectomized man (a study with the aid of an artificial endocrine pancreas).

The effect of insulin withdrawal and exogenous glucagon infusion upon blood glucose concentration was investigated in a totally pancreatectomized patient with the aid of an artificial endocrine pancreas. Blood glucose remained unchanged at about 100 mg/100 ml, when insulin infusion was stopped, but rose up to 300 mg/100 ml, during a 12-h period of exogenous glucagon infusion at a rate of 3 ng/kg/min. Fractionation of whole plasma on Bio Gel P-30 revealed no immunoreactive glucagon in the region of true glucagon. This study seems to reinforce the hypothesis that true glucagon is essential in the fasting condition at least in the short term to produce hyperglycemia in insulin deprived diabetics.

Aged↗