Biomedical subjects

L Luzi

Publications and source records attributed to L Luzi.

78 records · Page 5Linked to original sources

PubMed1989

Effect of loss of first-phase insulin secretion on hepatic glucose production and tissue glucose disposal in humans.

To examine the importance of first-phase insulin secretion on total body glucose homeostasis, six normal subjects (age, 24 +/- 1 yr; ideal body wt, 100 +/- 1%) received three hyperglycemic (+75 mg/100 ml) clamp studies in combination with [3-3H]glucose: study I, 150 min hyperglycemic clamp; study II, hyperglycemic clamp plus somatostatin (6 micrograms/min) plus basal glucagon replacement (0.4 ng.kg-1.min-1) plus an insulin infusion designed to mimic only the second phase of insulin secretion; and study III, hyperglycemic clamp plus somatostatin plus basal glucagon plus an insulin infusion designed to mimic both the first and second phase of insulin secretion. Basal plasma C-peptide concentrations averaged 0.21 +/- 0.01 pmol/ml in the three study protocols. In study I the plasma C-peptide response demonstrated an early burst within the first 10 min followed by a gradually increasing phase of C-peptide secretion that lasted until the end of the study. In studies II and III plasma C-peptide declined within the first 10 min after somatostatin was started and averaged 0.06 +/- 0.01 and 0.05 +/- 0.01 pmol/min, respectively. Basal hepatic glucose production (2.3 +/- 0.2 mg.kg-1.min-1) was suppressed by 90% at 20 min and remained suppressed thereafter in studies I and III. In contrast, in study II hepatic glucose production was inhibited by only 50% (1.1 +/- 0.2 mg.kg-1.min-1) at 60 min (P less than 0.01 vs. studies I and III) and remained incompletely suppressed even after 150 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1988

Metabolic effects of low-dose insulin therapy on glucose metabolism in diabetic ketoacidosis.

The effect of low-dose insulin treatment (5-10 U/h) on hepatic glucose production (HGP) and peripheral glucose disposal was determined in 5 insulin-dependent diabetes mellitus (IDDM) subjects who were admitted with diabetic ketoacidosis (DKA; plasma glucose 598 +/- 50 mg/dl, blood pH 7.20 +/- 0.06, plasma bicarbonate 12 +/- 2 meq/L). Basal hepatic glucose production (4.3 +/- 0.5 mg.kg-1.min-1) in the DKA patients was 1.5- to 2-fold greater (P less than .01) than in controls (2.1 +/- 0.1 mg.kg-1.min-1) and nonketotic IDDM subjects (2.9 +/- 0.3 mg.kg-1.min-1), whereas tissue glucose disposal was significantly reduced (1.7 +/- 0.1 vs. 2.1 +/- 0.1 mg.kg-1.min-1, P less than .05). After the institution of insulin therapy (1 mU.kg-1.min-1), the plasma glucose concentration fell at the rate of 60 +/- 5 mg.dl-1.h-1 to reach a value of 220 +/- 10 mg/dl, which was maintained constant for 2 h (insulin-clamp technique). Blood pH (7.21 +/- 0.06 to 7.35 +/- 0.05) and plasma bicarbonate (12 +/- 3 to 18 +/- 2 meq/L) both increased during insulin therapy (P less than .01). The decline in plasma glucose concentration during insulin therapy primarily resulted from a suppression of HGP (from 4.3 +/- 0.5 to 1.7 +/- 0.2 mg.kg-1.min-1, P less than .01) and to a lesser extent from the stimulation of tissue glucose disposal (1.7 +/- 0.2 to 2.6 +/- 0.3 mg.kg-1.min-1, P less than .01). At this time, urine glucose excretion decreased from 2.6 +/- 0.2 to 0.6 +/- 0.1 mg.kg-1.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

3-Hydroxybutyric Acid↗

PubMed1987

Effect of insulin and plasma amino acid concentrations on leucine metabolism in man. Role of substrate availability on estimates of whole body protein synthesis.

We examined the effect of insulin and plasma amino acid concentrations on leucine kinetics in 15 healthy volunteers (age 22 +/- 2 yr) using the euglycemic insulin clamp technique and an infusion of [1-14C]leucine. Four different experimental conditions were examined: (a) study one, high insulin with reduced plasma amino acid concentrations; (b) study two, high insulin with maintenance of basal plasma amino acid concentrations; (c) study three, high insulin with elevated plasma amino acid concentrations; and (d) study four, basal insulin with elevated plasma amino acid concentrations. Data were analyzed using both the plasma leucine and alpha-ketoisocaproate (the alpha-ketoacid of leucine) specific activities. In study one total leucine flux, leucine oxidation, and nonoxidative leucine disposal (an index of whole body protein synthesis) all decreased (P less than 0.01) regardless of the isotope model utilized. In study two leucine flux did not change, while leucine oxidation increased (P less than 0.01) and nonoxidative leucine disposal was maintained at the basal rate; endogenous leucine flux (an index of whole body protein degradation) decreased (P less than 0.01). In study three total leucine flux, leucine oxidation, and nonoxidative leucine disposal all increased significantly (P less than 0.01). In study four total leucine flux, leucine oxidation, and nonoxidative leucine disposal all increased (P less than 0.001), while endogenous leucine flux decreased (P less than 0.001). We conclude that: (a) hyperinsulinemia alone decreases plasma leucine concentration and inhibits endogenous leucine flux (protein breakdown), leucine oxidation, and nonoxidative leucine disposal (protein synthesis); (b) hyperaminoacidemia, whether in combination with hyperinsulinemia or with maintained basal insulin levels decreases endogenous leucine flux and stimulates both leucine oxidation and nonoxidative leucine disposal.

Adult↗

PubMed1987

Different effects of glyburide and glipizide on insulin secretion and hepatic glucose production in normal and NIDDM subjects.

Glyburide (GB) and glipizide (GZ) differ in their pharmacokinetics, but it is not known whether they also differ in mode of action. To examine this question, 10 young healthy subjects and 6 non-insulin-dependent diabetic (NIDDM) patients participated in each of three studies: 1) infusion of saline for 120 min followed by a 100-min hyperglycemic (125 mg/dl) clamp; 2) 120-min primed continuous infusion of GZ followed by a 100-min hyperglycemic clamp; and 3) 120-min primed continuous infusion of GB followed by a 100-min hyperglycemic clamp. The GB and GZ infusions were continued throughout the hyperglycemic clamp. Similar plasma concentrations of GB and GZ were obtained in both groups. All studies were performed with [3-3H]glucose to allow quantification of hepatic glucose production. When administered under basal conditions of glycemia, the acute phase (0-10 min) of plasma insulin and C-peptide increase in both control and NIDDM subjects was twice as great with GZ compared with GB (P less than .01). During the hyperglycemic-clamp studies performed in normal subjects, both GB and GZ increased the first- (1.6-fold) and second- (2.2-fold) phase plasma insulin responses more than hyperglycemia alone. During the hyperglycemic clamp in NIDDM subjects, the first-phase plasma insulin response was absent, and the second-phase insulin response was markedly impaired. Neither GB nor GZ improved first-phase insulin secretion in the NIDDM patients. In both NIDDM and control subjects, the effects of hyperglycemia and sulfonylurea drugs (both GB and GZ) on the first- and second-phase plasma insulin responses were simply additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1984

Urea, creatinine, and glucose determined in plasma and whole blood by a differential pH technique.

We report the conditions (buffer composition and enzyme activity) required for estimating three frequently determined analytes--urea, glucose, and creatinine--by use of an improved version of the differential pH apparatus previously described (Clin Chem 29: 80-85, 1983). For each analyte, we used only one specific enzyme, thus avoiding a chain of auxiliary and indicator reactions. The method requires about a minute for each determination in undiluted plasma or whole blood.

Blood Glucose↗

PubMedDate not supplied

Whole blood L-lactate assay by a new differential pH method: application to metabolic investigations.

We propose a new quantitative method for L-lactate assay in whole blood, based on the measurement of pH variation caused by specific and irreversible oxidation of L-lactate to pyruvate in the presence of an electron acceptor (hexacyanoferrate) and of the enzyme cytochrome b2 (EC 1.1.2.3.). No sample pretreatment is needed; the method is simple and fast (1.5 min/analysis) and requires 10 microliters whole blood per assay. Linearity is confirmed up to 20 mmol/l L-lactate. Within-day and between-day variability was (as C.V.) 3.6% and 8.1% for blood lactate 1.3 and 1.0 mmol/l, respectively. The results by the present method correlate well with those from two reference methods (test method vs a lactate sensor based method: r = 0.996; test method vs a spectrophotometric method: r = 0.987). An application of the present method to the continuous monitoring of L-lactate in patients after combined kidney and pancreas transplantation, under conditions of euglycemic hyperinsulinemia and hyperglycemic hyperinsulinemia is reported. We conclude that the method is simple and reproducible and can be employed to measure whole blood lactate concentration continuously both in clinical protocols and in basic research.

Adult↗