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Biomedical subjects

G Mingrone

Publications and source records attributed to G Mingrone.

At least 37 records · Page 2Linked to original sources
PubMed2001

Oxidation of D-[U-(14)C] glucose and [1,12-(14)C] dodecanedioic acid by pancreatic islets from Goto-Kakizaki rats.

In pancreatic islets from hereditarily diabetic GK rats, [1,12 -(14)C] dodecanedioic acid (5.0 mM) was oxidized at a rate representing about 5 % of that of D-[U - (14)C] glucose (8.3 mM). Dioic acid and hexose failed to exert any significant reciprocal effects on their respective oxidation. The production of (14)CO(2) from [1,12 -(14)C] dodecanedioic acid was proportional to its concentration in the 0.2 - 5.0 mM range. These results were essentially comparable to those obtained in islets from control rats. They extend, therefore, to GK rats the knowledge that dodecanedioic acid acts as a nutrient in pancreatic islet cells.

Animals↗
PubMed2001

Unreliable use of standard muscle hydration value in obesity.

Intramuscular water content is assumed to be constant in humans independent of their anthropometric characteristics. To verify whether this assumption is correct, intramuscular water, proteins, glycogen, and both total and intramyocytic triglycerides were measured in 51 samples of rectus abdominis muscle obtained from 16 lean and 35 overweight and obese subjects (body mass index cutoff 24.9 kg/m2). Data (referred to as wet tissue) were analyzed by means of a composition model at the cellular level of the skeletal muscle (SM). The average SM water content was 76.3 +/- 3.3% in normal-weight individuals and 65.7 +/- 5.8% in obese subjects (P < 0.0001). Total triglycerides were 5.5 +/- 2.3% in controls and 19.0 +/- 7.0% in obese subjects (P < 0.0001). The intramyocytic triglyceride fraction was also increased in obese subjects. The composition model provides an explanation for the negative correlation between total triglycerides and intramuscular water, and some of the model parameters were determined from the experimental data. In conclusion, although the hydration of fat-free SM mass may be unchanged in obese subjects, the hydration of in toto muscle mass decreases as its lipid content increases.

Adult↗
PubMed2001

Glucose disposal in morbidly obese patients in the early post-operative period.

BACKGROUND: In surgical patients, operative stress causes protein catabolism, muscle mass loss, and impaired glucose tolerance. We investigated fuel metabolism and glucose and protein turnover in 15 obese subjects who underwent biliopancreatic diversion (BPD) by using stable labelled isotopes. METHODS: 6 males and 9 females (age 45.11 +/- 8.9 years, BMI of 48.85 +/- 4.43 kg/m2) who underwent BPD were studied, and the APACHE II score was calculated. Patients were studied 3 times (before BPD, 1st and 3rd postoperative day). Glycemia was stable--maintained by continuously infusing Rapid insulin. Each day of the study, the patients received a primed, constant infusion of [15N2] urea, and, 180 min after, a [6.6-2H] glucose infusion started and continued for 3 hours. Indirect calorimetry was performed during the study, under TPN (30 kcal/kg). RESULTS: The APACHE score was lower on the 3rd postoperative day than on the 1st postoperative day (7.4 +/- 2.7 vs 6.3 +/- 2.6, p < 0.05). The npRQ was different throughout the post-operative period (0.82 +/- 0.03 vs 0.9 +/- 0.06, p < 0.05), while urinary nitrogen excretion, energy expenditure and glycemia did not change. The insulin amount infused was lower during the 3rd post-operative day (44.25 +/- 12.3 vs 64.12 +/- 11 UI on the 1st one, p < 0.05). Insulinemia was lower during the 3rd than during the 1st postoperative day (66.4 +/- 9.49 vs 117.44 +/- 8.49 microU/ml, p < 0.05). Non-essential fatty acid levels were higher on the 3rd post-operative day than on the 1st one (0.98 +/- 0.6 vs 0.45 +/- 0.34 mmol/L, p < 0.01). No differences were observed in glucose and urea turn-over. CONCLUSION: The metabolic pattern of morbidly obese patients operated by BPD was similar to that of other critically ill patients previously studied in the literature. Furthermore, the increased glucose oxidation rate observed on the 3rd post-operative day was coupled with an improved clinical condition.

APACHE↗
PubMed2001

A model for glucose control of insulin secretion during 24 h of free living.

The aim of this work was to develop a mathematical model describing the functional dependence of insulin secretion on plasma glucose concentrations during 24 h of free living. We obtained hourly central venous blood samples from a group of healthy volunteers who spent 24 h in a calorimetric chamber, where they consumed standardized meals. Insulin secretory rates were reconstructed from plasma C-peptide concentrations by deconvolution. The relationship between insulin release and plasma glucose concentrations was modeled as the sum of three components: a static component (describing the dependence on plasma glucose concentration itself, with an embedded circadian oscillation), a dynamic component (modeling the dependence on glucose rate of change), and a residual component (including the fraction of insulin secretion not explained by glucose levels). The model fit of the individual 24-h secretion profiles was satisfactory (within the assigned experimental error of glucose and C-peptide concentrations). The static component yielded a dose-response function in which insulin release increased quasi-linearly (from 40 to 400 pmol/min on average) over the range of 4-9 mmol/l glucose. The dynamic component was significantly different from zero in coincidence with meal-related glucose excursions. The circadian oscillation and the residual component accounted for the day/night difference in the ability of glucose to stimulate insulin release. Over 24 h, total insulin release averaged 257+/-58 nmol (or 43+/-10 U). The static and dynamic component together accounted for approximately 80% of total insulin release. The model proposed here provides a detailed robust description of glucose-related insulin release during free-living conditions. In nondiabetic subjects, non-glucose-dependent insulin release is a small fraction of total insulin secretion.

Adult↗
PubMed2000

Insulin resistance directly correlates with increased saturated fatty acids in skeletal muscle triglycerides.

A close relationship between elevated plasma free fatty acid (FFA) levels and insulin resistance is commonly reported in obese subjects. The aim of the present study was to evaluate the role of intramuscular triglyceride (mTG) and FFA levels in insulin sensitivity in 30 nondiabetic normal-weight or obese subjects (18 with body mass index [BMI] = 21.8 +/- 3.3 kg/m2 and 12 with BMI = 34.6 +/- 2.7 kg/m2) who underwent minor abdominal surgery. Body composition was estimated by isotopic dilution, substrate oxidation by indirect calorimetry, and whole-body glucose uptake by euglycemic-hyperinsulinemic clamp (EHC). Glucose uptake (M) value negatively correlated with the MTG level (R2 = -.56, P < .0001), which was increased in obese patients (11.6 +/- 2.2 v 6.2 +/- 1.4 micromol/g wet weight muscle tissue, P < .0001). The TG fatty acid profile was significantly different in the 2 groups: an increased concentration of saturated fat was present in obese patients (unsaturated to saturated ratio, 1.89 +/- 0.40 v2.19 +/- 0.07, P < .0001). Stepwise linear regression analysis of total mTGs and palmitic and oleic fractions on the M value showed that only TGs and palmitic acid were significantly related to glucose uptake (R2 = .66, P < .0001). Furthermore, among the other anthropometric variables, only the BMI was significantly correlated with MTGs (R2 = .71, P < .0001). In conclusion, not only the MTG concentration but also the FFA pattern seems to affect insulin-mediated glucose uptake. A pivotal role might be played by a high saturated fatty acid content in the TGs.

Adult↗
PubMed2000

Serum leptin levels in post-hepatitis liver cirrhosis.

BACKGROUND/AIMS: Little information is available on the involvement of leptin in clinical conditions associated with malnutrition, such as liver cirrhosis. The behaviour of serum leptin in patients with different Child-Pugh score, post-hepatitis liver cirrhosis and insulin sensitivity has therefore been investigated and compared with that in alcoholic Child C patients. METHODS: Sixty-four patients, aged 51 to 62 years, with different degrees of post-hepatitis cirrhosis or Child C alcoholic cirrhosis were compared with 15 age-matched control subjects. Body composition was estimated by skinfold thickness. Serum leptin, glucose and insulin were assayed. RESULTS: In post-hepatitis patients a significant reduction in leptin levels was observed as the Child-Pugh score worsened (men: 2.94+/-1.61 in Child C vs 6.78+/-2.49 ng/ml in controls, p<0.001; women: 4.14+/-0.66 in Child C vs 16.16+/-3.90 ng/ml in controls, p<0.02). Conversely, only the men with alcoholic liver cirrhosis showed a significant difference in leptin concentration compared to controls (8.5+/-2.1 vs 16.4+/-7.9 kg, p<0.05). In particular, Child C, alcoholic cirrhotic women had a significantly (p=0.03) higher level of leptin than post-hepatitis matched women. A positive correlation was observed between leptin and fat mass (men R2=0.59, p<0.0001 and women R2=0.65, p<0.0001). While fasting levels of serum leptin correlated significantly with insulin concentrations in controls, a similar relationship was not observed in the cirrhotic population, which displayed higher insulin concentrations than controls. CONCLUSIONS: In contrast to findings in alcoholic cirrhotic women, low leptin values in post-hepatitis cirrhotic patients mainly represent the expression of a reduced fat mass.

Adipose Tissue↗
PubMed2000

Acetyl-L-carnitine infusion increases glucose disposal in type 2 diabetic patients.

Little information is available in the literature on the effect of L-carnitine to improve glucose disposal in healthy control subjects and type 2 diabetic patients. No data are reported on the pharmacological properties of acetyl-L-carnitine (ALC) in type 2 diabetes mellitus. The present study evaluates glucose uptake and oxidation rates with either ALC or placebo administration in 18 type 2 diabetic patients. On different days, each patient received both a primed-constant infusion of ALC (5 mg/kg body weight [BW] priming bolus and either 0.025, 0.1, or 1.0 mg/kg BW/min constant infusion) and a comparable placebo formulation. During the infusion period, continuous indirect calorimetric monitoring and a euglycemic-hyperinsulinemic clamp (EHC) study were performed. The total end-clamp glucose tissue uptake (M value) was significantly increased by the administration of ALC (from 3.8 to 5.2 mg/kg/min, P = .006), and the dose dependence of this effect reached borderline statistical significance (P = .037). The increase in the M/I ratio was also highly significant after ALC administration (from 3.9 to 5.8 x 10(-2) mg/kg/min/(microUI/mL, P < .001), while no statistically significant effect was attributable to the different dosages. The increase in the M value was related to increased glucose storage (highly significant effect of ALC) rather than increased glucose oxidation (no statistical significance). In conclusion, the effect of ALC on glucose disposal has no relationship to the amount administered. This could be due to an effect of ALC on the enzymes involved in both the glycolytic and gluconeogenetic pathways, and a possible reversibility of glycogen synthase inhibition in diabetic subjects.

Acetylcarnitine↗
PubMed2000

Body composition and energy expenditure after weight loss following bariatric surgery.

OBJECTIVES: To assess the effectiveness of biliopancreatic diversion (BPD) in the treatment of morbid obesity and to evaluate how the procedure affects body weight. SUBJECTS: Fourteen morbidly obese subjects studied before and 30 months after BPD and fifteen healthy volunteers matched for age, sex and height (controls). METHODS: Comparison of the following parameters were made in the study groups before surgery and 30 months after BPD and with those of the controls group: fat mass, fat-free mass, non-protein substrate oxidation, basal metabolic rate, plasma glucose, insulin and free fatty acid concentrations. RESULTS: Obese subjects lost 60.38+/-10.71 kg of weight during 18 months following surgery and then remained stable for another 12 months, when this study was performed. Weight loss was substantially due to a loss of fat mass (FM: 60.13+/-13.01 kg before and 19.02+/-8.61 kg after BPD; p<0.001). FM were not statistically different between post-obese subjects and controls; however, post-obese patients retained significantly more fat free mass (FFM) than controls. Subsequently, basal metabolic rates of post-obese subjects were higher than those of the control group (p<0.05). Fasting non-protein respiratory quotient (npRQ) was significantly lower before BPD than 30 months after the surgery (0.798+/-0.04 vs. 0.90+/-0.048, p<0.001), suggesting that, while obese, patients oxidized more lipids than carbohydrates. Moreover, fasting and two-hour plasma glucose and insulin concentrations decreased significantly after BPD to values comparable to those of the control group. CONCLUSION: Weight loss in obese patients after BPD is mainly due to lipid malabsorption, but increased energy expenditure associated with retaining a high FFM in physically active post-obese subjects may also play a role, enabling them to maintain long-term reduced body weights.

Adult↗
PubMed2000

Changes in body composition, substrate oxidation, and resting metabolic rate in adult celiac disease patients after a 1-y gluten-free diet treatment.

BACKGROUND: The incidence of celiac disease has been on the rise in both Europe and the United States. Celiac disease patients are at high risk of undernutrition because of nutrient malabsorption. OBJECTIVE: The aim of the present study was to evaluate changes in body composition and energy metabolism in a group of patients with celiac disease before and after consumption of a gluten-free diet (GFD). DESIGN: Body composition (by anthropometry and isotopic dilution), resting metabolic rate (RMR), and substrate oxidation rates (by indirect calorimetry) were assessed in 39 adult celiac disease patients (16 men and 23 women) with a mean (+/-SD) age of 29. 9 +/- 7.6 y, weight of 58.3 +/- 6.6 kg, and percentage body fat of 20.1 +/- 6.7%, and in 63 (29 men and 34 women) age- and height-matched control subjects (age: 33.2 +/- 8.1 y; weight: 66.8 +/- 6.6 kg; and percentage body fat: 25.4 +/- 3.7%). Celiac disease patients were studied twice, at diagnosis and 1 y after treatment with a GFD. RESULTS: Before treatment, celiac disease patients had a lower body weight (P < 0.05) and a higher carbohydrate oxidation rate (P < 0.01) than did control subjects. Carbohydrate oxidation rates correlated positively with fecal lipid loss in untreated celiac disease patients (r = 0.80, P < 0.0001). After the GFD, percentage body fat was higher in celiac disease patients than in control subjects (P < 0.01), and lipid intakes tended to be higher than before treatment. CONCLUSIONS: This longitudinal study showed that the GFD treatment significantly increased body fat stores. Untreated patients preferentially utilized carbohydrates as a fuel substrate, probably as a consequence of both lipid malabsorption and a high carbohydrate intake, and lipid utilization increased with the restoration of the intestinal mucosa.

Adolescent↗
PubMed2000

Effect of a vegetable-protein-rich polymeric diet treatment on body composition and energy metabolism in inactive Crohn's disease.

OBJECTIVE: Since malnutrition and lactose intolerance are frequently reported in Crohn's disease (CD), we evaluated the differences in terms of compliance-to-treatment and nutritional status in inactive CD patients after two different treatments using either a standard polymeric diet or a vegetable-protein-rich and lactose-free diet. STUDY DESIGN: A case-control study. SUBJECTS: Forty CD patients with inactive disease were randomly divided into two groups. Group A (10 men; aged 33.9+/-7.2 years; BMI, 21.8+/-1.7 kg/m2) received a conventional polymeric enteral diet, while group B (10 men; aged 35.6+/-6.8 years; BMI, 21.4+/-1.8 kg/m2) was administered a soy-rich and lactose-free polymeric diet, over a 4-week period. METHODS: All the patients had a clinical and laboratory examination. Body composition was assessed by isotopic dilution and resting metabolic rate (RMR), and substrate oxidation rates were measured by indirect calorimetry. RESULTS: Body weight significantly increased after treatment in both groups (A, P<0.05; and B, P<0.01), as well as fat-free mass (A, P<0.05; and B, P<0.05) and fat mass (A, P<0.05; and B, P<0.01). RMR slightly increased, although it did not reach statistical significance. Treatment did not influence substrate oxidation rates. Group B lactose-intolerant patients reported a greater compliance-to-treatment than those in group A. CONCLUSIONS: This study showed that a polymeric enteral diet rich in vegetable protein and not containing milk protein, eaten at home, with no need for positioning a nasogastric tube, significantly improved body composition in inactive and lactose-intolerant CD patients, with no effect on energy metabolism, suggesting that it could be useful in improving nutritional status in these patients.

Adult↗
PubMed2000

Oxidation of [1,12-14C]dodecanedioic acid by rat pancreatic islets.

Several aliphatic dioic acids were recently reported to stimulate insulin release in isolated rat pancreatic islets incubated at close-to-physiological D-glucose concentrations. In order to gain insight into the mode of action of these acids in pancreatic islet B-cells, the oxidation of [1,12-14C]dodecanedioic acid (5.0 mM) was now measured in rat islets. Expressed as pmol of [1, 12-14C]dodecanedioic acid equivalent, the production of 14CO2 was close to 1.0 pmol/islet per 120 min, representing about 8% of that attributable to the oxidation of D-[U-14C]-glucose (8.3 mM). The dioic acid and the hexose failed to exert any significant reciprocal effect upon their respective oxidation rate. These findings support the view that the insulinotropic action of dodecanedioic acid, and presumably other aliphatic dioic acids, is causally linked to their capacity to act as nutrients in pancreatic islet cells.

Animals↗
PubMed2000

Disposition of dodecanedioic acid in humans.

The disposition of dodecanedioic acid (C12) was investigated in six overnight-fasting healthy male volunteers, who received a 165-min i. v. infusion of 42.45 mmol of C12 added to 150 microCi of [1-12-(14)C]C12. Blood samples were collected up to 360 min after the start of infusion, and concentration of serum labeled C12 was determined. Expired radioactivity (microCi/min) was measured up to 600 min and at 24 h. The 24-h C12 urinary excretion was around 5% of the administered amount. The percentage of C12 oxidized was 81.7 +/- 9.5% (mean +/- S.D.) of administered amount as estimated from the area under the curve of measured (14)CO(2) expiration rate. C12 kinetics was described by assuming a single compartment. A saturable rate of C12 tissue uptake (model A) and a linear rate of tissue uptake (model B) were considered. The kinetics of CO(2) produced by C12 oxidation was described by a fast pathway acting in parallel to a slow pathway modeled by first order kinetics. Parameters of model B were estimated for each subject, whereas model A was identified by fitting the pooled data of all subjects. On the basis of estimates obtained from model B, an average calorie delivery of 500 kcal/day was predicted in the plateau phase for the infusion rate of our experiments. When estimated from model A, the maximal rate of tissue uptake was 0.38 +/- 0.08 mmol/min, with a maximal calorie delivery of 750 kcal/day. These results appear promising for C12 utilization in parenteral nutrition, because C12 elimination with urine is low, whereas tissue uptake and oxidation are rather efficient.

Adult↗
PubMed2000

Subclinical hepatic encephalopathy: role of tryptophan binding to albumin and the competition with indole-3-acetic acid.

BACKGROUND: The role of tryptophan (TRY) and its metabolites in the pathogenesis of hepatic encephalopathy is conflicting. The aim of the present study is to investigate in posthepatitis cirrhotic patients with encephalopathy the serum levels of TRY and those of its metabolite indole-3-acetic acid, as well as TRY binding curve to serum albumin and the competition with indole-3-acetic acid. The presence of a relationship between encephalopathy severity and circulating free TRY was also investigated. METHODS: Serum TRY and indole-3-acetic acid were analyzed by HPLC; binding of TRY to serum albumin and the competition with indole-3-acetic acid was studied by equilibrium dialysis. RESULTS: Serum-free TRY was significantly higher in cirrhotic patients (43.33 +/- 14.70 vs 28.87 +/- 8.77 mumol/L, P = 0.02). The binding capacity of albumin was reduced in cirrhotics and further decreased by the addition of indole-3-acetic (K = 6.63 +/- 0.97 x 10(3) mol/L-1, gamma = 1.16 +/- 0.45 x 10(2) mol/L-1 in normal sera vs K = 1.04 +/- 0.20 x 10(3) mol/L-1, gamma = 1.91 +/- 0.92 10(2) mol/L-1 in cirrhotic sera). A multivariate analysis showed that among the psychometric tests the only independent predictor of serum levels of free TRY was the Block Design (R2 = 0.94, B = 0.16 +/- 0.01, beta = 0.97; P < 0.0001). CONCLUSIONS: A high percent ratio of free/total TRY and indoleacetic acid (IAA) was found in cirrhotic patients with hepatic encephalopathy. The concentrations of serum-free IAA and TRY correlated with the degree of subclinical encephalopathy, suggesting a role of these compounds in the development of mental derangement in liver cirrhosis.

Adult↗
PubMed2000

Effects of aliphatic dioic acids and glycerol-1,2,3-tris(dodecanedioate) on D-glucose-stimulated insulin release in rat pancreatic islets.

Aliphatic dioic acids have been proposed as alternative nutrients in selected clinical situations. In this study, their possible insulinotropic action was investigated in isolated rat pancreatic islets prepared from fed rats. Azelaic acid, sebacic acid and tridecanedioic acids, when tested at a 10.0 mm concentration, were found to augment insulin release evoked by D-glucose (7.0 mm) in the pancreatic islets. Likewise, glycerol-1,2,3-tris(dodecanoedioate), when used at concentrations close to 1.0 mm, increased the secretory response to the hexose. It is speculated that these findings may extend to insulin-producing cells, the knowledge that aliphatic dioic acids or their esters may act as energy substrates, e.g. in parenteral nutrition.

Animals↗
PubMed1999

Comparison of insulin response to intravenous glucose in healed myocardial infarction, in "cooled-off" unstable and stable angina pectoris, and in healthy subjects.

Fasting and postglucose hyperinsulinemia are recognized risk factors for acute coronary events. The insulin reactivity of patients with acute coronary syndromes, however, has not been carefully compared with that of patients with chronic stable angina. We used Bergman's minimal model to analyze the insulin response to intravenous glucose in 21 subjects: 8 patients with previous (>3 months) acute coronary syndrome but no effort-related angina; 6 patients with stable effort angina but no prior acute event; and 7 healthy controls. Diabetes mellitus, systemic hypertension, dyslipidemias, and obesity were excluded. All patients underwent coronary angiography. Insulin sensitivity, glucose effectiveness, and glucose tolerance were determined from insulin and glucose concentrations measured frequently up to 3 hours after a 0.33 g/kg intravenous glucose bolus. Patients with previous unstable angina or acute myocardial infarction had less extensive disease at angiography than patients with stable angina (p = 0.007). Both patient groups had higher basal and 180-minute insulinemia than controls (p <0.0007). However, patients with stable angina did not differ significantly from controls with regard to early and late insulinemic response to glucose. In contrast, patients with previous acute onset of ischemia had significantly greater 180-minute integrated insulinemia (p = 0.04) and reduced insulin sensitivity (p = 0.05) after the glucose challenge than did the stable angina group. These data suggest that patients with acute presentation of coronary artery disease, compared with patients with uncomplicated chronic stable angina, have an impaired insulin response to glucose despite less extensive coronary disease at angiography.

Analysis of Variance↗