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Biomedical subjects

G Pozza

Publications and source records attributed to G Pozza.

At least 73 records · Page 4Linked to original sources
PubMed1997

Personality traits and metabolic control: a study in insulin-dependent diabetes mellitus patients.

BACKGROUND: In the present study the authors evaluated the relationship between personality traits (according to DSM-III-R) and poor metabolic control in an adult onset insulin-dependent diabetes mellitus sample (n = 77). METHODS: Personality traits were assessed with the Personality Diagnostic Questionnaire--Revised. Metabolic control was evaluated through glycosilated hemoglobin (HbA1c): poor metabolic control was defined as HbA1c > or = 9% (normal values < 6.0%). RESULTS: Principal Component Analysis revealed three personality profiles: 'Cluster A/C Mixed', 'Cluster B Dependent' and 'Cluster B Aggressive'. Oneway ANCOVA, using sex as covariate, revealed a significant association (p = 0.01) only between poor metabolic control and Cluster B Dependent profile. No correlation was found between HbA1c and the other profiles. CONCLUSION: These data suggest that a specific personality profile is associated with poor metabolic control.

Adult↗
PubMed1997

Insulin and glucagon release of human islets in vitro: effects of chronic exposure to glucagon.

Hyperglucagonemia is commonly found in insulin-dependent as well as in non-insulin-dependent diabetes mellitus, and is likely to be caused by absolute or relative insulin deficiency. The aim of the present study was to evaluate whether a chronic glucagon exposure (1.0 microM for 4 h) modifies the insulin response to acute stimuli with glucagon (1.0 microM), arginine (10.0 mM) and glucose (16.7 mM), or the glucagon response to arginine and glucose, in human islets. Chronic exposure to glucagon did not affect the insulin response to glucose and arginine, but inhibited its response to glucagon (44.6 +/- 9.3 vs 168.6 +/- 52.3 pg/islet per 20 min, P < 0.05); the latter effect was not observed when exposure to glucagon was discontinuous (2.0 microM glucagon alternated with control medium for 30 min periods). The chronic exposure to glucagon also reduced the glucagon response to arginine (- 4.9 +/- 5.7 vs 19.9 +/- 7.9 pg/islet per 20 min, P < 0.05) without affecting the inhibition of glucagon release exerted by glucose. These data indicate that chronic exposure to glucagon desensitizes pancreatic alpha and beta cells in response to selected stimuli.

Arginine↗
PubMed1997

Cancer arising after pancreas and/or kidney transplantation in a series of 99 diabetic patients.

OBJECTIVE: Recipients of solid organ transplants have an increased risk of developing certain types of malignancies as compared with the general population. The majority of the literature has reported on neoplasms in kidney and heart transplant recipients. RESEARCH DESIGN AND METHODS: We describe 9 neoplasms occurring in 7 out of 73 IDDM patients after simultaneous pancreas and kidney transplantation. No cases were recorded among 26 IDDM recipients of kidney transplantation. RESULTS: Among the neoplasms found were 2 cases of posttransplant lymphoproliferative disorder (PTLD), malignant melanoma, basal-cell and squamous-cell carcinoma of the skin in the same patient, squamous-cell carcinoma in situ of the vulva, hepatocarcinoma, small-cell lung cancer, and ductal carcinoma of the breast. Four patients died. Among immunological risk factors, over-immunosuppression for steroid-resistant kidney rejection was administered only in the 2 cases of PTLD. CONCLUSIONS: Increased dosage of immunosuppressive agents may be necessary in some patients of prevent or treat rejection in view of their reduced survival on hemodialysis.

Adult↗
PubMed1997

A method for assessing catheter patency in implanted pumps for long-term intraperitoneal insulin delivery.

Catheter complications are a common problem during long-term insulin therapy with implanted pumps. The purpose of this study was to test the feasibility of imaging intraperitoneal catheters with technetium (Tc) 99m in implantable devices for insulin delivery. Testing physical stability of an insulin/Tc 99 mixture did not show formation of insulin aggregates during a period up to 48 h on a rotating wheel. Five hundred microCurie (equal to 18 MBq) of Tc 99m were injected in the flush port of a pump for intraperitoneal insulin delivery implanted in patients with type I (insulin dependent) diabetes mellitus, and gamma camera images were obtained for 30 min. In patent catheters the tracer rapidly imaged the whole length of the catheter while in occluded catheters the tracer remained in the flush port, imaging only the portion of the catheter before the occlusion. In patent catheters in which insulin absorption was impaired, the tracer rapidly imaged the whole length of the catheter, but its removal from the peritoneum was delayed. Tc 99m imaging of intraperitoneal catheters for insulin delivery can be used to assess catheter patency and impaired delivery into the peritoneal cavity.

Catheterization↗
PubMed1997

[Is echography an adequate method for assessing the thickness of intra-abdominal fat? A comparison with computed tomography].

PURPOSE: The methods to measure intraabdominal fat amount and to distinguish visceral from subcutaneous fat are useful and needed because visceral obese people are at risk of developing cardiovascular disorders. We investigated US capabilities in measuring intraabdominal fat thickness and distribution distinguishing visceral from subcutaneous fat. The results were compared with those obtained with CT, the gold standard, and with the waist-hip ratio (W/H). MATERIAL AND METHODS: Thirty obese women admitted to the Internal Medicine I Department, Ospedale S. Raffaele (Milan, Italy) were examined. The patients, aged 18-60 years and with BMI ranging 29.0-47.3, were submitted to consecutive double blind measurements with US and CT. The following anthropometric values were compared for every patient: W/H, US visceral/subcutaneous thickness, CT visceral/subcutaneous thickness, CT visceral area, CT subcutaneous adipose area and CT visceral/subcutaneous adipose area. RESULTS: The classification of visceral obesity by W/H (> .85) was confirmed by CT visceral/subcutaneous adipose area (> .491). The W/H correlated significantly with CT visceral/subcutaneous adipose thickness and CT visceral/subcutaneous adipose area (r = .52, p < .004; r = .51, p < .004), but not with US visceral/subcutaneous adipose thickness (r = .42, p < .06). Significant correlations were found between Ct visceral/subcutaneous adipose area and with both US and CT visceral/subcutaneous adipose thickness (r = .59, p < .006; = .71, p < .0001). A high correlation was found between US visceral/subcutaneous adipose thickness and CT visceral/subcutaneous adipose thickness (r = .96, p < .0001). CONCLUSION: Analyzing the results of the different methods, we conclude that US can always be used to study abdominal fat amount and distribution in obese women because this method exhibits significant correlations with CT, the gold standard. The W/H is not sufficient to distinguish visceral from subcutaneous intraabdominal fat.

Abdomen↗
PubMed1996

Effects of low-dose heparin infusion on arterial endothelin-1 release in humans.

BACKGROUND: The aim of this study was to evaluate the effect of low-dose heparin infusion on arterialized endothelin-1 (ET-1) release in the presence of fasting or high insulin levels in healthy humans. METHODS AND RESULTS: Eleven normal subjects underwent two tests in random order lasting 240 minutes. A primed (250 IU), continuous heparin (600 IU/h) infusion was performed in test 1; saline was infused in test 2 as control. At 120 minutes, a euglycemic hyperinsulinemic clamp (25 mU.kg-1.h-1) was started that lasted 2 hours in both tests. Two hours after heparin infusion (test 1), ET-1 levels decreased by 32% (3.52 +/- 0.60 to 3.02 +/- 0.73 pg/mL), while nitric oxide (NO) and forearm blood flow increased by 29% and 14%, respectively. During saline infusion, ET-1, nitric oxide, and forearm blood flow remained unchanged. There was a significant interaction between the effect of decreasing ET-1 levels and the heparin treatment (F, 4.06; df, 3.30; P < .01). The decrease in ET-1 levels was significantly correlated with the increase in forearm blood flow in test 1 (r = .74; P < .01) but not in test 2. During the heparin/insulin period, ET-1 increased by 25%, returning to fasting values; nitric oxide levels increased by 12%; and forearm blood flow remained unchanged. CONCLUSIONS: The present study showed that it is possible to decrease ET-1 levels by use of low-dose heparin infusion in humans. This effect seems mediated by a simultaneous increase in nitric oxide levels and is completely reversed by a mild increase in insulin concentrations.

Adult↗
PubMed1996

Metabolic effects of successful intraportal islet transplantation in insulin-dependent diabetes mellitus.

The intraportal injection of human pancreatic islets has been indicated as a possible alternative to the pancreas transplant in insulin-dependent diabetic patients. Aim of the present work was to study the effect of intraportal injection of purified human islets on: (a) the basal hepatic glucose production; (b) the whole body glucose homeostasis and insulin action; and (c) the regulation of insulin secretion in insulin-dependent diabetes mellitus patients bearing a kidney transplant. 15 recipients of purified islets from cadaver donors (intraportal injection) were studied by means of the infusion of labeled glucose to quantify the hepatic glucose production. Islet transplanted patients were subdivided in two groups based on graft function and underwent: (a) a 120-min euglycemic insulin infusion (1 mU/kg/min) to assess insulin action; (b) a 120-min glucose infusion (+75 mg/di) to study the pattern of insulin secretion. Seven patients with chronic uveitis on the same immunosuppressive therapy as grafted patients, twelve healthy volunteers, and seven insulin-dependent diabetic patients with combined pancreas and kidney transplantation were also studied as control groups. Islet transplanted patients have: (a) a higher basal hepatic glucose production (HGP: 5.1 +/- 1.4 mg/kg/ min; P < 0.05 with respect to all other groups) if without graft function, and a normal HGP (2.4 +/- 0.2 mg/kg/min) with a functioning graft; (b) a defective tissue glucose disposal (3.9 +/- 0.5 mg/kg/min in patients without islet function and 5.3 +/- 0.4 mg/kg/min in patients with islet function) with respect to normals (P < 0.01 for both comparisons); (c) a blunted first phase insulin peak and a similar second phase secretion with respect to controls. In conclusion, in spite of the persistence of an abnormal pattern of insulin secretion, successful intraportal islet graft normalizes the basal HGP and improves total tissue glucose disposal in insulin-dependent diabetes mellitus.

Adult↗
PubMed1996

Intercellular Ca2+ waves sustain coordinate insulin secretion in pig islets of Langerhans.

Insulin release was investigated in parallel with changes in cytosolic calcium concentration, [Ca2+]i, in pig islets stimulated by glucose. After two days in culture, glucose stimulation failed to induce insulin release, and caused limited [Ca2+]i changes in few cells. After ten days, insulin response was partially restored and [Ca2+]i recordings revealed a slow oscillatory activity of the whole islet. Slow oscillations appeared to be due to the average [Ca2+]i variations resulting from the spreading of waves throughout the islet. These waves demonstrate the reestablishment of functional cell coupling, which appears to play a critical role in insulin release.

Animals↗
PubMed1996

Effects of an acute decrease in non-esterified fatty acid levels on muscle glucose utilization and forearm indirect calorimetry in lean NIDDM patients.

The aim of the study was to evaluate an acute decrease in NEFA levels during an oral glucose tolerance test and its effects on glucose tolerance, muscle glucose uptake and muscle indirect calorimetry in ten lean non-insulin-dependent diabetic subjects. Two 75-g oral glucose tolerance tests were performed in random order. Placebo or 250 mg acipimox (to inhibit lipolysis) were administered orally 2 h before the start of the oral glucose tolerance test. Two hours after acipimox administration (time 0), non-esterified fatty acid, glycerol and 3-hydroxybutyrate levels decreased by 84, 68 and 77% respectively, compared to basal levels. Concomitantly, muscle lipid oxidation and non-oxidative glycolysis also decreased significantly. After placebo administration, non-esterified fatty acids, glycerol and 3-hydroxybutyrate and lipid oxidation increased by 29, 28, 106 and 33%, respectively (NS vs basal levels; p < 0.001 vs acipimox). There was a negative rate of net glucose storage (interpreted as glycogenolysis) during post-absorptive conditions and at time 0 after administration of both drugs. After oral glucose tolerance test, the incremental areas of blood glucose and insulin were significantly decreased by 18 and 19% after acipimox compared to placebo. In addition, the ratio between the incremental area of forearm muscle glucose uptake and the insulin levels was significantly increased by 45% during acipimox compared to placebo administration. Glucose oxidation and non-oxidative glycolysis were significantly higher while lipid oxidation was significantly lower after acipimox than after placebo. In conclusion, our study found that in lean non-insulin-dependent diabetic subjects, an acute decrease in non-esterified fatty acid levels improves glucose tolerance, muscle glucose uptake, glucose oxidation and non-oxidative glycolysis, but is unable to normalize glucose storage.

3-Hydroxybutyric Acid↗
PubMed1996

Prevalence of diabetic peripheral neuropathy and its relation to glycaemic control and potential risk factors: the EURODIAB IDDM Complications Study.

The EURODIAB IDDM Complications Study involved the examination of 3250 randomly selected insulin-dependent diabetic patients, from 31 centres in 16 European countries. Part of the examination included an assessment of neurological function including neuropathic symptoms and physical signs, vibration perception threshold, tests of autonomic function and the prevalence of impotence. The prevalence of diabetic neuropathy across Europe was 28% with no significant geographical differences. Significant correlations were observed between the presence of diabetic peripheral neuropathy with age (p < 0.05), duration of diabetes (p < 0.001), quality of metabolic control (p < 0.001), height (p < 0.01), the presence of background or proliferative diabetic retinopathy (p < 0.01), cigarette smoking (p < 0.001), high-density lipoprotein cholesterol (p < 0.001) and the presence of cardiovascular disease (p < 0.05), thus confirming previous associations. New associations have been identified from this study - namely with elevated diastolic blood pressure (p < 0.05), the presence of severe ketoacidosis (p < 0.001), an increase in the levels of fasting triglyceride (p < 0.001), and the presence of microalbuminuria (p < 0.01). All the data were adjusted for age, duration of diabetes and HbA1c. Although alcohol intake correlated with absence of leg reflexes and autonomic dysfunction, there was no overall association of alcohol consumption and neuropathy. The reported problems of impotence were extremely variable between centres, suggesting many cultural and attitudinal differences in the collection of such information in different European countries. In conclusion, this study has identified previously known and new potential risk factors for the development of diabetic peripheral neuropathy.

Adolescent↗
PubMed1996

Benfluorex in obese noninsulin dependent diabetes mellitus patients poorly controlled by insulin: a double blind study versus placebo.

Most obese patients with noninsulin-dependent diabetes mellitus (NIDDM) are initially treated with diet, then with oral hypoglycemic agents, eventually with insulin. However several reports indicate that in these patients insulin therapy has little chance to control glucose metabolism, promotes weight gain and arterial hypertension, and is likely to aggravate insulin resistance. In this randomized, double-blind trial vs. placebo (P) we evaluated in 29 obese NIDDM patients poorly controlled by insulin (daily insulin doses 48.7 +/- 4.0 U/day, HbA1c 10 +/- 0.27%, mean daily blood glucose levels 12.3 +/- 0.3 mmol/L, fasting C-peptide 1.8 +/- 0.2, C-peptide after 1 mg iv glucagon 3.2 +/- 0.3 ng/mL, means +/- SE), the clinical and metabolic effects of benfluorex (B), a lipid-lowering drug able to improve insulin sensitivity. After a 2-3 week run-in period (1 tablet P at dinner and diet 800 cal/day to lose 5% of the initial body weight (BWi), patients received a 1000 kcal/day diet and were randomized to B, 150 mg/ tablet, or P (3 tablets/day); the time limit was set at a 10% decrease of BWi or at 90 days. At the end of run-in there was a significant reduction of BWi (P < 0.001), fasting (P = 0.002) and mean daily blood glucose levels (P < 0.001), triglycerides (P = 0.02), cholesterol (P < 0.001) and daily insulin doses (P < 0.001). At the end of the double-blind trial, weight-loss was greater (P < 0.05), faster (P = 0.018), and more frequent (P < 0.05) with B than with P, and systolic blood pressure (P < 0.05) decreased only with B. Considering only patients with a 10% decrease of BWi (B = 15, P = 10), HbA1c (P < 0.001) decreased only with B, while fasting insulin levels decreased with both B (P < 0.01) and with P (P < 0.05). Insulin sensitivity was evaluated by means of a double infusion test (LDIGIT, insulin 25 mU/Kg/h plus glucose 4 mg/kg/min, lasting 150 min) at the end of run-in and at the end of the double-blind trial; at the end of the double-blind trial steady state blood glucose (SSBG, P < 0.05), free fatty acids (FFA, P < 0.05) and blood beta-hydroxybutyrate (P < 0.05) decreased only with B, while blood glycerol decreased both with both P (P < 0.05) and B (P < 0.06). At the end of the double-blind trial, C-peptide release was unchanged with either P or B. In conclusion, benfluorex potentiates the effects of hypocaloric diet on weight loss and on glycemic control in obese NIDDM patients treated with insulin, and this effect seems to be the result of an improved insulin sensitivity.

3-Hydroxybutyric Acid↗
PubMed1996

Dihydropyridine-sensitive and -insensitive voltage-operated calcium channels participate in the control of glucose-induced insulin release from human pancreatic beta cells.

Calcium ion entry through voltage-operated calcium channels is a crucial step in the coupling of beta cell depolarization with insulin secretion. Various calcium channel subtypes have been shown to be coexpressed in single neurons and endocrine cells. Using the patch-clamp technique, we investigated the biophysical and pharmacological properties of calcium channels in freshly dispersed human pancreatic beta cells. Both low and high voltage activated currents were expressed, the two current types being easily distinguishable on the basis of biophysical criteria. The high voltage activated currents were not homogeneous: one component was affected by the dihydropyridine antagonist nitrendipine and the agonist Bay-K-8644; the other was insensitive to both dihydropyridines and omega-conotoxin GVIA. In line with this pharmacology, nitrendipine reduced and Bay-K-8644 increased glucose-induced insulin secretion from perifused human islets, whereas omega-conotoxin GVIA had no effect. However, about 20% of the glucose-induced insulin release was found to be resistant to high nitrendipine concentrations. These data show that human pancreatic beta cells express heterogeneous voltage-operated calcium channels, only one of which is dihydropyridine-sensitive (L type). The L type channels are clearly involved in the control of insulin secretion, but our data suggest that dihydropyridine- and omega-conotoxin GVIA-insensitive channels may also play a role in the stimulus-secretion coupling of human beta cells.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1996

Hypertriglyceridemia and hyperinsulinemia are potent inducers of endothelin-1 release in humans.

The purpose of the study was to evaluate fasting endothelin-1 levels in subjects with syndrome X, in subjects with insulinoma, and in normal subjects. The single and synergistic contributions of insulin and triglyceride levels to endothelin-1 release were studied in normal subjects. This was achieved by the evaluation of endothelin-1 levels in response to an insulin bolus combined with a euglycemic clamp (protocol A) and during intralipid (test 1) or saline (test 2) infusions lasting 360 min (protocol B). In protocol B, a euglycemic two-step hyperinsulinemic (25 and 125 mU x kg-1 x h-1) clamp was started at 120 min. Subjects with syndrome X showed significantly higher endothelin-1 levels than normal subjects and subjects with insulinoma (7.22 +/- 0.89 vs. 2.61 +/- 0.38 and 2.49 +/- 0.24 pg/ml, P < 0.01). After an insulin bolus, endothelin-1 levels peaked at 10 min (3.71 +/- 0.96 pg/ml). The incremental area of endothelin-1 was significantly higher after insulin than after a saline bolus. In test 1, an acute increase in triglyceride levels significantly enhanced endothelin-1 levels, with were further increased by the synergistic contribution of high insulin and triglyceride levels. In test 2, endothelin-1 release was achieved at high insulin levels but remained significantly lower than in test 1. In conclusion, subjects with syndrome X showed higher endothelin-1 levels than normal subjects and subjects with insulinoma. These levels were reproduced in normal subjects by a simultaneous increase in insulin and triglyceride levels.

Adult↗
PubMed1996

Effect of pancreas transplantation on free fatty acid metabolism in uremic IDDM patients.

To assess the effect of pancreas transplantation on free fatty acid (FFA) and glucose metabolism, we studied seven uremic IDDM patients (HbA1c 9.1%), nine IDDM patients after combined kidney-pancreas transplantation (HbA1c 5.8%), seven patients with chronic uveitis (HbA1c 5.6%), and nine normal control subjects (HbA1c 5.5%) by means of the [3(- 3)H]glucose and [1(-14)C]palmitate infusion techniques combined with indirect calorimetry and euglycemic insulin clamp. In the postabsorptive state, pancreas-transplant patients had similar plasma glucose and FFA concentrations and non-statistically different rates of hepatic glucose production (HGP) and FFA turnover, while demonstrating a reduced rate of FFA oxidation (42 +/- 5 vs. 73 +/- 10 micromol x m-2 x min-1; P < 0.05) compared with control subjects. After 180 min of tracer equilibration, all subjects underwent a low-dose (100 min, 8 mU x m-2 x min-1) followed by a high-dose (100 min, 40 mU x m-2 x min-1) euglycemic insulin infusion. During insulin infusion, pancreas-transplant patients showed a greater inhibition of FFA concentration (609 +/- 76 to 58 +/- 15 micromol/l) compared with healthy subjects (681 +/- 90 to 187 +/- 25 micromol/l; P < 0.01 vs. pancreas-transplant patients). FFA turnover and oxidation rates during both low-dose and high-dose insulin infusions were lower in pancreas-transplant patients compared with healthy subjects (P < 0.03 and P < 0.01, for turnover and oxidation, respectively). Uremic IDDM patients demonstration altered basal and insulin-mediated glucose metabolism. Pancreas transplantation normalized only insulin-mediated glucose oxidation, leaving the stimulation of non-oxidative glucose disposal still markedly defective. In conclusion, patients after pancreas transplantation have normal basal FFA turnover and reduced basal FFA oxidation rates. During hyperinsulinemia, pancreas-transplant patients show a normal inhibition of FFA turnover and FFA oxidation. Insulin-mediated glucose metabolism remained abnormal after pancreas transplantation. Our findings may be related to the effect of chronic immunosuppressive therapy on glucose and FFA metabolism.

Adult↗
PubMed1995

Lipoprotein profile after combined kidney-pancreas transplantation in insulin dependent diabetes mellitus.

In order to evaluate the effect of a combined kidney-pancreas (KP) transplantation in insulin-dependent diabetes mellitus (IDDM) patients on the lipid and lipoprotein profile, 15 KP patients were compared with 11 kidney (K)--transplanted IDDM patients, 19 IDDM patients on hemodialysis (HD), and 15 nondiabetic control subjects. Cholesterol, triglycerides, apo AI, and apo B were measured in total plasma and in VLDL, LDL, and HDL of all participants. VLDL cholesterol, VLDL-triglycerides, and VLDL-apo B were significantly lower in KP patients, but not in K patients, than in HD patients. In addition, patients in the K, but not in the KP, group showed high levels of apo B in LDL and an increased triglyceride/apo B ratio in VLDL, compared with patients in the HD group. The percentage of apo AI associated with HDL was significantly higher in both transplanted groups than in the HD group. However, compared with a nondiabetic control population, an increase in VLDL particles and in triglyceride content in LDL and HDL still persisted following combined KP transplantation. Insulin resistance (probably due to steroid therapy) associated with high peripheral and potentially low hepatic insulin levels (due to the systemic drainage of the transplanted pancreas) could be the main causes of the remaining lipoprotein abnormalities.

Adult↗