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F D'Onofrio

Publications and source records attributed to F D'Onofrio.

At least 19 recordsLinked to original sources
PubMed2006

Psoriatic arthritis and Klinefelter syndrome: case report.

Psoriatic arthritis (PsA) is a well-known disease characterized by psoriasis and inflammatory joint disease, with distinct clinical and radiological features to differentiate it from other arthropathies. Whereas many cases of coexistence of arthritis and other autoimmune disorders with chromosomal abnormalities have been reported, the occurrence of PsA and Klinefelter syndrome has not been reported previously. A case of Klinefelter syndrome and PsA was reported. This case report emphasizes the role played by sex hormones and chromosomal abnormalities in the pathogenesis of autoimmune disorder, and to our knowledge, this is an uncommon case of a patient with Klinefelter syndrome who developed PsA.

Androgens↗
PubMed2006

Pathogenesis, clinical findings and management of acute and chronic gout.

Gout is a chronic metabolic disease caused by a disorder of the purine metabolism leading to hyperuricaemia. It is determined by the deposition of monosodium urate crystals in joints and other tissues which causes an acute inflammatory response and can induce a permanent tissue damage which defines the urate chronic joint disease which is characterised by the appearance of ulceration of the joint cartilage, marginal osteophytosis, geodic and erosive lesions and chronic inflammation of synovial membrane. Gout and hyperuricaemia usually occur after the age of 30 years and more frequently in men. Hyperuricaemia is the result of an increased production of uric acid or its hypoexcretion by the kidneys, or both. In the pathogenesis of gout and hyperuricaemia are involved genetic and environmental factors; further, different pathologic condition such as glycogenosis, renal insufficiency, use of some drugs, are associated with gout. Treatment of acute gout includes colchicine, nonsteroidal anti-inflammatory drugs and glucocorticoids, whereas in the intercritical periods colchicine is effective for preventive purposes. Urate-lowering therapy with xanthine-oxidase inhibitors or uricosuric agents is indicate only in patients with more than two gout crisis per year, tophaceous deposits, uric acid nephrolithiasis, and interstitial renal disease, as asymptomatic hyperuricaemia does not requires any treatment but can be controlled with preventive dietetic measures and changes in lifestyle.

Acute Disease↗
PubMed2005

[Fibromyalgic syndrome: new perspectives in rehabilitation and management. A review].

Fibromyalgia is a chronic syndrome, characterized by widespread body pain and pain at specific tender points, whose etiology and pathogenesis is still unknown. Patient can also exhibit a range of other symptoms including irritable bowel syndrome, chest pain, anxiety, fatigue, sleep disturbance, headache. The prevalence of fibromyalgia ranges from 1-3% in the general population, and the condition is more common among female than males. Contrary to the situation a few years ago, the most widely accepted hypothesis now evoke central nervous system mechanisms, whose local functions could influence also periferical microvascular activity at tender points. There are many findings supporting the hypothesis of different endogenic and exogenic factors that lead to chronic local hypoxia in muscle tissue. Currently, therapy is polipragmatic and is aimed at reducing the pain. A range of medical treatment had been used to treat fibromyalgia. Pharmacological therapy aims to enhance the pain threshold and to support sleep. Nonpharmaceutical treatment modalities, such as exercise, massage, idrotherapy can be helpful. Future studies should investigate the possible benefits of new strategies that may combine the effects of hot pool water, stretching exercises, massage and relaxation benefits of balneotherapy.

Fibromyalgia↗
PubMed2004

Does headache represent a clinical marker in early diagnosis of cerebral venous thrombosis? A prospective multicentric study.

The main aim of this study is to look for early clinical markers of cerebral venous thrombosis (CVT). As headache represents the major clinical manifestation at presentation we focused our attention on this symptom. We present the preliminary results of a prospective multicentric study that includes cases diagnosed as CVT in the participating centres. We have so far studied 35 patients (5 males and 30 females) from the ages of 18 to 78. The most frequent manifestation was headache (77.1%). It was more frequently localised (66.7%) and continuous (77.8%). The onset of pain was mostly acute-subacute (38.5%-50.0%) and the intensity moderate-severe (37.0%-51.9%). On univariate analysis, we found a positive correlation between CVT, acute headache onset (p=0.001) and severe headache (p=0.004). These preliminary results seem in accordance with our previous findings in the retrospective study, suggesting that CVT is more often associated with acute-onset headache of severe intensity.

Acute Disease↗
PubMed1998

Lowering fatty acids potentiates acute insulin response in first degree relatives of people with type II diabetes.

Studies have shown that a high plasma non-esterified fatty acid concentration may inhibit glucose induced insulin secretion in vitro and in vivo. The effect of lowering the fatty acid concentration on the acute insulin response was investigated in first degree relatives of people with Type II diabetes in a double-blind, randomised, placebo-controlled trial. Fifty first degree relatives of people with Type II diabetes volunteered for the study. Twenty five were given acipimox (250 mg/day, four times daily) and 25 placebo. The group treated with acipimox had a lower 2-h plasma glucose concentration (6.1 +/- 0.2 vs 7.7 +/- 0.3 vs mmol/l, p < 0.01); better insulin-mediated glucose uptake (35.4 +/- 0.5 vs 28.3 +/- 0.4 mumol/kg fat free mass per min, p < 0.01), acute insulin response (68 +/- 4.4 vs 46 +/- 7.3 mU/l, p < 0.01) and respiratory quotient (0.81 +/- 0.02 vs 0.77 +/- 0.03, p < 0.05); and a rise in the plasma glucagon (164 +/- 63 vs 134 +/- 72 ng/1, p < 0.05), growth hormone (1.31 +/- 0.13 vs 0.97 +/- 0.21 microgram/l, p < 0.03) and cortisol (325 +/- 41 vs 284 +/- 139 nmol/l, p < 0.05) concentrations. The difference in the acute insulin response persisted, even after adjustment for the 2-h plasma glucose concentration, insulin-mediated glucose uptake, the fasting plasma glucagon concentration and the growth hormone concentration (p < 0.05). In a subgroup of eight patients acipimox was compared with acipimox plus intralipid. The acute insulin response (44 +/- 5.1 vs 71 +/- 5.3 mU/l, p < 0.01) and the insulin-mediated glucose uptake (27.4 +/- 0.4 vs 36.7 +/- 0.5 mumol/kg fat free mass per min, p < 0.003) were lower with acipimox plus intralipid treatment than with acipimox alone. It is concluded that long term acipimox treatment lowers the plasma fasting free fatty acid concentration and improves the acute insulin response and the insulin mediated glucose uptake.

Adult↗
PubMed1998

Hemodynamic and metabolic effects of transdermal clonidine in patients with hypertension and non-insulin-dependent diabetes mellitus.

The aim of this study was to evaluate the effect of transdermal clonidine on hemodynamic and metabolic parameters in patients who have elevated blood pressure and non-insulin-dependent diabetes mellitus (NIDDM). After a 2-week run in placebo period, 20 NIDDM patients who had diastolic blood pressure in the range of 90 to 105 mm Hg underwent a randomized, single blind, placebo controlled, cross-over study of 4 week treatment with clonidine (transdermal patch 2.5 mg/week) or placebo (inactive patch). Compared with placebo, clonidine significantly reduced systolic (153 +/- 6 v 163 +/- 8) and diastolic (88 +/- 2 v 98 +/- 3.5 mm Hg, P = .001) blood pressure, left ventricular mass (94 +/- 11 v 99 +/- 12 g/m2, P < .01) and fasting glucose levels. Total glucose disposal (glucose clamp) was 6.5 +/- 1.5 with placebo and 7.1 +/- 1.6 mg/kg/min with clonidine (P < .01). Oxidative glucose disposal (indirect calorimetry) was also greater after clonidine. Plasma glucose, insulin, and C-peptide responses following oral glucose (75 g) were significantly lower after clonidine, as well as urinary albumin excretion. Transdermal clonidine is effective in reducing blood pressure in hypertensive NIDDM patients and is well tolerated. It may be useful to reduce the cardiovascular impact of hypertension in diabetes mellitus.

Administration, Cutaneous↗
PubMed1998

Plasma sex hormones are significantly associated with plasma leptin concentration in healthy subjects.

OBJECTIVE: In humans a sexual dimorphism of plasma leptin concentration has been demonstrated but its significance remains to be established. Sex hormones may have a role. PATIENTS: Eighty healthy, non-obese subjects (41M/39F) were studied. MEASUREMENTS: In the whole group of subjects plasma sex hormones, leptin and insulin concentrations were determined, body fat content assessed by bioimpedance analysis, body fat distribution evaluated and insulin-mediated glucose uptake measured by euglycemic hyperinsulinemic glucose. RESULTS: After adjustment for age, gender, amount of body fat, waist/hip ratio (WHR) and fasting plasma insulin concentration, fasting plasma leptin was still significantly correlated with plasma DHEAS (r = -0.30, P < 0.006), oestradiol (r = 0.53, P < 0.001) and testosterone (r = -0.43, P < 0.001) in all subjects (n = 80). Independently of age, amount of body fat and WHR, fasting plasma leptin concentration correlated with plasma oestradiol (r = 0.38, P < 0.01) and total testosterone (r = -0.58, P < 0.001) in males (n = 41) and with fasting plasma oestradiol (r = 0.48, P < 0.002) in females (n = 39). To investigate the independent contribution of anthropometric and hormonal variables to fasting plasma leptin concentration, a multivariate stepwise regression analysis with fasting plasma leptin concentration as dependent variable was made. In the entire group (n = 80), the whole model explained 43% of fasting plasma leptin concentration with fasting plasma insulin, total testosterone and oestradiol concentrations significantly and independently associated with plasma leptin concentration. In this model, fasting plasma DHEAS, testosterone and oestradiol explained 25% of the variability in plasma leptin concentration. CONCLUSION: Our study demonstrates that plasma sex hormone concentrations are associated with plasma leptin concentration.

Analysis of Variance↗
PubMed1998

Effect of metformin on food intake in obese subjects.

BACKGROUND: It has been hypothesized that metformin inhibits food intake, but in humans such effect needs to be demonstrated. Our study aims at investigating the effect of metformin administration on food intake in obese, non-diabetic, normotensive patients. METHODS: Thirty patients underwent a double-blind, randomized study. Placebo (P; n = 15) and metformin (M; n = 15) were both given for 15 days, and food intake (FI) was recorded at baseline and in the last 4 days of each treatment period. RESULTS: M administration allowed a stronger decline in body weight (BW) (-2.8 +/- 1.6 vs. -0.3 +/- 0.4 kg P < 0.01), body fat (BF) (-1.4 +/- 1.2 vs. -0.3 +/- 1.1 kg P < 0.01), plasma leptin concentration (-5.2 +/- 8.9 vs. -1.8 +/- 10.4 ng mL-1 P < 0.05) and FI (-642 +/- 491 vs.-70 +/- 1165 kJ per 24 h P < 0.01) than P. In M-treated subjects, changes in FI significantly correlated with those in BW (r = 0.63, P < 0.007) and BF (r = 0.74, P < 0.001). Independently of sex and change in BF, the changes in FI and in fasting plasma leptin concentration (r = 0.58, P < 0.01) were still correlated. CONCLUSION: Our study suggests that metformin administration is useful to inhibit FI and to lower BW and BF in obese non-diabetic patients.

Adolescent↗
PubMed1998

Advancing age and insulin resistance: role of plasma tumor necrosis factor-alpha.

In 70 healthy subjects with a large age range, the relationships between plasma tumor necrosis factor-alpha (TNF-alpha) and body composition, insulin action, and substrate oxidation were investigated. In the cross-sectional study (n = 70), advancing age correlated with plasma TNF-alpha concentration (r = 0.64, P < 0.001) and whole body glucose disposal (WBGD; r= -0.38, P < 0.01). The correlation between plasma TNF-alpha and age was independent of sex and body fat (BF; r = 0.31, P < 0.01). Independent of age and sex, a significant relationship between plasma TNF-alpha and leptin concentration (r = 0.29, P < 0.02) was also found. After control for age, sex, BF, and waist-to-hip ratio (WHR), plasma TNF-alpha was still correlated with WBGD (r = -0.33, P < 0.007). Further correction for plasma free fatty acid (FFA) concentration made the latter correlation no more significant. In a multivariate analysis, a model made by age, sex, BF, fat- free mass, WHR, and plasma TNF-alpha concentrations explained 69% of WBGD variability with age (P < 0.009), BF (P < 0.006), fat-free mass (P < 0.005), and plasma TNF-alpha (P < 0.05) significantly and independently associated with WBGD. In the longitudinal study, made with subjects at the highest tertiles of plasma TNF-alpha concentration (n = 50), plasma TNF-alpha concentration predicted a decline in WBGD independent of age, sex, BF, WHR [relative risk (RR) = 2.0; 95% confidence intervals (CI) = 1.2-2.4]. After further adjustment for plasma fasting FFA concentration, the predictive role of fasting plasma TNF-alpha concentration on WBGD (RR = 1.2; CI = 0.8-1.5) was no more significant. In conclusion, our study demonstrates that plasma TNF-alpha concentration is significantly associated with advancing age and that it predicts the impairment in insulin action with advancing age.

Adult↗
PubMed1998

Effects of perindopril and carvedilol on endothelium-dependent vascular functions in patients with diabetes and hypertension.

OBJECTIVE: To compare the effects of the ACE inhibitor perindopril and the beta-blocker carvedilol on blood pressure and endothelial functions in NIDDM patients with hypertension. RESEARCH DESIGN AND METHODS: We conducted a double-blind randomized trial in 26 patients with NIDDM and mild hypertension. A 4-week run-in placebo period preceded the active 12-week treatment with perindopril (4-8 mg daily) or carvedilol (25-50 mg daily). Endothelial functions were assessed by evaluating the hemodynamic (mean blood pressure, leg blood flow) and rheological (platelet aggregation, blood viscosity, and blood filterability) responses to an intravenous bolus of 3 g L-arginine, the natural precursor of nitric oxide. RESULTS: Both perindopril and carvedilol significantly reduced mean blood pressure (P < 0.001) and increased leg blood flow (P < 0.05) to the same extent; blood filterability remained unchanged in both perindopril- and carvedilol-treated groups. Carvedilol reduced platelet aggregation and blood viscosity significantly (P < 0.05) but perindopril did not. Before treatment, the hemodynamic and rheologic responses to L-arginine were significantly lower in patients (P < 0.05-0.01) than in 20 nondiabetic nonhypertensive control subjects. After 12 weeks of treatment, both drugs normalized the hemodynamic responses to L-arginine. Platelet aggregation response to L-arginine was ameliorated by carvedilol and remained unchanged in the perindopril group. CONCLUSIONS: At the doses used, both drugs effectively reduce blood pressure and normalize the hemodynamic responses to L-arginine. The implications of the ameliorated endothelial function for the poor cardiovascular outlook of the NIDDM hypertensive patient need further assessment.

Adrenergic beta-Antagonists↗
PubMed1998

[Canalith repositioning maneuver: proposal of a new therapy for benign paroxysmal positional vertigo of the posterior semicircular canal].

A new therapy is proposed for the treatment of Benign Paroxysmal Positional Vertigo (B.P.P.V.) of the Posterior Semicircular Canal (P.S.C.): the Canalith Repositioning Maneuver (C.R.M.). The need for a new maneuver to treat B.P.P.V. of the P.S.C. arises from the difficulties encountered in daily practice, under particular conditions (i.e. elderly, obese, traumatized patients and in the presence of rachis pain, etc.), to perform the most common rehabilitative techniques such as the Semont Maneuver and Epley's Canalith Repositioning Procedure (C.R.P.). The results achieved using this new technique on a group of 47 consecutive out-patients are presented and compared to those achieved using the Semont Maneuver in an analogous group of 23 patients. C.R.M. and the Semont Maneuver were performed once per treatment session and all patients were checked every 3 days until the symptoms of B.P.P.V. disappeared. Thereafter they were invited to return for check-up if signs of vertigo returned (follow-up 6-25 months). The two techniques proved equally effective: 87.5% of the cases were resolved with C.R.M., 82.6% with the Semont Maneuver. However, the C.R.M. provided other advantages as it resolved the problem immediately (i.e. in a single session) in 81% of the cases vs. 68.4% for the Semont Maneuver. In view of the Canalith theory, the action mechanism envisaged for all three maneuvers--C.R.M., the Semont Maneuver and the Epley C.R.P.--can be explained assuming that the canalith passes from the ampullar to the non ampullar branch of the (P.S.C.) passing finally through the Common Duct and into the Utricle. C.R.M. is a specific treatment for the B.P.P.V. of the P.S.C. and is simple to perform, well tolerated and quite effective. It is indicated in all cases of B.P.P.V. of the P.S.C. both as initial treatment and as alternative to other treatment methods which have proved ineffective or difficult to perform. Indeed, in therapy it is best to be quite skilled in more than one technique, availing oneself of a full range possibilities; in this way the cure can be tailored to the patient in each individual case and not vice versa.

Adolescent↗
PubMed1997

Association of fasting plasma free fatty acid concentration and frequency of ventricular premature complexes in nonischemic non-insulin-dependent diabetic patients.

We investigated the association between free fatty acid (FFA) concentration and ventricular premature complexes (VPCs) in nonischemic patients with non-insulin-dependent diabetes mellitus using 3 approaches: cross-sectional analysis (n = 142), intervention including induction of elevated FFA levels with Intralipid heparin (n = 15), and reduction in FFA levels with Acipimox (n = 34) and a longitudinal follow-up study (n = 59). Patients at the third tertile of fasting plasma FFA concentration had the strongest increase in VPCs. Independently of age, sex, body mass index (BMI), waist/hip ratio, left ventricular mass index, glycated hemoglobin, fasting plasma insulin and triglyceride concentration, and daily physical activity, FFA concentration and VPCs were significantly correlated (r = 0.21 p <0.01). At multiple logistic regression analysis independently of age, sex, BMI, waist/hip ratio, left ventricular mass index, mean arterial blood pressure, glycated hemoglobin, fasting plasma insulin, triglycerides and potassium concentration, fasting plasma low-density lipoprotein/high-density lipoprotein cholesterol ratio, and daily physical activity, plasma FFA concentration was a significant determinant of VPCs (odds ratio 1.2, 95% confidence interval 1.0 to 2.3). Intralipid infusion (10% in 24 hours) (n = 15) and acipimox administration (250 mg, 4 times/day) (n = 34) increased, and decreased fasting plasma FFA concentration, respectively. In those studies, change in VPCs paralleled the effects on plasma FFA. In the longitudinal study (n = 59), plasma FFA concentration predicted the development of VPCs (RR 1.4 95% confidence interval 1.0 to 1.9) independently of age, sex, BMI, waist/hip ratio, left ventricular mass index, mean arterial blood pressure, fasting plasma triglyceride concentration, fasting plasma low-density lipoprotein/high-density lipoprotein cholesterol ratio, and daily physical activity. In conclusion, in nonischemic patients with non-insulin-dependent diabetes mellitus, plasma FFA concentration is associated with the frequency of ventricular premature complexes.

Aged↗
PubMed1997

Metabolic and cardiovascular effects of carvedilol and atenolol in non-insulin-dependent diabetes mellitus and hypertension. A randomized, controlled trial.

BACKGROUND: Diabetic patients are considered less suitable than nondiabetic patients for beta-blocker therapy because of the risk for worsened glucose and lipid metabolism and more severe hypoglycemic attacks. OBJECTIVE: To compare the metabolic and cardiovascular effects of carvedilol with those of atenolol in diabetic patients with hypertension. DESIGN: Randomized, double-blind, 24-week trial. SETTING: University hospital clinic. PATIENTS: 45 patients with non-insulin-dependent diabetes mellitus and hypertension. INTERVENTION: After a 4- to 6-week run-in period during which placebo was given in a single-blind manner, patients were randomly assigned to carvedilol or atenolol. MEASUREMENTS: An oral glucose tolerance test; assessment of insulin sensitivity and hormonal responses to insulin hypoglycemia; and assessment of lipid levels, blood pressure, left ventricular mass, and lipid peroxidation. RESULTS: Changes in systolic and diastolic blood pressure and left ventricular mass index were similar with carvedilol and atenolol (P > 0.2). Fasting plasma glucose and insulin levels decreased with carvedilol and increased with atenolol. Responses to carvedilol were greater than those to atenolol, as follows: increase in total glucose disposal, 9.54 mumol/kg of body weight per minute (95% CI, 7 to 11.9 mumol/kg per minute); decrease in plasma glucose response to oral glucose, 61 mmol/L x 180 minutes (CI, -101 to -21 mmol/L x 180 minutes); decrease in insulin response to oral glucose, 6.2 nmol/L x 180 minutes (CI, -9.8 to -2.6 nmol/L x 180 minutes); decrease in triglyceride level, 0.56 mmol/L (CI, -0.75 to -0.37 mmol/L; P < 0.001); increase in high-density lipoprotein cholesterol level, 0.13 mmol/L (CI, 0.09 to 0.17 mmol/L; P < 0.001); and decrease in lipid peroxidation, 0.25 mumol/L (CI, -0.34 to -0.16 mumol/L). CONCLUSIONS: By improving glucose and lipid metabolism and reducing lipid peroxidation, carvedilol may offer advantages in patients with diabetes and hypertension.

Adrenergic alpha-Antagonists↗
PubMed1997

Vascular effects of acute hyperglycemia in humans are reversed by L-arginine. Evidence for reduced availability of nitric oxide during hyperglycemia.

BACKGROUND: Acute hyperglycemia may increase vascular tone in normal humans via a glutathione-sensitive, presumably free radical-mediated pathway. The objective of this study was to investigate whether or not the vascular effects of hyperglycemia are related to reduced availability of nitric oxide. METHODS AND RESULTS: Acute hyperglycemia (15 mmol/L, 270 mg/dL) was induced in 12 healthy subjects with an artificial pancreas. Systolic and diastolic blood pressures, heart rate, and plasma catecholamines showed significant increases (P < .05) starting after 30 minutes of hyperglycemia; leg blood flow decreased significantly (15%; P < .05) at 60 and 90 minutes. Platelet aggregation to ADP and blood viscosity also showed significant increments (P < .05). The infusion of L-arginine (n = 7, 1 g/min) but not D-arginine (n = 5, 1 g/min) or L-lysine (n = 5, 1 g/min) in the last 30 minutes of the hyperglycemic clamp completely reversed all hemodynamic and rheological changes brought about by hyperglycemia. Infusion of NG-monomethyl-L-arginine (L-NMMA; 2 mg/min) to inhibit endogenous nitric oxide synthesis in 8 normal subjects produced vascular effects qualitatively similar to those of hyperglycemia but quantitatively higher (P < .05); however, heart rate and plasma catecholamine levels decreased during L-NMMA infusion, presumably as a consequence of baroreflex activation. Infusion of L-NMMA during hyperglycemia produced changes not different from those obtained during infusion of L-NMMA alone. CONCLUSIONS: The results show that acute hyperglycemia in normal subjects causes significant hemodynamic and rheological changes that are reversed by L-arginine. Moreover, the effects of hyperglycemia are mimicked to a large extent, but not entirely, by infusion of L-NMMA. This suggests that hyperglycemia may reduce nitric oxide availability in humans.

Acute Disease↗
PubMed1997

The vascular effects of L-Arginine in humans. The role of endogenous insulin.

This study aimed at evaluating whether increased availability of the natural precursor of nitric oxide, L-arginine, could influence systemic hemodynamic and rheologic parameters in humans and whether the effects of L-arginine are mediated by endogenous insulin. 10 healthy young subjects participated in the following studies: study I, infusion of L-arginine (1 g/min for 30 min); study II, infusion of L-arginine plus octreotide (25 microg as i.v. bolus + 0.5 microg/min) to block endogenous insulin and glucagon secretion, plus replacement of basal insulin and glucagon; study III, infusion of L-arginine plus octreotide plus basal glucagon plus an insulin infusion designed to mimic the insulin response of study I. L-Arginine infusion significantly reduced systolic (11+/-3, mean+/-SE) and diastolic (8+/-2 mmHg, P < 0.001) blood pressure, platelet aggregation (20+/-4%), and blood viscosity (1.6+/-0.2 centipois, P < 0.01), and increased leg blood flow (97+/-16 ml/min), heart rate, and plasma catecholamine levels (P < 0.01). In study II, plasma insulin levels remained suppressed at baseline; in this condition, the vascular responses to L-arginine were significantly reduced, except for plasma catecholamines which did not change significantly. In study III, the plasma insulin response to L-arginine was reestablished; this was associated with hemodynamic and rheologic changes following L-arginine not significantly different from those recorded in study I. These findings show that systemic infusion of L-arginine in healthy subjects induces vasodilation and inhibits platelet aggregation and blood viscosity. These effects are mediated, in part, by endogenous released insulin.

Adult↗
PubMed1997

L-arginine but not D-arginine stimulates insulin-mediated glucose uptake.

Our study aims at investigating a possible role for L-arginine and D-arginine in insulin-mediated glucose uptake. Twelve lean healthy subjects volunteered for the study and were submitted to three euglycemic-hyperinsulinemic glucose clamps to investigate the effect of L-arginine (0.5 g/min in the last 60 minutes of the clamp), D-arginine (0.5 g/min in the last 60 minutes of the clamp), and saline 0.9% NaCl on insulin-mediated glucose uptake. All tests were made in random order. In study 1, L-arginine versus saline infusion was associated with a significant increase in blood flow (131% +/- 7% v 87% +/- 5%, P < .001) and whole-body glucose disposal ([WBGD] 61.4 +/- 4.4 v 41.3 +/- 3.5 mumol/kg fat-free mss [FFM].min, P < .001). Analysis of substrate oxidation demonstrated that both oxidative and nonoxidative glucose metabolism was improved by L-arginine delivery. After adjustment for the change in blood flow, WBGD was still greater after L-arginine than after saline infusion. Along with L-arginine infusion and independently of the change in blood flow, the percent change in WBGD correlated with the percent change in plasma cGMP (r = .55, P < .05). D-Arginine infusion did not affect insulin-mediated glucose uptake. In particular, WBGD (42.1 +/- 3.4 v 41.3 +/- 3.5 mumol/kg FFM.min, P = NS) was similar in both experimental conditions. Basal levels (2.8 +/- 0.2 v 2.7 +/- 0.3 nmol/L, P = NS) and the insulin-mediated increase (43% +/- 5% v 39% +/- 4%, P = NS) in plasma cGMP were also superimposable along with insulin plus D-arginine and insulin alone, respectively. Finally, blood flow (224 +/- 29 v 230 +/- 35 mL/min, P = NS) was not different at baseline and was similarly stimulated (84% +/- 4% v 87% +/- 5%, P = NS) by insulin infusion. In conclusion, L-arginine but not D-arginine stimulates insulin-mediated glucose uptake. Nitric oxide (NO), the metabolic mediator for L-arginine, potentiates insulin-mediated glucose uptake through the increase in blood flow. Nevertheless, an independent effect of intracellular cGMP on WBGD cannot be ruled out.

Adult↗
PubMed1997

L-arginine for testing endothelium-dependent vascular functions in health and disease.

The objective of this study was to assess the role of L-arginine, the natural precursor of nitric oxide, for testing endothelial function in physiological and pathophysiological conditions. In an initial study of 20 healthy subjects, mean blood pressure decreases in response to increasing doses of L-arginine (1, 2, 3, and 5 g) were 1.1 +/- 1.3, 2.6 +/- 1.5, 7.6 +/- 1.3, and 7.7 +/- 2 mmHg, respectively, P < 0.01. The enantiomer D-arginine (3 g) did not produce any change in mean blood pressure and platelet aggregation (n = 10), whereas the infusion of the L-arginine analog NG-monomethyl-L-arginine (6 mg/min) reduced by 70% the vascular effects of L-arginine. In the whole population of 52 healthy subjects, there was an inverse correlation between age and blood pressure or platelet aggregation changes after L-arginine. Compared with matched controls (n = 20), the changes in mean blood pressure and platelet aggregation after L-arginine were significantly lower in non-insulin-dependent diabetic (n = 20) and hypercholesterolemic (n = 16), but not in hypertensive (n = 20), subjects. Changes in blood viscosity were significantly lower only in hypercholesterolemic subjects. Our findings suggest that an intravenous bolus of 3 g L-arginine may be a simple and useful tool to assess the endothelial control of blood pressure and platelet activity in health and disease.

Adenosine Diphosphate↗