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F Belfiore

Publications and source records attributed to F Belfiore.

82 records · Page 5Linked to original sources
PubMedDate not supplied

A formula for quantifying the effects of substrate cycles (futile cycles) on metabolic regulation. Its application to glucose futile cycle in liver as studied by glucose-6-phosphatase/glucokinase determinations.

Substrate cycles (SC) are formed by a 'forward pathway' (FP) and a 'backward pathway' (BP), the difference between FP and BP forming the 'metabolic flux' (MF) through the route of which the cycle is part. SC modulate regulatory effects, i.e. amplify or reduce the % change in MF compared to the % change in FP and BP, thus affecting the sensitivity to regulatory factors, including hormones. A formula is given to calculate (with an approximation of +/- 0.5) the 'flux response index' (FRI), i.e. the factor by which the % change in FP plus the % change in BP must be multiplied to obtain the % change in metabolic flux, when FP and BP undergo opposite, non-unidirectional changes (as is often the case in metabolic regulation). The formula is: FRI = [( FP + BP)/(FP-BP)]/2. By this formula we evaluated the hepatic activities of glucose-6-phosphatase and glucokinase (which roughly reflect hepatic glucose production and uptake, respectively), i.e. the two enzymes that catalyze the cycle between glucose-6-phosphate (glucose-6-P) and glucose. Based on data obtained in normal, nonobese diabetic and obese diabetic subjects as well as in normal, streptozotocin-diabetic, and obese diabetic (ob/ob) mice, we found that FRI was reduced in non-obese diabetic humans and animals whereas it was increased in obese-diabetic humans and mice, compared to normal controls. Thus, diabetes without obesity decreases, and obesity with diabetes increases, the sensitivity of the glucose-6-P/glucose cycle to regulatory agents.

Animals↗
PubMedDate not supplied

Rabbit lens and retina phosphorylate glucose through a glucokinase-like enzyme: study in normal and spontaneously hyperglycemic animals.

After having previously shown that some noninsulin-sensitive tissues (capillaries and optic nerve) phosphorylate glucose in a concentration-dependent manner through a glucokinase-like enzyme, here, we report data on glucose phosphorylation in rabbit lens and retina at various glucose concentrations (1, 5, 10, 25, 50, and 100 mmol/L). In the 3000 g supernatant of lens and retina homogenates from two separate groups of female albino rabbits ten animals in each group; 1.8-2.0 kg body weight; mean +/- SEM morning glycemia: 8.19 +/- 0.28 and 8.12 +/- 0.24 mmol/L, respectively) was assayed glucose phosphorylating activity (NADP reduction measured as change in optical density at 366 nm at pH 7.5). The enzyme activity did not reach the maximum at low glucose concentration (1 mmol/L), as it occurs in several tissues, but increased progressively in both tissues with the increase in glucose concentration. Values (mean +/- SEM) for lens were 0.197 +/- 0.031 nmol/min/mg protein at 1 mmol/L and 0.327 +/- 0.051 (the highest value) at 50 mmol/L glucose (+65.99%, p < 0.01; r = 0.31, p < 0.05). Values for retina were 36.02 +/- 2.12 at 1 mmol/L glucose and 42.48 +/- 2.79 (the highest value) at 25 mmol/L glucose (+17.93%, p < 0.001; r = 0.32, p < 0.05). These kinetic characteristics, somewhat reminiscent of those shown by hepatic glucokinase, are still more pronounced when we calculated the "glucokinase component," obtained by subtracting the activity at 1 mmol/L glucose (hexokinase component) from that at the highest glucose concentration (total glucose phosphorylating activity). In five rabbits of similar age and weight, with spontaneous hyperglycemia (mean +/- SEM morning glycemia: 11.71 +/- 0.60) glucose phosphorylation in the retina was lower than normal, value at pH 7.5 and 1 mmol/L glucose being 24.52 +/- 2.20 versus 36.02 +/- 2.12 of normal animals (-31.93%, p < 0.01). This, if occurs also in other tissues, could contribute to the hyperglycemia by reducing glucose utilization. In these animals, however, the glucose phosphorylating activity retained the responsivity to increasing glucose concentrations, with value at 100 mmol/L of 28.65 +/- 2.10, corresponding to + 16.84% over the value at 1 mmol/L (p < 0.01). Therefore, the actual glucose phosphorylation in the retina of these animals would depend both upon the enzyme level (which is reduced) and glucose concentration (which is increased). Due to the in vivo inhibition of the hexokinase component by glucose 6-phosphate, the glucokinase component in retina and lens may be predominant in vivo, making the stimulating effect of hyperglycemia much more important than it would appear from our in vitro data. This might play a role in the chronic diabetic complications.

Animals↗
PubMedDate not supplied

In vitro inhibition of glucose phosphorylation by an aldose-reductase inhibitor (Tolrestat) in some non-insulin-sensitive rabbit tissues.

We have previously demonstrated that in some non-insulin-sensitive tissues (capillaries of eel swimbladder Rete mirabile, and rabbit eye choroidocapillary lamina, optic nerve, retina, and lens) glucose phosphorylation increases with the increase in the concentration of glucose, a characteristic relevant to the hyperglycemia of diabetes. In the present research we demonstrate an effect of the aldose reductase inhibitor, Tolrestat, on the glucose-phosphorylating activity of rabbit lens and optic nerve, by assaying the enzyme activity of tissue homogenates (in the presence of 10 mmol/L glucose) without or with 10 min preincubation with increasing concentrations of Tolrestat (2, 4, and 8 micromol/L). In the lens, a 18% inhibition (p < 0.01) was observed in the presence of 8 micromol/L Tolrestat. In the optic nerve, a 12% (p < 0.05) and a 21% (p < 0.01) reduction was recorded at 4 and 8 micromol/L Tolrestat, respectively. Significant inverse correlations existed between the concentration of Tolrestat and the phosphorylation rate of glucose of rabbit lens and optic nerve. The dose-dependent inhibition of glucose phosphorylation observed by us suggests that the inhibitory action of Tolrestat on glucose metabolism extends beyond the well-known effects of this compound on the polyol pathway, and might contribute to the refraining action of Tolrestat on the development and progression of late diabetic complications in non-insulin-sensitive tissues.

Aldehyde Reductase↗
PubMedDate not supplied

[Tophaceous gout in plurimetabolic syndrome].

Aim of this paper is to describe and discuss, on the basis of the available current literature, the case of a female patient affected by a tophaceous gout associated with plurimetabolic syndrome. Hyperuricemia and gout may be seen today in all the populations of developed countries, with increasing frequency on the last fifty years. Increased production or reduced urinary excretion of uric acid (and hypoxanthine and xanthine) are the most important pathogenetic mechanisms of primary or secondary hyperuricemia. Gout is an acute rheumatic disorder (characterized by a limited range of manifestations) which occurs in humans in connection with deposition of crystals of monosodium urate (the final product of purine metabolism) in the articular and soft periarticular tissues. Hyperuricemia and/or gout are often associated with hyperinsulinemia, obesity, diabetes mellitus, hyperlipemia, hypertension and atherosclerosis to form the syndrome called "Plurimetabolic syndrome" or "Syndrome X". Here we report the clinical case of a 64-year-old female patient who had android obesity, type 2 diabetes mellitus, hypertension, dyslipidemia and hyperuricemia and had been suffering (over many years) from intermittent episodes of severe pain and inflammatory joint swelling (first metacarpo- and metatarso-phalangeal joints) with development of pronounced multiple tophi in bone articular and soft periarticular tissues. Hyperuricemia and acute episodes had never been treated with anti-hyperuricemic drugs because gouty arthritis had never been diagnosed. This severe tophaceous gout associated to multiple metabolic disorders prompted us to present knowledge on gout and to focus on the interrelationships between hyperuricemia and/or gout and plurimetabolic syndrome, important risk factors for coronary heart disease.

Arteriosclerosis↗
PubMedDate not supplied

[Bilateral sclerosing lipogranuloma of the gluteal region with calcification. Report of a clinical case and review of the literature].

A rare case of large bilateral sclerosing lipogranuloma with multiple calcifications of gluteal region is described in an old female patient affected by a cerebrovascular disease. The lesions appeared as firm, nontender, plaques, 9-10 cm in diameter, covered with hyperpigmented skin. This uncommon disorder is discussed on the basis of data obtained from an extensive literature review. The term "sclerosing lipogranuloma" was coined in 1950, and it defines a disease of the subcutaneous fat, which for a trauma or unknown reasons undergoes necrosis of fat cells with the release of fat droplets into intercellular spaces and a peculiar local sclerosing granulomatous reaction of fatty tissue. The cytosteatonecrosis and sclerosing lipogranuloma, post-traumatic or secondary to injection of exogenous oily substances, usually localized in the breast of women and in genitalia of men, are relatively well known. Sclerosing lipogranulomatosis of the orbita and eyelides, an infrequent but severe complication after endonasal surgery, has also been reported. Rarely, the lipogranuloma can be spontaneous or idiopathic or primitive. A particular form of genetic diffuse lipogranulomatosis is the Farber's syndrome, firstly described on 1947. In our patient, the absence of trauma seems to indicate a primitive lipogranuloma. The presence of an acute rheumatic syndrome responsive to corticosteroids, and the positivity of antimitochondrial autoantibodies are in accordance with the report of sclerosing multiple lipogranulomatosis associated with a lupus-like syndrome. Because of the long duration and the absence of acute local symptoms, this syndrome can be considered benign with favorable prognosis, but the physician should know it.

Aged↗
PubMedDate not supplied

[Italian Consensus Conference; overweight, obesity and health (ICC S.O.S. 1991)].

On April 5th and 6th 1991, at the National Research Council (CNR) in Rome, a Consensus Conference on the relationship between Overweight, Obesity and Health was held. The Conference was sponsored by FATMA (Applied Project on Disease Factors of the CNR) and UICO (Italian Society for the Study of Obesity) with the purpose of establishing guidelines for health employees. The development of the Conference followed the methodology set down by OMAR to obtain a rational and significant consensus on the answers to 6 basic questions prepared by the Planning Committee. The questions were the pivotal point of the Conference and were brought to the attention of all the attendees and widely diffused among the medical community; they were proposed with the aim of giving an exhaustive definition of obesity, to investigate its relationship with mortality and morbidity, to highlight its social characterization, to indicate methods of evaluation and recommendations for weight loss, to select groups at risk, and to focus general guidelines for research. After the presentation of the state of the art on 18 topics by experts in the field, the 22 members of the Consensus Panel, impartial experts from a vast area of the scientific community, discussed a draft document representing the answers to the questions, which was subsequently illustrated to the 307 attendees, discussed and then approved. This paper is the definitive document of the Consensus Conference. The introduction explains the reasons which led to the decision to promote the Conference six years after the one held in the United States. The methodology is then set out. The questions are answered in the form of recommendations and backed up by data and scientific demonstrations from the literature.

Adolescent↗
PubMedDate not supplied

[Use of an automatic blood glucose measurement system for the assessment of insulin resistance during the oral glucose tolerance test].

An automatic glycemic control system (Beta-like, Esaote) was used to calculate the insulin area (IA) required to keep glycemia within the normal range during OGTT (using NDDG criteria). IA was calculated by adding total endogenous insulin to insulin infused by the Betalike system (Actrapid HM, Novo). During the test, glycemia was obliged to follow a mean normal curve using an insulin infusion according to a special algorithm which automatically adapted to individual parameter variations during the different stages of OGTT. Fourteen blood samples were collected to assay metabolites (glucose, NEFA, lactate and alanine) and hormones (insulin, C peptide, glucagon). Data on insulinemia and glycemia were used to calculate the respective areas under the total and incremental curve (IA expressed in UL-1 min-1 and GA expressed in mM.L-1.min-1); an insulin resistance index was then calculated (total and incremental) using the following formula: IA/(normal GA/patient GA). This test allows us: a) to evaluate the insulin secretory response to a standard glycemic stimulus represented by a glycemic curve within the normal range; b) to calculate the quantity of insulin necessary to maintain the glycemic curve within the normal range; c) to evaluate the body's total insulin resistance according to an index calculated on the basis of the insulin area required; d) to compare the calculated insulin resistance index with NEFA and glucagon data obtained during the test; e) to identify the exact evolution of these events over time during OGTT.

Blood Glucose↗
PubMedDate not supplied

[Diffuse symptomatic polypoid lipomatosis of the colon with hyperplasia of epiploic appendices: a case report].

Diffuse and symptomatic lipomatosis of the colon, particularly when associated with hyperplasia of the appendices epiploicae, is a rare disease. We report here the case of a lean, 26-year-old woman who had polypoid lipomatosis of the colon with submucosal and subserous expression (involving the mesentery and peritoneum) associated with extreme hyperplasia of the appendices epiploicae. Her disease led to a recurrent subocclusive syndrome which required total colectomy. We discuss the case and review the literature on this subject. The particular characteristics of this case and early onset of disease would suggest that our patient was affected by a congenital lipomatous syndrome linked to mesenchymal dysplasia. Long-term monitoring will enable prompt intervention in the case of reformation of lipomatous tissue.

Adult↗
PubMedDate not supplied

[Protein S deficiency and thrombophilia: presentation of a clinical case and review of the literature].

We report the case of a 22-year-old obese woman with severe protein S deficiency, probably genetic in nature, associated with recurrent venous thrombosis. Protein S deficiency is a rather rare disease: it may be an inherited, either homozygous (purpura fulminans at neonatal age), heterozygous, or acquired disorder. The thrombophilic state may be manifested as deep vein thrombosis or thrombophlebitis of the superficial veins with a high risk of pulmonary embolism in the young, and it is often exacerbated by pregnancy. In our case, the presenting event, bilateral deep venous (iliac-femoral) thrombosis complicated by disseminated intravascular coagulation, had occurred when the patient was 13 years old. We started long-term therapy with oral coagulants, i.e. warfarin even if the latter may cause skin necrosis ("warfarin dermatitis") in some patients with protein S deficiency. The clinician must consider protein S deficiency in cases of recurrent thrombosis, particularly in young patients: the importance of early implementation of long-term preventive therapy should not be underestimated.

Adult↗