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Heart failure may promote metabolic changes such as insulin resistance, in part through neurohumoral activation, and determining an increased utilization of non-carbohydrate substrates for energy production. In fact, fasting blood ketone bodies as well as fat oxidation have been shown to be increased in patients with heart failure. The result is depletion of myocardial ATP, phosphocreatine and creatine kinase with decreased efficiency of mechanical work. A direct approach to manipulate cardiac energy metabolism consists in modifying substrate utilization by the failing heart. To date, the most effective metabolic treatments include several pharmacological agents that directly inhibit fatty acid oxidation. The results of current research are supporting the concept that shifting the energy substrate preference away from fatty acid metabolism and toward glucose metabolism could be an effective adjunctive treatment in patients with heart failure. Trimetazidine is the most studied drug in this context. Several small studies have evidenced the usefulness of such additional therapeutic tools for heart failure. More specifically, recent meta-analyses and a multicenter retrospective study have shown that additional use of trimetazidine in patients with heart failure, along with symptoms and cardiac function improvement, also provides a significant protective effect on all-cause mortality, cardiovascular events and hospitalization due to cardiac causes. Nevertheless, the exact role of metabolic therapy in heart failure is yet to be established, and a large multicenter randomized trial is necessary.

In today's diagnostic imaging the heart with Pet 18F - FDG finds its highest expression in' identify the extent, severity, and the possibility of recovery of dysfunctional myocardium. Aim of this study was to extract some parameters "unique" as the regional metabolic rate, the speed of fractional irreversible binding of the tracer to the receptor sites in order to obtain a quantization of a possible damage of the tissue under examination. We used a dedicated software, the PMOD, implemented with compartmental models and graphical analysis methods in order to obtain absolute and repeatable results. In our results these parameters can give a qualitative data integration and definition to which, as is known, do not allow the identification of objective criteria to identify a possible ischemic damage and, most important, a possible recovery of dysfunctional myocardium.

Aim: Recently, numerous studies have shown significant correlation between hyperandrogenism and elevated insulin levels in many patients with polycystic ovarian syndrome (PCOS). Insuline-Resistance (IR) results in increased circulating levels of this hormone and it is the basis of the metabolic syndrome, characterized by the presence of fatty liver disease (NAFLD), which is pathologically characterized by the accumulation of triglycerides as macro or micro vesicles, in more than 5% of hepatocytes. The aim of our study was to evaluate the incidence of NAFLD in young women with PCOS, who were lean, overweight or obese., Methods: Particularly, the levels of glucose and insulin, the lipidic profile, and all liver function indices were evaluated; the severity and degree of steatosis were established on the basis of parenchymal echogenicity and the view of intrahepatic venous circulation., Results: Our study showed that NAFLD is a common disease in women with polycystic ovaries, especially with high BMI, but an incidence rate of 40% in lean women too was found. Because steatohepatitis is a risk factor for the developmente of cirrhosis and hepatocellular carcinoma, it is therefore prudent to carry out an ultrasound evaluation of liver in all young patients suffering from polycystic ovary syndrome, regardless of their BMI and the results of serological evaluation of liver., Conclusion: This collateral diagnosis that accompanies the diagnosis of Polycystic Ovary Syndrome seems important since this type of patients could be treated with metformin or with thiazoles to reduce insulin-resistance and steatosis as well.

It has been known for about 50 years that different obesity phenotypes do exist. Nonetheless, how abdominal, namely visceral, obesity is burdened by metabolic and cardiovascular diseases has been established only in recent years. The association between abdominal obesity and diabetes, which is well documented, has been mainly explained by the lower insulin sensitivity of subjects with excess visceral fat. However, more recent studies support the hypothesis that several molecules released in greater or lower amount by visceral adipocytes can exert also a detrimental role on beta-cell function. Among these molecules free fatty acids and adipokines should be mentioned. The latter include inflammatory cytokines, such as tumor necrosis factor-alpha and interleukin-6 and hormones synthesized by adipocytes, such as adiponectin, leptin and resistin. Visceral obesity is also associated with an excessive depot of triglycerides and other lipid products (e.g., ceramide) within the key organs of glucose metabolism (liver, skeletal muscle, pancreatic islets). This phenomenon seems to contribute to both insulin resistance and beta-cell dysfunction, favoring abnormalities of glucose homeostasis.

Corticosteroid therapy is widely used in the acute and chronic treatment of different diseases, with consequent possible onset of typical side effects on multiple systems of the organism, including also energy metabolism and metabolism of water and minerals (sodium, potassium, calcium and phosphorus). Clinical signs, related to the type and dosage of the steroidal drug, may lead to secondary illnesses with variable degrees of severity, depending on proneness of the individual patient and on the underlying disease that motivated the treatment. The role of dietetic intervention in the management of a patient chronically receiving corticosteroid therapy is not ancillary, although often underestimated, its aim being the reduction of some long-term therapy related side effects, and the correction of major metabolic derangements. In particular, the diet shall be moderately rich in protein (1.5 g/Kg/day of proteins) and low in fat (< 30% of calories, obtained mostly from unsaturated fatty acids), based mainly on complex carbohydrates (80%), providing 50% of the caloric intake. Diet has to be specifically characterized by food containing little sodium and yielding high amounts of water, calcium, magnesium and potassium. Minor directions concern the reduced intake of ethanol and purines. The efficacy of supplementation with antioxidant vitamins (vitamin C and E) and selenium is currently under investigation.

Background: Ventricular arrhythmias (VA) are prevalent in hypertensives, as well as in diabetics and dyslipidemics. The aim of our study is to evaluate if alterations in glucose or lipid metabolism increase the risk of VA in hypertensive patients., Methods: Sixty-eight patients (24 males, 44 females, aged 45-78), with mild-moderate hypertension, were divided into 2 groups: group A (n=24) normoglycemic and normolipemic, and group B (n=44) with serum cholesterol >220 mg% and/or triglycerides >165 mg% and/or glucose >110 mg%. Patients with clinical or ECG signs of ischemia or kaliemia <3.5 mEq/l, were not admitted to the study. After a 15-days pharmacological wash-out, 24-hour Holter ECG and echocardiography were performed on all patients., Results: Ventricular ectopic beats (VEB) were found in 66% of group A and 100% of group B (difference =34%, 95% C.I. =18-50%). VEB were less severe in group A (Lown's class 1-2), while group B had VEB ranging from class 1 to 5. Left ventricular hypertrophy (LVH) was found in 33% of group A and in 72.7% of group B, and was not closely correlated to VA. Group B patients with LVH had more severe VA (4 A, 4 B and 5 Lown's class)., Conclusions: Hyperglycemia and/or dyslipidemia, even mild, seem to increase the risk of VA in the hypertensive patient with or without LVH. It suggests that 24 hour Holter ECG may be useful to select, among patients with metabolic alterations, those at high risk for VA.

Background: The aim of the study is to evaluate the nutritional stats in candidates to radical cystectomy in order to minimize post-operative complications., Methods: The evaluation is carried out on the basis of anthropometric, bio-humoral and immunologic indexes in a retrospective analysis of patients who underwent major urologic surgery during the last two years. Twenty cases of invasive bladder cancer (mean age 71 years) who underwent radical cystectomy have been studied: in 13 cases urinary diversion by Camey II technique, in 7 cases by Bricker technique has been performed. In 5 cases of orthotopic neo-bladder, endovenous parenteral protein sparing nutrition was carried out for 4 days, in the remaining 15 cases glucidic and saline solutions have been administered., Results: In all the 20 evaluated patients post-operative complications have not been observed., Conclusions: On the basis of the data obtained, the conclusion is drawn that patients with bladder cancer are generally not so malnourished to need an artificial feeding regimen. Considering the urinary tract substitution effects on renal function and metabolism, particularly for the role of glucose on proximal and distal tubule the usefulness of administering only glucidic solutions and maintaining a good diuresis is underlined.

Background and Aims: The aim of this study was to evaluate the results obtained using Scopinaro's biliopancreatic diversion technique (AHS-BPD) in the surgical treatment of morbid obesity., Methods: A retrospective study was carried out in 69 patients with a follow-up ranging between 6-44 months. All patients were operated and monitored by the Obesity Surgery Centre operating in Sardinia since february 1995 at the Department of Emergency Surgery of Sassari University. All the patients were severely obese with a mean BMI of 51.58 and, in the majority of cases, presented associated metabolic diseases with the following incidence: type 2 diabetes in 40.57%, arterial hypertension in 36.23%, severe alteration of lipid status in 52.17%; in overall terms, a plurimetabolic syndrome was present in 24.63% of cases. All patients underwent biliopancreatic diversion using Scopinaro's classic technique (AHS-BPD). Controls were carried out at set intervals (1-3-6-12-18 and 24 months) to evaluate weight loss and the metabolic effects of surgery in terms of the lipid, glucose and protein status., Results: Results were good, as confirmed by the marked weight loss (BMI after 24 months: 30) and the normalisation of cholesterol and glycemia. No major reductions were observed in proteinemia and albuminemia levels., Conclusions: In the light of these results, the authors affirm that Scopinaro's technique is a valid solution for the treatment of morbid obesity. Its relatively invasive nature is justified by the results obtained in terms of weight control and its effect on associated metabolic diseases.

The liver plays a major role in the regulation of glucose metabolism: plasma glucose concentration is the result of peripheral glucose utilization and liver production. Several hormones, including insulin, glucagon, growth hormone, cortisol, and catecholamines contribute to the regulation of glucose metabolism by the liver. In this review, we examine hepatic glucose metabolism, in particular the actions of insulin and contrainsular hormones on glucose hepatic uptake and production in patients with diabetes or chronic liver disease. The most frequent patterns of hepatic involvement that take place during diabetes, i.e. nuclear glycogenesis, steatosis, portal fibrosis, and diabetic steatonecrosis, are discussed. Also considered are anomalies of glucose homeostasis observed in chronic liver disease, including glucose intolerance, diabetes, and hypoglycemias. There is a strong correlation between diabetes mellitus and the liver: diabetic patients have typical histological lesions, while several glucose metabolism alterations are commonly found in subjects with chronic liver disease. The pathogenesis of impaired glucose metabolism during chronic liver disease has not yet been fully understood: further clinical and experimental studies should clarify this issue.

Women receiving estrogen replacement therapy after menopause have a reduced risk of cardiovascular and cerebrovascular mortality when compared to untreated controls. Estrogens are thought to protect women primarily through an effect on lipid metabolism. However estrogen-induced increase of HDL-cholesterol and decrease of total and LDL-cholesterol appear to account only in part for the protective effect of ovarian hormones. Direct effects of estrogens on the arterial wall appear to contribute to the over-all cardiovascular benefits.

Diabetes mellitus is one of the most important cardiovascular risk factors. An increased prevalence of silent or paucisymptomatic myocardial ischaemia has been described in diabetic patients. The authors examined the relationship between glucose metabolism balance and acute ischemic heart disease symptoms in 174 patients: 46 diabetics and 128 non diabetics. Diagnosis of diabetes mellitus was made during admission to hospital in four patients. No differences of strength, length, type, site and radiation of pain between 46 diabetic patients and 128 non diabetics were found. As regards the other symptoms, the authors found that only dyspnoea and palpitations were prevalent in diabetic patients with ten-year or more-disease length. On the other hand, the prevalence of these two symptoms was not different between non diabetics and diabetics with less than ten-year-disease length.

Chronic renal failure is characterized by abnormalities in glucose metabolism. In fact there are present a normal fasting plasma glucose level )or mild hyperglycemia) in the presence of hyperinsulinemia, blunted decrease in the plasma glucose concentration in response to exogenous insulin administration, and diminished effect of intravenous insulin on glucose uptake in forearm perfusion studies. The glucose intolerance is not the result of reduced insulin secretion, or circulating insulin antagonists, and does not correlate with the coexisting metabolic acidosis. Glucose intolerance exists because the peripheral insulin-sensitive tissue (muscle, adipose tissue, liver) of the patients with chronic renal failure are insulin resistant. However there are two subgroups of uremic patients with regard to glucose tolerance: about half of uremic patients can augment their insulin secretion sufficiently to maintain normal glucose tolerance despite glucose intolerance. In the other half, insulin secretion following glucose loads is not different from normal values, so that glucose intolerance results. The cause of the peripheral insulin resistance remain unclear. Besides deranged renal function can result in the development of hypoglycemia. The most important predisposing mechanism to hypoglycemia is diminished glucose availability due to substrate limitation; the second important mechanism (alcohol, insulin, propranolol, etc.). Finally, in chronic renal failure persistent hyperinsulinemia can contribute hyperlipemia and to high incidence of cardiovascular disease.

Cyclosporin A (CsA) is an immunosuppressive drug, but it has also a marked action on carbohydrate metabolism. This study was designed to define the role of a single CsA administration in glucose load distribution. Results show that CsA seems to modify glucose load distribution; in fact it influences considerably glycemia and hepatic, cardiac and muscular glycogen levels, particularly after glucose load. The present experiments suggest that CsA has an antagonist action on insulin release elicited by glucose. This effect may be due to a modification of Ca2+ cellular levels in pancreatic beta-cells. Reduction of insulin release may develop a "pharmacologic diabetes" with metabolism deviated towards gluconeogenesis.

Renal hemodynamic changes and insulin-resistance are normally observed in pregnancy. This study was aimed at evaluating the presence of microalbuminuria in normotensive pregnant subjects with normal or abnormal glucose tolerance. Nineteen pregnant women have been evaluated by oral glucose tolerance test (OGTT, 100 g) and by urine testing for microalbuminuria at 10 weeks of gestation. Eighteen and 14 women have been reexamined respectively at 24 and 32 weeks of gestation. In the subjects examined there was no correlation between microalbuminuria and abnormal glucose tolerance. Microalbuminuria, however, absent when the subjects were examined at 10 weeks of pregnancy, was present in 36% of women examined at 32 weeks of gestation. In conclusion, probably due to renal hemodynamic changes, microalbuminuria appears frequently in late pregnancy.

The coexistence of Graves' disease and insulin-dependent diabetes mellitus is well known among autoimmune polyglandular syndromes and sustained by common underlying immune pathogenic factors. Hyperthyroidism itself may lead to impaired glucose tolerance in subjects with intact beta-cell function through various not well clarified mechanisms and treatment of thyroid hyperfunction, on the other side, generally ameliorates the degree of metabolic control when diabetes is pre- and/or coexisting. We report a case of Graves' disease associated with diabetes mellitus, in which a partial recovery of insulin secretion is documented after euthyroidism was restored.

The onset of a protein-energy malnutrition represents a real risk for patients on CAPD. In order to verify the nutritional status and the effectiveness of the dietetic surveillance in preventing this complication, dietary intake, anthropometric measurements and biochemical parameters were monitored in 46 patients (27 males, 19 females, mean age: 58.7 +/- 14.8 years), suffering from ESRF and treated with CAPD, for a total observation period of 1731.67 months (mean: 37.64 +/- 25.17 months). The mean glucose concentration in the dialysate was 2.00 +/- 0.36 g/dl, the glucose reabsorption from dialysate per kg of ideal body weight (kg-IBW) was equivalent to 5.1 kcal, the mean dialysate protein loss was 13.08 +/- 5.52 g/day and the incidence of peritonitis episodes was 1 every 30.38 months-patient. The daily total caloric intake (by mouth and dialysate) was 30.8 kcal/kg-IBW with a normal subdivision for each diet component: there were not statistically significant differences in distribution according to age, sex and in the follow-up. The mean daily value of protein intake (PI) evaluated by dietary interviews was 0.99 g/kg-IBW, with a significant increase 1 year since the beginning of CAPD; the PI evaluated from urea nitrogen appearance was 1.22 g/kg-IBW. The PI remained stable later in the follow-up and in patients that made use of dietetic supplements, the mean daily increase by this way was 0.47 g/kg-IBW. Anthropometric measurements showed a statistically significant increase of %RBW after 1 year and of TS and % body fat after 3 years.(ABSTRACT TRUNCATED AT 250 WORDS)

Unlabelled: Eleven insulin-dependent diabetic patients (IDDM) with angiographically normal coronary arteries and normal echocardiographic dipyridamole test, and 12 normal controls were studied at rest and after atrial pacing. Simultaneous sampling from arterial and coronary sinus blood was performed. In IDDM patients, despite hyperglycemia, myocardial glucose uptake was slightly lower than in controls. This process was significantly activated in both groups by atrial pacing. The isotopically calculated net flux of lactate across myocardium, in agreement with the net balance value based on unlabeled lactate-pyruvate arterio-venous differences, showed a net uptake in controls (3.5 +/- 0.6 mumol/min/1.73 m2) and a net release in IDDM (12.4 +/- 2.6; p less than 0.01). Atrial pacing stimulated lactate uptake in both groups. Myocardial uptake of ketone bodies was significantly higher in IDDM than in controls (37.0 +/- 6.3 mumols/min/1.73 m2 vs 10.1 +/- 3.4; p less than 0.01). Free fatty acid uptake was also significantly greater in IDDM than in controls (44.1 +/- 7.0 mumols/min/1.73 m2 vs 24.1 +/- 5.1; p less than 0.01). Alanine and branched chain amino-acids were released by diabetics but not by control hearts at rest. The normalization of blood glucose concentrations restored normal patterns of lactate and ketone body kinetics across diabetic myocardium., In Conclusion: at rest, myocardial lactate and aminoacids uptake is markedly impaired in IDDM without coronary artery disease; the metabolic abnormalities of the diabetic myocardium is not a primary phenomenon but rather a consequence of hypoinsulinemia and hyperglycemia because insulin administration, resulting in normoglycemia, restored normal patterns of cardiac metabolism.

To assess the value of myocardial substrate in the occurrence of ischemic-reperfusion damage, isolated, electrically paced rabbit hearts were perfused for 60 min under aerobic condition (25 ml/min with oxygenated Krebs-Henseleit solution containing glucose 11 mM). Thereafter the hearts were made ischemic for 30 min by reducing coronary flow to 3 ml/min. During ischemia, 3 different substrates were used glucose 11 mM (Group I), palmitate 1.2 mM (Group II) and palmitate 1.2 mM + glucose 11 mM (Group III). The hearts were then reperfused (25 ml/min) for 30 min under aerobic condition using glucose 11 mM as the only substrate. In the presence of glucose with or without palmitate (Group I and III) ischemic damage was mild. Recovery of the developed pressure was 95% and there was no contracture during ischemia and or reperfusion. During ischemia and reperfusion there was a small release of CPK, GSSG and GSH. In the presence of palmitate (Group II) ischemic and reperfusion damage was profound. Recovery of developed pressure was reduced (25%) and diastolic pressure significantly increased (68 +/- 5.1 vs 3 +/- 1.5, 5 +/- 1.8 mmHg). These mechanical data were concomitant with an important release of CPK (580 +/- 50 vs 180 +/- 35, 210 +/- 48 mU/min/gww) and oxidised glutathione (0.38 +/- 0.3 vs 0.05 +/- 0.001, 0.09 +/- 0.003 nmoles/min/gww). In addition the redox state of the cells of the Group II was significantly shifted through the oxidative state at the end of ischemia and of reperfusion. These results indicate that palmitate as substrate increases the deleterious effects of ischemia; glucose is able to overcome the negative effects of palmitate.

As it's well known from the clinic, human syndromes depending on pituitary GH, ACTH and PRL secreting tumors are associated with alteration of glucose homeostasis. There is an hypothetical but convincing explanation for this, based on a number of concrete observations and experiments. The main mechanism for glucose intolerance or overt diabetes is related to insulin-resistance. The increased concentration of the three hormones would alter the action of insulin on its target cells at binding and (mainly) post-binding level. Besides recent researches indicate that the hypothalamus may play an important role in the pathogenesis of at least some cases of pituitary adenomas and, directly or indirectly, of the glucose homeostasis derangement.

In this report the Authors have verified the effects of Ketanserin on glycaemic metabolism of type II diabetic subjects with a moderately high blood pressure. They think that a therapeutic dose of drug is not able to considerably inhibit insulin production. The Authors can assert that the Ketanserin does not influence the glycaemic regulation by therapeutic dose, neither does it increase the diabetic disease, nor disturb the oral hypoglycaemic therapy though it normalizes high blood pressure.

NMR is still considered essentially, in the field of ischemic brain vascular disease, an imaging method. On the contrary, Authors review MR-spectroscopy possibilities, emphasizing that by this method it is possible to achieve a complete and dynamic study of brain energy metabolism, and therefore to identify markers of cellular injury clearly more sensitive and precocious than MRI morphological findings. Moreover, this method allows to easily evaluate cerebral blood flow, pharmacologic treatment efficacy, effects of eventual metabolic abnormalities on ischemia's evolution.

The study of the intra- and post-operative intestinal absorption of glucose, xylose and a radionuclide, 99mTc, shows that laparotomy does not influence jejunal function, thus leaving the possibility of an immediate post-operative nutrition with a naso-jejunal tube, a needle catheter jejunostomy or, even, an oral feeding. Parenteral nutrition, for the future, could have a little role in post-operative period and the too much used nasogastric tube should be avoided.

A glucose metabolism impairment occurs in about 2-3% of all pregnancies. Two different groups of women are involved: diabetic women who become pregnant and healthy women developing gestational diabetes or glucose intolerance during pregnancy. Due to therapeutic improvements and new techniques of fetal monitoring, maternal and perinatal mortality now approaches that of normal pregnancies. On the contrary, congenital anomalies are still four times more frequent. A good control of the mother metabolism is necessary to reduce complications in fetal development, especially during the first six weeks, a crucial period for the early cell division. Fetal monitoring is very important not only to control the normality of the growth and the well-being of the fetus, but also for early identification of possible anomalies.

Diabetic renal microangiopathy accounts for enormous morbidity and mortality, particularly in patients who develop diabetes in childhood or early youth; in the last few years its pathogenesis has been therefore extensively studied, aiming to prevent renal complications or at least of slowing down its progression toward uremia. Though not always in accordance with theoretical expectations, the results of clinical trials have nevertheless widened our therapeutic possibilities; in fact, besides the attainment of an optimal metabolic control, other possible interventions include a careful correction of albeit minimal elevations in arterial pressure; the interference with intrarenal hemodynamic parameters; the correction of insulin-independent metabolic pathways, abnormally activated in the diabetic, such as non enzymatic glycation and polyol pathway; the treatment of endothelial and platelet alterations; the improvement of the rheologic properties of blood.

The effect of sodium salicylate perfused at constant rate for 30 minutes on Glucose-3-H3 kinetics has been studied in anestethyzed normal Wistar rats, controlling blood glucose levels, Ra and Rd. While blood glucose levels and Rd were not affected, the Ra values were influenced between the 20th and the 30th minute of salicylate perfusion.

The behaviour of glycaemia, insulinaemia, phosphoraemia, somatotropinaemia,free glycerol and triglyceridaemia was studied in six patients with A.L.S. following sugar load (1 g/Kg) in fasting. The results of glycaemia and insulinaemia were in tune with published data which have pointed to reduced sugar tolerance and reduced insulin secretion in patients with A.L.S. In the present experiments, particularly significant were the phosphoraemia responses. The failure of inorganic phosphorus values to fall after glucose loading suggests that the glycidic intolerance of these patients is related above all to a reduction in functioning muscular mass rather than to insufficient insulin secretion. The reduction in nervous tissue may also be of importance in this sense. In fact, not all biohumoral parameters investigated were similar to those of diabetes because the behaviour of somatotropinaemia, free glycerol and plasma triglycerides was normal. The changed behaviour of phosphorus would thus indicate altered glucose uptake at peripheral tissue level.

The severe impairment of the nutritional state, which usually accompanies malignant diseases, heavily contributes to the high morbidity and mortality rates observed in cancer patients. Nevertheless, the utility of an artificial energy supply to these patients is still controversial because the nutrients given to replete the host may also stimulate tumor growth. Consequently, a correct nutritional approach for cancer patients should be based upon a well-defined understanding of tumor as well as host-metabolic needs. In this regard, the most typical metabolic abnormalities observed in cancer patients and experimental animals are examined. Specific modifications of the plasma levels of different groups of amino acids--including glucogenic, aromatic, sulphur-containing and branched-chain amino acids--have been observed in cancer patients independently of the their degree of malnutrition, glucose tolerance and tumor diffusion. This may reflect a series of specific modifications induced by the neoplastic tissue on host's protein turnover. Little information is available regarding the protein metabolism in the neoplastic tissue. A number of attempts have been made to reduce tumor growth by withholding single amino acids considered essential to the tumor; nevertheless, the results obtained are still controversial. The two major abnormalities of carbohydrate metabolism observed in cancer patients are an increased glucose turnover and an impaired glucose tissue disposal. The former seems to be due to an increased glucogenesis, whereas the latter may be attributed to an insulin resistance in contrast to the high anaerobic glucose utilization observed in the neoplastic tissue.(ABSTRACT TRUNCATED AT 250 WORDS)