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Biomedical subjects

N Ferrara

Publications and source records attributed to N Ferrara.

At least 73 records · Page 4Linked to original sources
PubMed1998

Congestive heart failure and cognitive impairment in an older population. Osservatorio Geriatrico Campano Study Group.

OBJECTIVE: Congestive heart failure (CHF) is potentially preventable, and the identification of modifiable risk factors for cognitive impairment (CI) for older persons is a very important issue. We examined the cross-sectional relationship between CHF and CI in an older population. DESIGN: A cross-sectional survey. SETTING AND PARTICIPANTS: A total of 1339 subjects aged 65 and older were selected from the electoral rolls of Campania, a region of southern Italy. MEASUREMENTS: Sociodemographic characteristics were recorded, as was the presence of cardiovascular diseases, including CHF classified according to the New York Heart Association (NYHA) guidelines for disease severity; CI evaluated by means of the Mini-Mental State Examination (MMSE), with a score of <24 indicating impairment; geriatric depression scale (GDS) rating; blood pressure (BP); and heart rate (HR). RESULTS: The final sample numbered 1075; 172 subjects were excluded because of neurological disorders and psychotropic therapy, and 92 were excluded because their BP, HR, or cognitive examination was not recorded. Prevalence of CHF was 8.2%, and 23.0% of subjects scored <24 on the MMSE. The prevalence of CHF in subjects with an MMSE score of <24 and > or =24 was 20.2% and 4.6%, respectively (P < .001). Logistic regression analysis showed that CHF was associated independently with CI by sex, age, educational level, GDS, diabetes, hypertension, alcohol consumption, smoking, atrial fibrillation, systolic and diastolic BP, and HR. The risk of CI was 1.96-fold greater in subjects with CHF (odds ratio: 1.96; 95% confidence interval: 1.07-3.58; P < .028). Systolic BP decrease was correlated negatively with NYHA classes only in subjects with CI (r = -0.981; P < .020), whereas HR increase was correlated positively with NYHA classes only in subjects without CI (r = 0.985; P < .015). CONCLUSIONS: In our population, CHF is associated with CI in subjects aged 65 years and older. Systolic BP reduction and the lack of HR increase, related to NYHA classes, might characterize cognitively impaired subjects with CHF.

Aged↗
PubMed1998

Prevalence of varicose veins in an Italian elderly population.

The prevalence of varicose veins (VV) in the elderly population of the Campania Region, in Southern Italy, was estimated. A random sample of the people aged more than 65 years was drawn by means of a stratified multistage sampling design warranting that observed percentages were direct estimates of population percentages. The investigation covered 1319 subjects, 560 (42.5%) men and 759 (57.5%) women, their ages ranging from 66 to 96 years with an average value of 74.2 years, who were interviewed and visited by trained physicians. VV were defined as any reticular or truncal visible varicosities of the lower limbs, and investigated symptoms were heaviness, pain, nightly cramps, edema, eczema, hyperpigmentation, and ulceration. Some variables were studied as risk factors: age, sex, lifetime occupation, smoking, alcohol, hypertension, diabetes, and obesity; previous treatment and use of elastic stockings were also studied. Statistical associations were evaluated by Chi-square test, a two-tailed P value of 0.05 being assumed as significance level. In total, 391 (29.6%) subjects were reported to be affected by VV, but the clinical examination was positive in only 362 (27.4%) with a good correspondence between answers and clinical findings. Prevalence was greatly affected by sex, the percentage being two times higher in women (35.2%) than in men (17%). VV developed after a pregnancy in 40.5% of women, but a high percentage of women (38.2%) also reported menopause as a time starting point. No significant association between reported risk factors and VV was found among men, whereas obesity was strongly related to VV in women. One or more symptoms were reported in 92.1% of persons affected by VV, but no previous therapy was reported by 58.9% of subjects. Only 16.9% of patients used elastic stockings with a significant difference between men (7.4%) and women (20.2%).

Age Distribution↗
PubMed1998

Corticotropin regulates vascular endothelial growth factor expression in human fetal adrenal cortical cells.

The human adrenal cortex has a complex vasculature that is essential for growth, organ maintenance, and access of secreted hormones to the circulation. Growth and function of the adrenal cortex are regulated by corticotropin (ACTH), the actions of which are in part mediated by locally produced growth factors. As cortical growth and vascularization must increase in a coordinated manner, we hypothesized that ACTH also influences adrenal cortical angiogenesis by stimulating the local expression of specific angiogenic factors. Vascular endothelial growth factor (VEGF) is a potent endothelial cell-specific angiogenic peptide, the expression of which has been detected in adrenal cortical cells. Therefore, we examined the localization of VEGF expression in the midgestation (16-20 weeks) human fetal adrenal cortex and determined whether VEGF expression and secretion by isolated human fetal adrenal cortical cells are regulated by ACTH. By immunohistochemical analysis, strong cytoplasmic staining for VEGF was detected in scattered clusters of fetal zone (inner cortical compartment) cells. In contrast, cells in the outer, definitive zone of the cortex stained only weakly for VEGF. The predominant staining for VEGF in the fetal zone correlated with the extensive vasculature of this zone as detected by immunohistochemical staining for von Willebrand factor, which is specific for endothelial cells. In primary cultures of human fetal adrenal cortical cells, ACTH (1 nmol/L) and forskolin (10 micromol/L) increased the abundance of messenger ribonucleic acid transcripts encoding VEGF, as assessed by Northern and slot blot analyses. The stimulatory effect of ACTH and forskolin on VEGF gene expression occurred within 2 h of agonist exposure and persisted for at least 24 h. ACTH and forskolin also increased VEGF protein secretion by fetal adrenal cortical cells, as assessed by enzyme-linked immunosorbent assay for VEGF in fetal adrenal cortical cell-conditioned medium. A significant (P < 0.05) increase in VEGF secretion was detected as early as 8 h after ACTH or forskolin treatment. By 24 h after the addition of ACTH or forskolin, VEGF secreted from isolated human fetal adrenal cells was increased 5- to 6-fold. These data demonstrate that the human fetal adrenal cortex, particularly the cells of the inner fetal zone, express VEGF and that VEGF expression and secretion by these cells are directly regulated by ACTH and the activation of adenylate cyclase. Thus, VEGF may be a local regulator of adrenal cortical angiogenesis and an important mediator of the tropic action of ACTH, ensuring the coordination of ACTH-stimulated cortical growth and vascularization.

Adrenal Cortex↗
PubMed1998

Magnetic resonance imaging detects suppression of tumor vascular permeability after administration of antibody to vascular endothelial growth factor.

Macromolecular contrast medium-enhanced magnetic resonance imaging (MRI) and tumor-volume measurements were applied to monitor the effects of anti-vascular endothelial growth factor (anti-VEGF) antibody on microvascular characteristics and tumor growth of MDA-MB-435 human breast cancer cells implanted in nude rats. Administration of anti-VEGF antibody (three 1 mg doses at 3-day intervals) induced significant reductions in tumor growth rates (p < 0.05) and in MRI-assayed microvascular permeabilities (p < 0.05). Results of the study were consistent with previous observations that new microvessels formed in response to angiogenesis are hyperpermeable, and with the hypothesis that hyperpermeability is a mechanistic element in angiogenesis. Variations in tumor-vessel hyperpermeability can be measured by contrast-enhanced MRI, which may prove useful for assessing antiangiogenesis therapy.

Adenocarcinoma↗
PubMed1998

Substantially attenuated hemodynamic responses to Escherichia coli-derived vascular endothelial growth factor given by intravenous infusion compared with bolus injection.

Vascular endothelial growth factor (VEGF) produces beneficial angiogenesis in animal models of coronary and peripheral ischemia. However, intravenous bolus injection of Chinese hamster ovary cell (CHO)-derived VEGF produces adverse effects on hemodynamics. The present study examined pharmacokinetic and hemodynamic responses to Escherichia coli-derived VEGF, which will be used in clinical patients, compared with responses to CHO-derived VEGF, and tested whether intravenous infusion of E. coli-derived VEGF attenuates the hemodynamic responses compared with the responses observed with intravenous bolus injection. Hemodynamic parameters were measured before and after administration of VEGF in conscious, instrumented rats. Intravenous injection of both CHO- and E. coli-derived VEGF produced a similar maximal reduction in arterial pressure, although E. coli-derived VEGF exhibited less of a depressor effect in the initial phase after injection. Either infusion or injection of E. coli-derived VEGF caused hypotension, tachycardia and reduced cardiac output and stroke volume, which were significantly attenuated when given by infusion compared with injection. The maximal hypotensive and tachycardiac responses to infusion were decreased by 50 to 60% compared with those responses observed after injection. Cardiac output was maximally reduced by 34% after injection, but only 18% after infusion. A sustained elevation in systemic vascular resistance observed after injection was avoided after infusion. Thus, the hemodynamic side effects of VEGF administration can be substantially attenuated by controlling the rate of VEGF infusion. The data indicate that infusion, instead of bolus injection, is a more appropriate regimen for VEGF administration.

Animals↗
PubMed1997

Hypercholesterolemia attenuates angiogenesis but does not preclude augmentation by angiogenic cytokines.

BACKGROUND: The impact of hyperlipidemia on collateral vessel development in vivo remains enigmatic. We sought to determine the anatomic extent and functional capacity of the collateral bed that develops in response to limb ischemia in a well characterized animal model of spontaneous hypercholesterolemia, the Watanabe heritable hyperlipidemic (WHHL) rabbit. We further characterized the impact of exogenous angiogenic cytokine administration on collateral vessel development and function in the same animal model. METHODS AND RESULTS: Weight-matched 6-month-old male homozygous WHHL (n=9) and normal New Zealand White (NZW) (n=9) rabbits underwent surgical resection of one femoral artery. Ten days later, the ischemic hindlimb was evaluated for collateral vessel formation, blood flow, and tissue damage. Collateral vasculature was less extensive among WHHL than NZW, as indicated by a significant reduction in angiographic score (0.19+/-0.02 versus 0.35+/-0.03, P<.001) and capillary density (46.4+/-4.1 versus 78.9+/-4.6/mm2, P<.0002). This was associated with a reduction in calf blood pressure index (9.5+/-3.5% versus 32.8+/-2.8%, P<.0001), arterial blood flow (7.5+/-0.6 versus 13.6+/-0.7 mL/min, P<.0001), and muscle perfusion index (40.1+/-3.2% versus 65.9+/-2.0%, P<.0001) and an increase in muscle necrosis (48.16+/-5.41% versus 25.90+/-3.83% negative 2,3,5-triphenyltetrazolium chloride staining, P<.004). Treatment of WHHL rabbits (n=9) with recombinant human vascular endothelial growth factor produced a statistically significant improvement in all functional as well as anatomic indices of collateral development. CONCLUSIONS: Collateral vessel development associated with hindlimb ischemia in vivo is severely attenuated in an animal model of spontaneous hypercholesterolemia but nevertheless may be augmented by administration of angiogenic cytokines.

Animals↗
PubMed1997

Humanization of an anti-vascular endothelial growth factor monoclonal antibody for the therapy of solid tumors and other disorders.

Vascular endothelial growth factor (VEGF) is a major mediator of angiogenesis associated with tumors and other pathological conditions, including proliferative diabetic retinopathy and age-related macular degeneration. The murine anti-human VEGF monoclonal antibody (muMAb VEGF) A.4.6.1 has been shown to potently suppress angiogenesis and growth in a variety of human tumor cells lines transplanted in nude mice and also to inhibit neovascularization in a primate model of ischemic retinal disease. In this report, we describe the humanization of muMAb VEGF A.4.6.1. by site-directed mutagenesis of a human framework. Not only the residues involved in the six complementarity-determining regions but also several framework residues were changed from human to murine. Humanized anti-VEGF F(ab) and IgG1 variants bind VEGF with affinity very similar to that of the original murine antibody. Furthermore, recombinant humanized MAb VEGF inhibits VEGF-induced proliferation of endothelial cells in vitro and tumor growth in vivo with potency and efficacy very similar to those of muMAb VEGF A.4.6.1. Therefore, recombinant humanized MAb VEGF is suitable to test the hypothesis that inhibition of VEGF-induced angiogenesis is a valid strategy for the treatment of solid tumors and other disorders in humans.

Adrenal Cortex↗
PubMed1997

Differential transcriptional regulation of the two vascular endothelial growth factor receptor genes. Flt-1, but not Flk-1/KDR, is up-regulated by hypoxia.

Vascular endothelial growth factor (VEGF) and its two endothelial cell-specific receptor tyrosine kinases, Flk-1/KDR and Flt-1, play a key role in physiological and pathological angiogenesis. Hypoxia has been shown to be a major mechanism for up-regulation of VEGF and its receptors in vivo. When we exposed human umbilical vein endothelial cells to hypoxic conditions in vitro, we observed increased levels of Flt-1 expression. In contrast, Flk-1/KDR mRNA levels were unchanged or slightly repressed. These findings suggest a differential transcriptional regulation of the two receptors by hypoxia. To identify regulatory elements involved in the hypoxic response, promoter regions of the mouse Flt-1 and Flk-1/KDR genes were isolated and tested in conjunction with luciferase reporter gene. In transient transfection assays, hypoxia led to strong transcriptional activation of the Flt-1 promoter, whereas Flk-1/KDR transcription was essentially unchanged. Promoter deletion analysis demonstrated a 430-bp region of the Flt-1 promoter to be required for transcriptional activation in response to hypoxia. This region includes a heptamer sequence matching the hypoxia-inducible factor-1 (HIF) consensus binding site previously found in other hypoxia-inducible genes such as the VEGF gene and erythropoietin gene. We further narrowed down the element mediating the hypoxia response to a 40-base pair sequence including the putative HIF binding site. We show that this element acts like an enhancer, since it activated transcription irrespective of its location or orientation in the construct. Furthermore, mutations within the putative HIF consensus binding site lead to impaired transcriptional activation by hypoxia. These findings indicate that, unlike the KDR/Flk-1 gene, the Flt-1 receptor gene is directly up-regulated by hypoxia via a hypoxia-inducible enhancer element located at positions -976 to -937 of the Flt-1 promoter.

Amino Acid Sequence↗
PubMed1997

Effects of melatonin in isolated rat papillary muscle.

Melatonin (N-acetyl-5-methoxytryptamine), the principal hormone of the vertebral pineal gland, elicits several neurobiological effects. However, the effects of melatonin on cardiac muscle are still unknown. The first goal of the study was to investigate the role of melatonin on myocardial contractility in isolated rat papillary muscle using dose-response curves to melatonin, to isoproterenol and calcium either in the presence or in the absence of melatonin (0.3 nM). Response curves to isoproterenol were additionally performed in the presence of melatonin plus the specific receptor antagonist N-acetyltryptamine (10 microM); the adenylate-cyclase stimulator forskolin (10 microM) was also used. Melatonin has no direct inotropic effect in isolated rat papillary muscle but counteracts isoproterenol but not [Ca2+] effects. In fact, the EC50 for isoproterenol was significantly higher in the presence than in the absence of melatonin (p < 0.001). This anti-adrenergic action occurs through an interaction to a specific cardiac receptor. Forskolin-stimulated adenylate cyclase induced an increase of contractile force (+118 +/- 25%) which was reduced in the presence of melatonin (+26 +/- 10%; p < 0.01). In conclusion, we found that melatonin possess anti-adrenergic effect in isolated rat papillary muscle. This phenomenon was abolished in the presence of its receptor antagonist N-acetyl-tryptamine demonstrating that melatonin operates through a specific cardiac receptor. The reduction of contractility increase, induced by forskolin-stimulated adenylate cyclase, shows that melatonin may act through a reduction of cyclic AMP accumulation.

Adenylyl Cyclases↗
PubMed1997

The role of Gi-proteins and beta-adrenoceptors in the age-related decline of contraction in guinea-pig ventricular myocytes.

A decline in contractility in myocytes from ageing guinea-pig hearts was demonstrated, which is more pronounced for maximum beta-adrenoceptor-stimulated activity than contraction in high Ca2+. In this study the role of the inhibitory G-proteins (Gi) in this process was investigated. Comparisons were made between young (Y, < 400 g, < 4 weeks), adult (A. > 600 g, > 8 weeks) and senescent guinea pigs (S, 58-65 weeks, 1136 +/- 30 g). Gi alpha activity, detected by pertussis toxin-catalysed ADP ribosylation, was significantly increased in senescent compared to young animals, but immunodetectable levels of Gi alpha were unchanged, beta-adrenoceptor number was decreased by 27% in senescent compared with young animals (P < 0.002). Pertussis toxin treatment increased the maximum response to isoproterenol in contacting myocytes so that there was no longer any significant decline with age. Maximum contraction amplitudes (sarcomere length change, micron) with isoproterenol before pertussis toxin were 0.144 +/- 0.011 (Y, n = 22 animals), 0.104 +/- 0.009 (A. 18) and 0.098 +/- 0.009 (S. 14), P < 0.01 by analysis of variance (ANOVA). Following toxin treatment amplitudes were 0.140 +/- 0.012 (Y. 12), 0.117 +/- 0.010 (A. 10) and 0.117 +/- 0.018 (S. 8), P = N.S. Pertussis toxin treatment also reversed the effects of ageing on contraction and relaxation velocity in isoproterenol. In contrast, the effect of age on contraction amplitude or velocity in maximum Ca2+ was more pronounced after toxin treatment. The EC50 value for isoproterenol increased with age: pertussis treatment decreased the EC50 in each group, but the effect was especially pronounced for senescent animals. There was no significant difference in the concentration-response curves for the negative inotropic effect of adenosine (in the presence of isoprotenerol) between the three age groups before toxin treatment. All effects of adenosine were abolished after pertussis exposure. We conclude that increased Gi alpha activity is likely to contribute to the decreased response to isoproterenol, but not to high Ca2+, in myocytes from ageing guinea-pigs.

Adenosine Diphosphate↗
PubMed1997

Alterations in beta-adrenoceptor mechanisms in the aging heart. Relationship with heart failure.

In chronic heart failure substantial and characteristic changes occur in the function of the adrenergic nervous system. Studies in isolated left ventricular muscle and in single cardiomyocytes from experimental models of aging and, recently, from humans show an age-related reduced contractile response to beta-adrenoceptor stimulation. "beta-adrenoceptor desensitization" is thought to be a general and common mechanism to explain the age- and heart failure-related decrease in beta-adrenoceptor response. The aim of this review is to compare alterations in beta-adrenoceptor mechanisms in physiological cardiovascular aging and chronic heart failure. From an analysis of the overall data on the role of aging in beta-adrenoceptor regulation in human and animal hearts, it is possible to conclude that the reduced response to beta-agonists is common to all species and all cardiac tissues. Moreover, the age-related changes are limited to beta-adrenoceptor-G-protein (s)-adenylyl cyclase system abnormalities, while the type and level of abnormalities change with species and tissues. The modifications shown in the aging heart are not very different from some observed in heart failure. In particular, both in aged and failing hearts we may see that the decrease in beta-adrenoceptor responsiveness is related to changes in G-protein function.

Aged↗
PubMed1997

Vascular endothelial growth factor attenuates myocardial ischemia-reperfusion injury.

BACKGROUND: Hypoxic endothelial cell activation plays a key role in the myocardial dysfunction resulting from ischemia-reperfusion injury. Recent evidence suggests that vascular endothelial growth factor (VEGF) may, in addition to promoting angiogenesis, modulate various aspects of endothelial function and repair. We examined whether administration of VEGF in the cardioplegic solution might have a beneficial effect on myocardial ischemia-reperfusion injury in an isolated rat heart model. METHODS: Hearts from Sprague-Dawley rats were perfused with Krebs-Henseleit solution in a modified Langendorff apparatus. Percent recovery of cardiac output, coronary flow, stroke work, and percent increase in coronary vascular resistance were measured after 2 hours of global ischemia and 40 minutes of reperfusion. Coronary effluent was collected after ischemia and reperfusion for measurement of creatine kinase. RESULTS: Hearts receiving cardioplegia solution containing 125 microg VEGF showed significantly improved recovery of cardiac output, coronary flow, and stroke work, and significantly reduced coronary vascular resistance compared with hearts receiving hyperkalemic cardioplegia only (p < 0.05). Coadministration of a nitric oxide synthase inhibitor attenuated the VEGF-induced cardiprotective effects. Hearts treated with VEGF released significantly less creatine kinase compared with control hearts. CONCLUSIONS: Addition of VEGF to hyperkalemic cardioplegia protects against myocardial ischemia-reperfusion injury in the isolated rat heart.

Animals↗
PubMed1997

Angina-induced protection against myocardial infarction in adult and elderly patients: a loss of preconditioning mechanism in the aging heart?

OBJECTIVES: The present study examined whether angina 48 h before myocardial infarction provides protection in adult and elderly patients. BACKGROUND: The mortality rate for coronary artery disease is greater in elderly than in young patients. In experimental studies, ischemic preconditioning affords an endogenous form of protection against ischemia-reperfusion injury in adult but not in senescent hearts. Angina before myocardial infarction, a clinical equivalent of experimental ischemic preconditioning, has a protective effect in adult patients. It is not known whether angina before myocardial infarction is also protective in aged patients. METHODS: We retrospectively verified whether antecedent angina within 48 h of myocardial infarction exerts a beneficial effect on in-hospital outcomes in adult (< 65 years old, n = 293) and elderly (> or = 65 years old, n = 210) patients. RESULTS: In-hospital death was more frequent in adult patients without than in those with previous angina (10% vs. 2.6%, p < 0.01), as were congestive heart failure or shock (10.7% vs. 3.3%, p < 0.02) and the combined end points (in-hospital death and congestive heart failure or shock) (20.7% vs. 5.9%, p < 0.0003). In contrast, the presence or absence of previous angina before acute myocardial infarction in elderly patients seems not to influence the incidence of in-hospital death (14.4% vs. 15.2%, p = 0.97), congestive heart failure or shock (11.0% vs. 11.9%, p = 0.99) and the combined end points (25.4% vs. 27.1%, p = 0.89). Logistic regression analysis models for in-hospital end points show that previous angina is a positive predictor in adult but not in elderly patients. CONCLUSIONS: The presence of angina before acute myocardial infarction seems to confer protection against in-hospital outcomes in adults; this effect seemed to be less obvious in elderly patients. This study suggests that the protection afforded by angina in adult patients may involve the occurrence of ischemic preconditioning, which seems to be lost in senescent patients.

Adult↗
PubMed1997

The role of blood pressure in cognitive impairment in an elderly population. Osservatorio Geriatrico Campano Group.

OBJECTIVE: The aim of this study was to investigate the cross-sectional relationship between arterial blood pressure and cognitive impairment in a group of elderly subjects, controlling for such confounding variables as age, education, depression, drug use and antihypertensive treatment. DESIGN AND SETTING: A cross-sectional survey in Campania, a region in southern Italy. SUBJECTS AND METHODS: A random sample of 1339 elderly subjects aged 65-95 years (mean 73.9 +/- 6.2 years) selected from the electoral rolls was interviewed by trained physicians. Sociodemographic characteristics, results of Mini-Mental State Examination (MMSE), Geriatric Depression Scale (GDS), blood pressure and whether antihypertensive treatment was being administered were recorded. When subjects with neurological diseases and those under psychotropic therapy were excluded from the analyses, the population numbered 1106. RESULTS: The MMSE score was less than 24 for 27.9% of the subjects and the mean GDS score was 10.8 +/- 6.3. The mean systolic blood pressure (SBP) was 145.3 +/- 19.0 mmHg and the mean diastolic blood pressure (DBP) was 82.0 +/- 9.2 mmHg. Logistic regression analysis showed that female sex, age, GDS score and DBP but not SBP were predictive of cognitive impairment. Educational level and antihypertensive treatment, on the contrary, play a protective role. DBP was associated with cognitive impairment in subjects aged 75 years (odds ratio 1.62, 95% confidence interval 1.16-2.25) and over (odds ratio 5.16, 95% confidence interval 1.50-17.71) but not in those aged 65-74 years. CONCLUSION: DBP but not SBP is predictive of cognitive impairment in subjects aged 75 years and over without neurological disorders independently from sex, age, education, GDS and antihypertensive treatment

Aged↗
PubMed1997

Glucose ingestion affects cardiac ANS in healthy subjects with different amounts of body fat.

Low-to-high frequency ratio (LF/HF) is an indirect index of sympathovagal balance derived by heart rate spectral analysis. We investigated the effect of glucose ingestion on LF/HF in 17 healthy, normotensive young subjects (9 male, 8 female) with a wide body fat content range (body fat = 29 +/- 5.9%; range = 19-42%) and a normal thyroid hormone status. Before and after an oral glucose tolerance test (OGTT), the Holter technique and indirect calorimetry allowed us to determine heart rate and substrate oxidation in all subjects. At baseline, LF/HF correlated with body fat (r = 0.60, P < 0.005), waist-to-hip ratio (r = 0.57, P < 0.01), fasting plasma insulin (r = 0.55, P < 0.04), leptin (r = 0.56, P < 0.01), and norepinephrine (r = 0.58, P < 0.009) concentrations. Age-, body fat-, content-, and fat-free mass-adjusted respiratory quotient (r = 0.59, P < 0.007) and basal metabolic rate (r = 0.61, P < 0.001) were also correlated with basal LF/HF. Along with OGTT plasma glucose, insulin and norepinephrine concentrations and basal LF/HF significantly rose at 60 min and then declined throughout the test. Area under the curve (AUC) for LF/HF correlated with body fat (r = -0.66, P < 0.004), fasting plasma leptin concentration (r = -0.57, P < 0.01), glucose induced thermogenesis (r = 0.62, P < 0.001), glucose uptake (r = 0.59, P < 0.007), and AUC for plasma norepinephrine concentration (r = 0.63, P < 0.001). Water instead of glucose ingestion does not significantly affect LF/HF (n = 8). In conclusion, our study supports the hypothesis that glucose ingestion affects LF/HF and that such change is related to the amount of body fat.

Adipose Tissue↗