Publications
342 results found
Leyva F, Chua TP, Godsland IF, et al., 1999, Loss of the normal coupling between the anaerobic threshold and insulin sensitivity in chronic heart failure, HEART, Vol: 82, Pages: 348-351, ISSN: 1355-6037
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- Citations: 8
Jolly M, Amin R, Godsland I, et al., 1999, A mechanism for insulin resistance in pregnancy? A study of insulin kinetics., DIABETOLOGIA, Vol: 42, Pages: A160-A160, ISSN: 0012-186X
Zoratti R, Godsland IF, Chaturvedi N, et al., 1999, Insulin resistance, lipid metabolism and body composition in Afro-Caribbean, South Asian and European-origin men., ATHEROSCLEROSIS, Vol: 145, Pages: S10-S10, ISSN: 0021-9150
Flanagan DE, Moore VM, Godsland IF, et al., 1999, Reduced foetal growth and growth hormone secretion in adult life, CLINICAL ENDOCRINOLOGY, Vol: 50, Pages: 735-740, ISSN: 0300-0664
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- Citations: 20
Leyva F, Godsland IF, Villar J, et al., 1999, Insulin sensitivity is modulated by the I/D ACE gene polymorphism, but not by the TRP64ARG β <inf>3</inf>-adrenoceptor gene polymorphism, the M235T angiotensinogen gene polymorphism or the ε2/ε3/ε4 apolipoprotein E gene polymorphism, Heart, Vol: 81, ISSN: 1355-6037
Background: Prospective studies have linked surrogate measures of insulin resistance, such as hyperinsulinemia and hyperglycemia, to coronary heart disease (CHD). The I/D polymorphism of the ACE gene has been linked to insulin resistance and to CHD risk, whereas the other polymorphisms cited above appear to modulate cardiovascular risk factor interrelationships. Methods: To explore the relation between these polymorphisms and insulin sensitivity (S i), healthy male Caucasian white subjects (n=78) underwent a metabolic assessment, including an iv. glucose tolerance test (IVGTT) for assessment of S i. Gene polymorphisms were identified using polymerase chain reaction (PCR) methodology. Results: Subjects with the ID genotype of the ACE gene polymorphism had the highest S i (ID v DD, p=0.020; ID v II, p=0.012; DD v II, ns), the lowest fasting insulin and IVGTT insulin and the lowest serum uric acid level (ID v DD, p<0.001; ID v II, p=0.002; DD v II, ns). ACE genotype emerged as a predictor of Si (F-ratio=4.73, p=0.012), independently of age and BMI (both ns, joint R 2=0.15). No consistent differences in any of the metabolic variables emerged with respect to the other gene polymorphisms. Conclusions: S i and serum urate are modulated by the by the I/D polymorphism of the ACE gene. This may be important in the CHD risk associated with this genotype.
Flanagan DE, Vaile JC, Petley GW, et al., 1999, The autonomic control of heart rate and insulin resistance in young adults, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, Vol: 84, Pages: 1263-1267, ISSN: 0021-972X
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- Citations: 50
Leyva F, Anker SD, Godsland IF, et al., 1998, Uric acid in chronic heart failure: A marker of chronic inflammation, EUROPEAN HEART JOURNAL, Vol: 19, Pages: 1814-1822, ISSN: 0195-668X
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- Citations: 225
Leyva F, Rauchhaus M, Proudler AJ, et al., 1998, Non-invasive assessment of vascular function: Paradoxical vascular response to intravenous glucose in coronary heart disease, CIRCULATION, Vol: 98, Pages: 848-848, ISSN: 0009-7322
Leyva F, Godsland IF, Worthington M, et al., 1998, Factors of the metabolic syndrome: Baseline interrelationships in the first follow-up cohort of the HDDRISC Study (HDDRISC-1) (vol 18, pg 208, 1998), ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 18, Pages: 1198-1198, ISSN: 1079-5642
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- Citations: 1
Godsland IF, Leyva F, Walton C, et al., 1998, Associations of smoking, alcohol and physical activity with risk factors for coronary heart disease and diabetes in the first follow-up cohort of the heart disease and diabetes risk indicators in a screened cohort study (HDDRISC-1), JOURNAL OF INTERNAL MEDICINE, Vol: 244, Pages: 33-41, ISSN: 0954-6820
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- Citations: 87
Leyva F, Godsland IF, Ghatei M, et al., 1998, Hyperleptinemia as a component of a metabolic syndrome of cardiovascular risk, ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 18, Pages: 928-933, ISSN: 1079-5642
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- Citations: 227
Leyva F, Wingrove CS, Godsland IF, et al., 1998, The glycolytic pathway to coronary heart disease: A hypothesis, METABOLISM-CLINICAL AND EXPERIMENTAL, Vol: 47, Pages: 657-662, ISSN: 0026-0495
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- Citations: 51
Crook D, Godsland I, 1998, Safety evaluation of modern oral contraceptives: Effects on lipoprotein and carbohydrate metabolism (vol 57, pg 189, 1998), CONTRACEPTION, Vol: 57, Pages: 420-420, ISSN: 0010-7824
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- Citations: 1
Leyva F, Rauchhaus M, Proudler AJ, et al., 1998, Non-invasive assessment of vascular function: Paradoxical vascular response to glucose in coronary heart disease, Heart, Vol: 79, ISSN: 1355-6037
Background: The vascular effects of insulin are nitric oxide-dependent, and independent of insulin's effect on glucose metabolism. Glucose, administered intravenously (iv.) as in the iv. glucose tolerance test (IVGTT), causes a physiological hyperinsulinaemia. We hypothesised that the this insulin response leads to forearm blood flow (FBF) changes in healthy individuals, and that such a response might be altered in patients with coronary heart disease (CHD). Methods: 10 healthy men and 13 men with angiographically proven CHD [aged 65.5±2.4 yrs, mean±SEM] underwent an IVGTT with simultaneous measurement of FBF (mercury-in-silastic venous occlusion plethysmography) at 28 time points over 3 hrs following iv. glucose administration. Results: In healthy controls, FBF increased to 31.7% above baseline at 7 mins and remained above baseline up to 180 mins after i.v. glucose. Significant group differences emerged in the % change in FBF from baseline at 180 mins (controls: +112.8±24.9%; CHD patients: -25.8±7.3%, p<0.001) and in he incremental areas under the FBF profiles (controls: +351.3±121.7; CHD patients: -244.3±72.4 min.ml/100ml, p<0.001). Conclusions: We have demonstrated for the first time that in healthy individuals, FBF increases after i.v. glucose, and that paradoxically this response is reduced in patients with CHD. Whilst the significance of the paradoxical FBF response observed in CHD requires further investigation, our findings provide the basis for a simple procedure for investigating endothelial function.
Leyva F, Godsland IF, Proudler AJ, et al., 1998, Hyperleptinaemia: A new component of the metabolic syndrome of cardiovascular risk, Heart, Vol: 79, ISSN: 1355-6037
Background: Production of leptin is linked to adiposity, insulin and insulin sensitivity. We therefore considered that alterations in plasma leptin concentrations could constitute an additional component of a metabolic syndrome of cardiovascular risk. Methods: Seventy four men [aged 48.4±1.3 years (mean±SEM), body mass index (BMI) 25.6±0.3 kg/m2 ], who were clinically free of coronary heart disease and diabetes, underwent anthropometric measurements (subscapular-to -triceps, S:T; - biceps, S:B), measurement of fasting plasma leptin, and an intravenous glucose tolerance test (IVGTT) for assessment of insulin sensitivity. Results: Plasma leptin concentrations correlated positively with BMI (r=0.57, p<0.001), S:T (r=0.34, p=0.003), S:B (r=0.37, p<0.001), systolic and diastolic blood pressure (both r=0.24, p=0.044), fasting triglycerides (0.31, p=0.007), serum uric acid (r=0.35, p=0.003), fasting glucose (r=0.32, p=0.003) and insulin (r=0.33, p=0.004), and IVGTT insulin (r=0.63, p<0.001), and negatively with insulin sensitivity (r=-0.32, p=0.006). In multivariate regression analyses, BMI (standardised coefficient, SC=0.40, p=0.001), fasting insulin (SC=0.23, p=0.036) and IVGTT insulin (SC=0.51, p<0.001) emerged as independent predictors of plasma leptin concentrations (R2=0.56, p<0.001). After adjustment for BM, only IVGTT insulin emerged as a significant predictor of plasma leptin concentrations (SC=0.56, p<0.001, R2= 0.45, p<0.001). Factor analysis revealed clustering of plasma leptin concentrations with a factor dominated by insulin resistance and high IVGTT insulin. Conclusion: Plasma leptin concentrations are strongly related to metabolic disturbances that precede coronary heart disease. Further studies are needed to determine whether the insulin-leptin axis plays a coordinating role in metabolic syndromes of cardiovascular risk.
Wingrove CS, Garr E, Godsland IF, et al., 1998, 17β-oestradiol enhances release of matrix metalloproteinase-2 from human vascular smooth muscle cells, BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE, Vol: 1406, Pages: 169-174, ISSN: 0925-4439
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- Citations: 141
Crook D, Godsland I, 1998, Safety evaluation of modern oral contraceptives -: <i>Effects on lipoprotein and carbohydrate metabolism</i>, CONTRACEPTION, Vol: 57, Pages: 189-201, ISSN: 0010-7824
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- Citations: 57
Leyva F, Godsland IF, Worthington M, et al., 1998, Factors of the metabolic syndrome - Baseline interrelationships in the first follow-up cohort of the HDDRISC study (HDDRISC-1), ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, Vol: 18, Pages: 208-214, ISSN: 1079-5642
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- Citations: 49
Leyva F, Godsland IF, Gathei M, et al., 1998, Hyperleptinemia as a component of a metabolic syndrome of cardiovascular risk, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 31, Pages: 197A-197A, ISSN: 0735-1097
Leyva F, Anker SD, Godsland IF, et al., 1998, Plasma leptin levels in chronic heart failure: Role of hyperinsulinemia and insulin resistance, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 31, Pages: 248A-249A, ISSN: 0735-1097
Leyva F, Godsland IF, Worthington M, et al., 1998, Erratum: Factors of the metabolic syndrome: Baseline interrelationships in the first follow-up cohort of the HDDRISC-1 study (HDDRISC-1) (Arteriosclerosis, Thrombosis and Vascular Biology (1998) 18 (208-214)), Arteriosclerosis, Thrombosis, and Vascular Biology, Vol: 18, ISSN: 1079-5642
Jovinge S, Hamsten A, Tornvall P, et al., 1998, Evidence for a role of tumor necrosis factor α in disturbances of triglyceride and glucose metabolism predisposing to coronary heart disease, METABOLISM-CLINICAL AND EXPERIMENTAL, Vol: 47, Pages: 113-118, ISSN: 0026-0495
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- Citations: 147
Godsland IF, Zoratti R, Chaturvedi N, et al., 1997, Lipid metabolism, insulin resistance, and body composition in Afro-Caribbean, South Asian and European-origin men, ATHEROSCLEROSIS, Vol: 135, Pages: 6-6, ISSN: 0021-9150
Anker SD, Leyva F, Godsland IF, et al., 1997, Skeletal muscle weakness is related to insulin resistance in patients with chronic heart failure, CIRCULATION, Vol: 96, Pages: 4227-4227, ISSN: 0009-7322
Spencer CP, Godsland IF, Stevenson JC, 1997, Is there a menopausal metabolic syndrome?, GYNECOLOGICAL ENDOCRINOLOGY, Vol: 11, Pages: 341-355, ISSN: 0951-3590
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- Citations: 109
Swan JW, Anker SD, Walton C, et al., 1997, Insulin resistance in chronic heart failure: Relation to severity and etiology of heart failure, JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, Vol: 30, Pages: 527-532, ISSN: 0735-1097
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- Citations: 425
Godsland IF, Bruce R, Walton C, et al., 1997, Insulin, HDL and coronary heart disease: 11.3 year evaluation of the first follow-up Cohort of the RISC study (RISC-1), Heart, Vol: 77, ISSN: 1355-6037
Hyperinsulinaemia has been identified as a predictor of CHD in some but not all prospective studies. High density lipoprotein (HDL) concentration is inversely related to hyperinsulinaemia, but the two have rarely been evaluated together as CHD predictors. The Risk Indicators in a Screened Cohort (RISC) Study has enabled further investigation of their relative importance. Methods: 728 male executives (age 26-70yr) initially free from vascular disease were followed for an average of 11.3 years. Metabolic (including oral glucose tolerance test glucose and insulin, and serum cholesterol and triglycerides), haematological, anthropometric and lifestyle variables were measured. HDL cholesterol was measured in 522 participants. 23 potential predictors of the development of CHD were considered. Significant predictors were identified by stepwise entry into the Cox model. Relative risks were estimated according to quintile cut-offs for each significant predictor. Results: 44 new cases of CHD were detected (31 in the subgroup with HDL measured). In the entire group the order of Cox model entry (HDL excluded) was high serum cholesterol (relative risk 4.2, 95% confidence interval 2.1-7.5), elevated mean arterial pressure (3.5, 1.6-5.8), current heavy cigarette smoking (2.8, 1.4-7.4), age in the range 49-54 years (3.1, 1.5-5.2), family history of heart disease (1.8, 0.9-3.4), and high erythrocyte sedimentation rate (1.9, 1.0-3.6). In the subgroup with HDL measurements, low HDL (2.7, 1.2-6.4) was an additional predictor and age was no longer significant. Neither fasting nor glucose tolerance test insulin emerged as significant. Conclusions: Hyperinsulinaemia was not a risk factor in this group of mainly social class 1 and 2 males, either in the presence or absence of HDL measurements. Future studies will need to consider insulin resistance, or groups with prevalent hyperinsulinaemia.
Godsland IF, Sidhu M, Crook D, et al., 1997, Coagulation and fibrinolytic factors, insulin resistance and the metabolic syndrome of coronary heart disease risk, Heart, Vol: 77, ISSN: 1355-6037
A number of independent risk factors for coronary heart disease (CHD) are now recognised to be part of a syndrome of metabolic disturbances centred on insulin resistance. However, links between this syndrome and the haemostatic system have only been explored in detail with regard to plasminogen activator inhibitor 1 (PAI-1). Methods: Fibrinogen, Factor VIIa, Factor X, protein C, protein S, antithrombin III, plasminogen, PAI-1, tissue plasminogen activator (tPA) and fibrinopeptide A were measured in 47 healthy males (aged 33-68 years, body mass index (BMI) 20.9-32.6 kg/m2). Insulin sensitivity (SI: inversely related to insulin resistance) was evaluated by mathematical modelling analysis of intravenous glucose tolerance test (IVGTT) glucose and insulin concentrations. Fasting serum lipids and lipoproteins were also measured. Results: Factor X was significantly associated with IVGTT insulin and C-peptide response (r=0.41, p=0.006 and r=0.32, p=0.04, respectively), SI (r=-0.38, p=0.02), BMI (r=0.41, p=0.006), systolic and diastolic blood pressures (r=0.35, p=0.02 and r=0.33, p=0.03, respectively), triglycerides (r=0.30, p=0.06) and HDL2 cholesterol (r=-0.32, p=0.04). Fibrinogen showed significant associations with IVGTT insulin and C-peptide response, SI, triglycerides and HDL2 cholesterol. Factor VII and PAI-1 were associated with IVGTT insulin response and SI. The association between PAI-1 and IVGTT insulin response was particularly strong (r=0.57. p<0.001) but PAI-1 was not related to any other measure. Conclusions: High Factor X and fibrinogen levels are strong candidates for inclusion in the metabolic syndrome. Factor VII and PAI-1 appear to be primarily related to insulin concentrations.
Leyva F, Anker SD, Chua TP, et al., 1997, Serum uric acid as a marker of impaired oxidative metabolism in chronic heart failure, Heart, Vol: 77, ISSN: 1355-6037
Elevated serum uric acid concentrations have been observed in clinical conditions associated with hypoxia. Since chronic heart failure (CHF) is a state of unpaired oxidative metabolism, we sought to determine whether serum uric acid concentrations relate to measures of functional capacity and disease severity. Methods: Patients with CHF (n=59) and healthy controls (n=20) underwent assessment of maximal oxygen consumption (MVO2) and regression slope relating to minute ventilation to carbon dioxide output (VE-VCO2) during a maximal treadmill exercise test. A metabolic assessment included measurement of serum uric acid and insulin sensitivity (obtained by minimal modelling analysis of glucose and insulin responses during an intravenous glucose tolerance test). Results: Compared to controls, patients with CHF had a 52% lower MVO2, 56.8% higher serum uric acid concentrations, and a 60.5% lower insulin sensitivity (all p<0.001). in the CHF group, serum uric acid correlated with exercise time (r=-0.53), MVO2 (r=-0.50) (both p<0.001), VE-VCO2 (r=0.45) and NYHA class (r=0.36) (both p<0.01). In multiple regression analysis, serum uric acid concentrations emerged as a significant predictor of MVO2, exercise time (both p<0.001), VE-VCO2 and NYHA class (both p<0.02), independently of diuretic dose, age, body mass index, serum creatinine, alcohol intake, plasma insulin levels, and insulin sensitivity. Conclusions: There is inverse relationship between serum uric acid concentrations and measures of functional capacity in patients with CHF. The strong inverse relationship between serum uric acid and MVO2 suggests that in CHF, serum uric acid concentrations can provide an index of an impairment of oxidative metabolism.
Leyva F, Anker S, Swan JW, et al., 1997, Serum uric acid as an index of impaired oxidative metabolism in chronic heart failure, EUROPEAN HEART JOURNAL, Vol: 18, Pages: 858-865, ISSN: 0195-668X
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- Citations: 257
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