bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the relationships between mineral metabolism, obesity and fat distribution
Authors: LIND L. , LITHELL H. , HVARFNER A. , POLLARE T. , LJUNGHALL S. 
Published: March 2008

Abstract. Alterations in calcium metabolism have been associated with cardiovascular risk factors. An altered binding of calcium to plasma proteins and raised levels of parathyroid hormone (PTH) have been described in morbid obesity. In the present study, indices of mineral metabolism were related to obesity (body mass index, BMI) and fat distribution (waist to hip ratio, w/h) in 194 subjects with a wide range of BMI and w/h. The ratio of total serum calcium to plasma ionized calcium (Ca2+) was found to be significantly correlated to both BMI (r = 0.20, P<0.02) and w/h (r = 0.22, P<0.005). Serum phosphate was also correlated to both of the indices of obesity in an inverse way (r= ‐0.24, P< 0.0008 for BMI and r= ‐0.33, P< 0.0001 for wl h). These relationships were still significant when the influences of age, sex and serum creatinine were included in the multiple regression analysis. This kind of analysis also disclosed that w/h was superior to BMI as a determinant of serum phosphate and the total calcium/Ca2+ ratio in serum. PTH was not significantly correlated to any of the indices of obesity.In conclusion, fat distribution rather than obesity per se was found to be associated with an altered mineral metabolism.
The platelet angiotensin II receptor in type I diabetes: studies in patients with and without nephropathy
Authors: MAKARIOUS M. , PAWLAK M. , CAMPBELL L. V. , TIMMERMANS V. , DUGGAN K. , CHARLESWORTH J. A. , MACDONALD G. J. 
Published: March 2008

Abstract. Experimental studies demonstrate impaired regulation of the mesangial angiotensin II (AII) receptor in diabetes. This could contribute to the disturbance of glomerular blood flow and the development of diabetic nephropathy. The aim of this study was to determine whether a similar receptor abnormality occurs in patients with type I insulin‐dependent diabetes mellitus (IDDM) and if so whether this is more prevalent in patients with micro‐ or macro‐albumi‐nuria. The platelet AII receptor was chosen because of its availability from the circulation and its comparable regulatory properties to tissue‐based receptors. The interaction between plasma All and its platelet receptor was examined in 45 patients with TDDM and 36 age‐ and sex‐matched control subjects. Seven patients had clinical nephropathy and two had persistent micro‐albuminuria. The duration of diabetes varied from 1 month to 42 years.There was a significant inverse correlation between plasma AIT and the logarithm of receptor number in the control group (r= ‐0.555, P <0.001). This relationship was not observed in the diabetic patients irrespective of the duration of disease or the presence of nephropathy. Receptor expression in patients without nephropathy showed no correlation with either duration of disease or the degree of glycaemic control. However, a significant relationship between AII receptor number and duration of diabetes was noted in the group with nephropathy (r = 0.723, P <0.05). Patients without nephropathy had a significantly lower receptor number than control subjects (i.e. 3.9 ± 0.4 and 5.1±0.7 sites per cell respectively; P = 0.02), while comparable values to controls were observed in patients with renal disease (5.7 ±1.2 sites per cell). Plasma renin and AII levels for both groups of patients were comparable to those observed in the control subjects.If these findings are representative of tissue‐based AII receptors, then the loss of ligand/receptor relationship in the presence of higher receptor expression in patients with nephropathy could provide an explanation for the glomerular haemodynamic abnormalities observed in human diabetes.
Heterozygous apolipoprotein C‐II deficiency: lipoprotein and apoprotein phenotype and Rsal restriction enzyme polymorphism in the Apo C'IIPadova kindred
Authors: GABELLI C. , BILATO C. , SANTAMARINA‐FOJO S. , MARTINI S. , JR H. B. BREWER , CREPALDI G. , BAGGIO G. 
Published: March 2008

Abstract. Deficiency of apolipoprotein C‐II (apo C‐II), the cofactor for lipoprotein lipase, results in the familial chylomicronaemia syndrome characterized by severe hypertriglyceridaemia and fasting chylomicronaemia. To investigate the biochemical features of the heterozygous state for apo C‐II deficiency, we characterized the lipid, lipoprotein and apolipoprotein profiles in 18 relatives of two affected individuals (brother and sister) homozygous for the apo C‐IIPadova gene defect which results in the synthesis of a truncated 36 amino acid apolipoprotein. Carrier status was established in first degree relatives as well as in seven non‐obligate heterozygotes by restriction enzyme analysis of amplified apo C‐II genomic DNA using RsaI.No significant differences in lipid, lipoprotein and apo C‐II levels were observed in heterozygotes when compared to unaffected family members. Thus, in this study, the carrier state was not associated with hypertriglyceridaemia or reduced plasma levels of apo C‐II.However, analysis of amplified DNA from members of the apo C‐IIPsdova kindred by digestion with the enzyme RsaI, which identifies the mutant apo C‐II, permitted the identification of heterozygous family members which could not be recognized by measuring either fasting triglycerides or plasma apo C‐II levels.This study provides further evidence that apo C‐II deficiency syndrome is a heterogeneous disease not only at the molecular level but also on the clinical ground with variable phenotypic expression in heterozygous individuals from different kindreds.
The influence of pretransplant lipoprotein abnormalities on the early results of renal transplantation
Authors: DIMÉNY E. , TUFVESON G. , LITHELL H. , LARSSON E. , SIEGBAHN A. , FELLSTRÖM B. 
Published: March 2008

Abstract. Lipoprotein patterns were investigated before and after renal transplantation in a prospective study including 151 patients. Kidney graft losses during the first 6 months were associated with higher total cholesterol (P= 0.03), LDL cholesterol (P= 0.003) and LDL triglyceride levels (P= 0.01) before transplantation. Patients with serum cholesterol ±6.9 mmol l‐1 before transplantation had more acute rejections (1.7 vs. 0.9), a worse graft function and more vascular intimal hyperplasia and glomerular mesangial changes in transplant biopsies at 6 months. Patients with serum creatinine levels exceeding 160 μmol l‐1 at 6 months had more severe lipid disorders already before transplantation.Serum creatinine at 6 months was influenced by the number of acute rejection episodes (P= 0.0001) and the age of the donor (P= 0.009) while the number of acute rejections was found to be related to pretrans plant total cholesterol levels (P= 0.0086) and the age of the recipient (P = 0.025).In conclusion, pretransplant lipoprotein disturbances have an impact on the early outcome of renal transplantation. Since there is a progresssion of hyperlipidaemia following transplantation, this may have an influence also on the cardiovascular morbidity and late graft dysfunction.
The impact of intermittent claudication on quality of life evaluated by the Sickness Impact Profile technique
Authors: ARFVIDSSON B. , KARLSSON J. , DAHLLÖF A.‐G. , LUNDHOLM K. , SULLIVAN M. 
Published: March 2008

Abstract. Unselected patients suffering from intermittent claudication (n= 148) were invited to take part in a prospective study. Physical examination and several circulatory investigations were performed including a treadmill walking test, bicycle ergometry and a quality of life examination (Sickness Impact Profile, SIP, technique). The SIP has been reported to be sensitive enough to identify specific dysfunction profiles in several clinical conditions, but it has not been used on patients with intermittent claudication. The aim of this study was to determine to what extent quality of life was influenced by reduced walking ability in patients with intermittent claudication. If so, the SIP technique should then be a useful tool for determination of the degree of reduced exercise capacity in patients who may benefit from surgery instead of conservative treatment. A majority of the SIP categories, Sleep and rest, Emotional behaviour, Body care and movement, Home management, Mobility, Social interaction, Ambulation and Overall SIP were shown to be useful in confirming objective dysfunctions in our patients. The correlation between maximum walking ability and SIP scores indicated an approximate cut‐off limit at 70 W walking capacity. Thus, significant reductions in everyday life function were demonstrated in patients with maximum walking ability below 70 W. Patients with intermittent claudication also suffered from several other dysfunctions in addition to walking disability. These factors may, as well, impact on quality of life without walking disability.Our results demonstrated that quality of life assessment by the SIP technique was a sensitive method for evaluation of overall dysfunction in patients with intermittent claudication. A comparison with a previous reference material from a general population showed that patients performing more than 70 W had only marginal dysfunctions in their everyday life. It may therefore be low cost‐effective to treat such patients particularly with surgery or angioplasty.
Human intestinal alkaline phosphatase—release to the blood is linked to lipid absorption, but removal from the blood is not linked to lipoprotein clearance
Authors: DOMAR U. , KARPE F. , HAMSTEN A. , STIGBRAND T. , OLIVECRONA T. 
Published: March 2008

Abstract. To evaluate a possible quantitative relationship between the rise in intestinal alkaline phosphatase (IAP) activity and triglyceride‐rich lipoproteins in the blood after an oral fat intake, a specific and sensitive immunocatalytic assay was used. First, day to day variation of the basal IAP activity in the blood of eight volunteers was evaluated. One group of subjects with high basal IAP activity and great variations from one day to the other was distinguished from a group with low basal IAP activity and small day to day variations. The subjects with high basal IAP activities were all secretors of red blood cell antigens, while those with low basal IAP activities were non‐secretors. The IAP activity in the blood rose after fat rich meals but not after fat free meals. To further investigate this, IAP activities were measured in the blood of 28 men before 3, 6, 9 and 12 h after a standardized oral fat load of a mixed meal type. The activity rose in all individuals and showed a similar time course as the rise in plasma TG concentration. The elevations of the IAP activity were, however, not quantitatively correlated with the elevations in TG concentration, nor were there any relations in time to peak levels. Subjects with high basal IAP increased their IAP activity more than those with low basal IAP, but within neither group there was any correlation between the basal IAP activity and the rise in IAP activity. IAP did not float with lipoproteins on ultracentrifugation of plasma, nor did IAP bind to lipid droplets from a fat emulsion added to plasma.It is concluded that transport of IAP from mucosal cells to the blood is greatly stimulated by fat absorption, but in the blood IAP was not bound to lipoproteins and no quantitative relationship between the rise in IAP activity and TG concentration was found. Therefore we suggest that the metabolism of TAP in the blood is not determined by intravascular lipoprotein metabolism, but by other factors, e.g. its glycosylation pattern.
Influence of platelet size before coronary angioplasty on subsequent restenosis
Authors: SMYTH D. W. , MARTIN J. F. , MICHALIS L. , BUCKNALL C. A. , JEWITT D. E. 
Published: March 2008

Abstract. Platelet size has been shown to reflect platelet activity. We prospectively measured the mean platelet volume (MPV) in 47 patients undergoing single vessel angioplasty for symptomatic angina. The patients underwent repeat angiography 4–8 months later irrespective of symptomatic status. Restenosis was assessed quantitatively by hand held calliper measurements of the lesion and qualitatively by a return of angina, ST segment changes on an exercise test and visual analysis of the lesion severity by two experienced angiogra‐phers. Twenty‐four patients developed recurrent angina during the follow‐up period, the MPV in the group with chest pain was 8.54 ± 0.60 fl compared to 8.1±0.69 fl in the asymptomatic group (P = 0.04). Twenty two patients had significant ST segment changes at exercise. In this group the MPV was 8.6 ± 0.56 fl compared to 8.0 ±0.70 fl for the group with a negative test (P = 0.002). Similarly visually assessed angiographic stenosis showed a significant increase in the restenotic group (8.6 ± 0.56 vs. 8.0 ± 0.61 fl, P=0.001). The relative odds for developing clinically defined restenosis were 10.2 times greater if the pre‐procedural MPV lay in the upper compared to the lowest quartile.There was a positive correlation between MPV and change in minimal luminal diameter between post angioplasty and follow‐up angiography, assessed quantitatively, r=+0.56, P = 0.016. There was no association between clinical or angiographic definitions of restenosis and haemoglobin, red cell count, mean corpuscular volume, white cell count or platelet count. Platelet size may influence the development of restenosis after succeesful coronary angioplasty.
Acute dexfenfluramine administration normalizes glucose tolerance in rats with insulin‐deficient diabetes
Authors: ARORA R. , DRYDEN S. , McKIBBIN P. E. , WILLIAMS G. 
Published: March 2008

Abstract. Dexfenfluramine has been shown to lower blood glucose concentrations independently of its effects in reducing food intake and body weight, in human and animal syndromes of non‐insulin dependent diabetes. This study aimed to determine whether dexfenfluramine could also reduce glycaemia in rats with severe insulin‐deficient diabetes induced by the β‐cell toxin, streptozotocin (55 mg kg‐1). Three weeks after diabetes induction, nine groups (each n= 10) of diabetic and non‐diabetic rats underwent oral glucose tolerance tests (1 g kg‐1, by gavage). These tests were preceded by 12–18 h of fasting to remove the confounding effects of hyperphagia in diabetic rats, and to stabilize glycaemia.Dexfenfluramine (1·0 mg kg‐1), given 2 h before the glucose challenge, significantly reduced basal glycaemia and decreased the post‐challenge glycaemic rise (P<0·01 vs. untreated diabetics). Dexfenfluramine dosages of 2·5 and 5·0 mg kg‐1 both further flattened the post‐challenge glycaemic profiles (both P<0·01 vs. untreated diabetics) and achieved levels that did not differ significantly from those in non‐diabetics (both P> 0·05). Subsequently, the studies using dexfenfluramine dosages of 2·5 and 5·0 mg kg‐1 were repeated to determine whether the drug affected plasma insulin levels 2 h after dosing. In diabetic rats, plasma insulin concentrations were reduced to 10–20% of non‐diabetic values, and were not significantly altered by dexfenfluramine.Acute dexfenfluramine administration therefore improves and (at dosages of 2·5 and 5·0 mg kg‐1) essentially normalizes glucose tolerance in rats with severe insulin‐deficient diabetes. As circulating insulin concentrations were not increased, dexfenfluramine probably acts by enhancing and/or mimicking insulin action. The magnitude of this effect suggests that dexfenfluramine could find application as adjunctive treatment in the management of human insulin‐dependent diabetic patients with insulin insensitivity, such as that associated with obesity.
Effect of adiposity on plasma lipid transfer protein activities: a possible link between insulin resistance and high density lipoprotein metabolism
Authors: DULLAART R. P. F. , SLUITER W. J. , DIKKESCHEI L. D. , HOOGENBERG K. , TOL A. VAN 
Published: March 2008

Abstract. The mechanisms responsible for the decreased high density lipoprotein (HDL) cholesterol levels associated with obesity and insulin resistance are not well understood. Lecithin: cholesterol acyltransferase (LCAT) and cholesterol ester transfer protein (CETP) are key factors in the esterification of cholesterol in HDL and the subsequent transfer of cholesteryl ester towards apolipoprotein B‐containing lipoproteins. Phospholipid transfer protein (PLTP) may be involved in the regulation of HDL particle size. We therefore measured the activities of LCAT, CETP and PLTP using exogenous substrate assays, as well as lipids, lipoproteins, insulin and C‐peptide in fasting plasma from eight healthy obese men (body mass index >27 kg m‐2) and 24 non‐obese subjects. The obese men had lower levels of HDL cholesterol (P<0·05) and higher levels of plasma triglycerides (P<0·05), insulin (P<0·05) and C‐peptide (P<0·01), as compared to the quartile of subjects with the lowest body mass index (BMI <22·4 kg m‐2). CETP and PLTP activities were elevated in the obese men by 35% (P<0·01) and by 15% (P<0·05), respectively. LCAT activity was comparable among the quartiles. Linear regression analysis showed that CETP activity was positively correlated with body mass index (P<0·02), fasting blood glucose (P7lt;0·05) and plasma C‐peptide (P<0·05). PLTP activity was positively related to body mass index (P<0·01), waist to hip circumference ratio (P<0·001), as well as to fasting blood glucose (P<0·05) and plasma C‐peptide (P<0·05)It is concluded that the activities of CETP and PLTP are influenced by adiposity and possibly by insulin resistance. Elevated lipid transfer protein activities may provide a mechanism that contributes to alterations in HDL in insulin resistant states.
Systemic interleukin‐1 α and interleukin‐2 secretion in response to acute stress and to corticotropin‐releasing hormone in humans*
Authors: SCHULTE H. M. , BAMBERGER C. M. , ELSEN H. , HERRMANN G. , BAMBERGER A. M. , BARTH J. 
Published: March 2008

Abstract Acute stress results in activation of the hypothalamic‐pituitary‐adrenal (HPA) axis. ACTH and cortisol secretion is stimulated by corticotropin‐releasing hormone (CRH). It has also been shown that activation of the HPA axis during stress is accompanied by changes in the immune response. However, little is known about the influence of acute stress on the release of cytokines such as inteleukin‐1 (IL‐1) or interleukin‐2 (IL‐2). In this study, we determined serum IL‐1 α and IL‐2 levels in 19 patients undergoing the acute stress of angioplasty for coronary artery disease. A second protocol was devised to determine serum IL‐1 α and IL‐2 concentrations as well as lymphocyte subpopulations in 10 normal volunteers receiving 1 μ kg‐1 human CRH intravenously. Finally, IL‐1 α concentrations were measured in CRH‐incubated mononuclear cell (MNC) and monocyte cultures.In response to the stress of angioplasty, ACTH and cortisol as well as IL‐1 α and IL‐2 concentrations were clearly above baseline levels (IL‐1 α, mean ± SEM, baseline: 1·39 ± 0·34 ng ml‐1, after angioplasty: 2·64 ± 0·73 ng ml‐1, P < 0·05; IL‐2, baseline: 1·2 ± 0·13 ng ml‐1, after angioplasty: 2·8 ± 1·14 ng ml, P < 0·05). A similar pattern was obtained in normal subjects in response to CRH (IL‐1 α, baseline: 0·8 ± 0·2 ng ml‐1, after angioplasty: 3·7 ± 1·4 ng ml‐1, P < 0·05; IL‐2, baseline: 1·9 ± 0·4 ng ml‐1, after angioplasty: 5·4 ± 2·2 ng ml‐1, P < 0·02). The percentage of IL‐2 receptor‐positive lymphocytes rose from 3·9 ± 1·2% to 6·2 ± 1·6% (P < 0·05), the relative number of CD‐3 lymphocytes rose from 74·5 ± 1·6% to 78·3 ± 2·0% (P < 0·05). No significant changes were observed in the number of CD‐4, CD‐8, natural killer and B cells. In vitro, IL‐1 α concentrations in cultures containing CRH were not significantly different from control cultures. Our data demonstrate significant activation of the HPA axis and secretion of IL‐1 α and IL‐2 in response to both angioplasty and CRH. Furthermore, CRH administration resulted in activation of the cellular immune system (indicated by an increase in IL‐2 receptor positive lymphocytes). Our in vitro data suggest that CRH may not directly act on blood mononuclear cells to induce IL‐1 α release or, alternatively, sources other than blood mononuclear cells may account for the elevated IL‐1 α levels observed in vivo. We conclude that CRH may play a major role in neuroendocrine‐immune interactions during acute stress.
Dietary supplementation with very long‐chain n‐3 fatty acids in man decreases expression of the interleukin‐2 receptor (CD25) on mitogen‐stimulated lymphocytes from patients with inflammatory skin diseases
Authors: SØYLAND E. , LEA T. , SANDSTAD B. , DREVON A. 
Published: March 2008

Abstract T‐cell activation and cytokine production play an important role in several chronic inflammatory diseases. Because n‐3 fatty acids exert beneficial effects on the clinical state of some of these diseases, we examined the effect of dietary supplementation of n‐3 fatty acids on T‐cell proliferation, expression of CD25 (interleukin‐2 receptor alpha‐chain), secretion of interleukin‐2, interleukin‐6 and tumour necrosis factor from T‐cells from patients with psoriasis and atopic dermatitis.During 4 months, 21 patients supplied 6 g of highly concentrated ethyl esters of EPA and DHA in gelatin capsules daily to their diet. In the control group 20 patients supplied 6 g per day of corn oil in gelatin capsules to their diet.Eicosapentaenoic acid (20:5, n‐3) of serum phospholipids increased from 14 (min 4‐max 42) to 81 (min 59‐max 144) mg l‐1 (P < 0·01) in patients with atopic dermatitis receiving n‐3 fatty acids, and from 25 (min 7‐max 66) to 74 (min 46‐max 142) mg l‐1 (P < 0·01) in patients with psoriasis, whereas docosahexaenoic acid (22:6, n‐3) increased from 65 (min 46‐max 120) to 92 (min 54‐max 121) mg l‐1 (P < 0·05) and from 81 (min 38‐max 122) to 92 (min 63‐max 169) mg l‐1 (NS) in atopic and psoriatic patients, respectively. The changes in the serum phospholipid fatty acid profile in the groups receiving n‐3 fatty acids, correlate to the dietary intake of corresponding fatty acids. There was no significant change in the fatty acid pattern of serum phospholipids in the corn oil group before and after supplementation.Mitogen‐induced secretion of interleukin‐6 was significantly higher in patients with psoriasis compared to patients with atopic dermatitis, whereas the secretion of interleukin‐2, tumour necrosis factor, PHA‐induced T‐cell proliferation and expression of CD25 on lymphocytes were similar in the two groups of patients.Patients receiving supplementation of n‐3 fatty acids decreased significantly the percentage of CD25 positive lymphocytes from 40·5 before start to 35·5 (P < 0·05) after the trial. The patients who received corn oil increased the level of tumour necrosis factor from 1095 pg ml‐1 before start to 1536 pg ml‐1 after the trial (P < 0·05). In conclusion, dietary intake of very long‐chain n‐3 fatty acids may suppress the expression of CD25 positive lymphocytes, which may partly account for the anti‐inflammatory effect exerted by these fatty acids.