Metabolic Markers (metabolic + marker)

Distribution by Scientific Domains


Selected Abstracts


Social experience organizes parallel networks in sensory and limbic forebrain

DEVELOPMENTAL NEUROBIOLOGY, Issue 3 2007
Eun-Jin Yang
Abstract Successful social behavior can directly influence an individual's reproductive success. Therefore, many organisms readily modify social behavior based on past experience. The neural changes induced by social experience, however, remain to be fully elucidated. We hypothesize that social modulation of neural systems not only occurs at the level of individual nuclei, but also of functional networks, and their relationships with behavior. We used the green anole lizard (Anolis carolinensis), which displays stereotyped, visually triggered social behaviors particularly suitable for comparisons of multiple functional networks in a social context, to test whether repeated aggressive interactions modify behavior and metabolic activity in limbic,hypothalamic and sensory forebrain regions, assessed by quantitative cytochrome oxidase (a slowly accumulating endogenous metabolic marker) histochemistry. We found that aggressive interactions potentiate aggressive behavior, induce changes in activities of individual nuclei, and organize context-specific functional neural networks. Surprisingly, this experiential effect is not only present in a limbic,hypothalamic network, but also extends to a sensory forebrain network directly relevant to the behavioral expression. Our results suggest that social experience modulates organisms' social behavior via modifying sensory and limbic neural systems in parallel both at the levels of individual regions and networks, potentially biasing perceptual as well as limbic processing. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source]


Auditory activation of ,visual' cortical areas in the blind mole rat (Spalax ehrenbergi)

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2002
Gilles Bronchti
Abstract The mole rat (Spalax ehrenbergi) is a subterranean rodent whose adaptations to its fossorial life include an extremely reduced peripheral visual system and an auditory system suited for the perception of vibratory stimuli. We have previously shown that in this blind rodent the dorsal lateral geniculate nucleus, the primary visual thalamic nucleus of sighted mammals, is activated by auditory stimuli. In this report we focus on the manifestation of this cross-modal compensation at the cortical level. Cyto- and myeloarchitectural analyses of the occipital area showed that despite the almost total blindness of the mole rat this area has retained the organization of a typical mammalian primary visual cortex. Application of the metabolic marker 2-deoxyglucose and electrophysiological recording of evoked field potentials and single-unit activity disclosed that a considerable part of this area is activated by auditory stimuli. Previous neuronal tracing studies had revealed the origin of the bulk of this auditory input to be the dorsal lateral geniculate nucleus which itself receives auditory input from the inferior colliculus. [source]


Vitamin K2 treatment for postmenopausal osteoporosis in Indonesia

JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH (ELECTRONIC), Issue 2 2006
Yuditiya Purwosunu
Abstract Aim: To investigate the effect of vitamin K2 (menatetrenone) treatment on bone mineral density (BMD) and a bone metabolic marker (osteocalcin) in postmenopausal women with osteoporosis living in Indonesia. Methods: A double-blind randomized placebo-controlled study of 63 postmenopausal women with osteoporosis. The vitamin K2 group (n = 33) received 45 mg menatetrenone and 1500 mg calcium carbonate per day and the control group (n = 30) received placebo and 1500 mg calcium carbonate per day for 48 weeks. BMD of lumbal spine (L2,L4), osteocalcin (OC) and undercarboxylated OC were measured before, 24 and 48 weeks after initiation of the treatment. Results: After 48 weeks of treatment, the mean percentage change of lumbar BMD in the vitamin K2 group was significantly higher (P < 0.05) than that of the control group. The undercarboxylated OC level decreased by 55.9% in the menatetrenone group and 9.3% in the control group compared with the baseline level. The difference between the two groups was significant (P < 0.01). The adverse events were three minor gastrointestinal cases, which subsided after temporary cessation of therapy. Conclusions: Treatment with 45 mg vitamin K2 with 1500 mg calcium per day for postmenopausal women with osteoporosis for 48 weeks resulted in a significant increase in lumbar BMD and a significant decrease in undercarboxylated OC levels. [source]


Characterization of oligodendrogliomas using short echo time 1H MR spectroscopic imaging

NMR IN BIOMEDICINE, Issue 1 2003
M. Rijpkema
Abstract Oligodendroglial tumors may not be distinguished easily from other brain tumors based on clinical presentation and magnetic resonance imaging (MRI) alone. Identification of these tumors however may have therapeutic consequences. The purpose of this study was to characterize and identify oligodendrogliomas by their metabolic profile as measured by 1H MR spectroscopic imaging (MRSI). Fifteen patients with oligodendroglial tumors (eight high-grade oligodendrogliomas, seven low-grade oligodendrogliomas) underwent MRI and short echo time 1H MRSI examinations. Five main metabolites found in brain MR spectra were quantified and expressed as ratios of tumor to contralateral white matter tissue. The level of lipids plus lactate was also assessed in the tumor. For comparison six patients with a low grade astrocytoma were also included in the study. The metabolic profile of oligodendrogliomas showed a decreased level of N -acetylaspartate and increased levels of choline-containing compounds and glutamine plus glutamate compared with white matter. The level of glutamine plus glutamate was significantly higher in low-grade oligodendrogliomas than in low-grade astrocytomas and may serve as a metabolic marker in diagnosis and treatment planning. In high-grade oligodendrogliomas large resonances of lipids plus lactate were observed in contrast to low-grade tumors. Copyright © 2003 John Wiley & Sons, Ltd. [source]


Serum metalloproteinase leukolysin (MMP-25/MT-6): a potential metabolic marker for atopy-associated inflammation

CLINICAL & EXPERIMENTAL ALLERGY, Issue 6 2010
M. N. Blumenthal
Summary Background Leukolysin is a novel matrix metalloproteinase (MMP-25/MT-6) released mainly by granulocytic cells, primarily neutrophils, which are implicated in chronic airways inflammation. Objective To determine if leukolysin might be a serum marker for atopic asthma or chronic obstructive pulmonary disease (COPD). Methods Three study populations were evaluated: (1) nuclear families with medical history of atopic asthma (N=337), (2) married-in individuals from an independent study of asthma genetics (N=122) and (3) randomly selected males with diagnosis of COPD (N=100). Each person was screened for asthma or COPD symptoms, respiratory function by standardized spirometry and serum total IgE and leukolysin and anti-IL1 levels by immunoassay. Study groups (1 and 2) were also screened by skin prick test using a battery of 14 common aeroallergens. Heritability estimates for leukolysin and total IgE were made by variance components analysis. Results For those without asthma or who had asthma defined as having symptoms, a physician's diagnosis and bronchial hyper-reactivity as demonstrated by reversibility in response to albuteral and/or bronchial reactivity as measured by a methacholine challenge, serum leukolysin levels were found to be higher for those with any positive skin test result. This paralleled trends for serum total IgE. In the nuclear families and COPD patients, serum leukolysin levels were significantly elevated for those who also had elevated total IgE levels (log[IgE]>2.0) compared with those with lower IgE (log[IgE]<2.0). Serum IL-1 levels correlated with the leukolycin levels. In contrast to IgE, leukolysin showed no apparent inherited component. Conclusion Among individuals with history of chronic airways inflammation (asthma and COPD) serum leukolysin may be a metabolic marker associated with chronic atopy-associated respiratory inflammation. Common factors may stimulate increased production or release of both leukolysin from myeloid cells and IgE from lymphoid cells. [source]


Characterizing the ADHD phenotype for genetic studies

DEVELOPMENTAL SCIENCE, Issue 2 2005
Jim Stevenson
The genetic study of ADHD has made considerable progress. Further developments in the field will be reliant in part on identifying the most appropriate phenotypes for genetic analysis. The use of both categorical and dimensional measures of symptoms related to ADHD has been productive. The use of multiple reporters is a valuable feature of the characterization of psychopathology in children. It is argued that the use of aggregated measures to characterize the ADHD phenotype, particularly to establish its pervasiveness, is desirable. The recognition of the multiple comorbidities of ADHD can help to isolate more specific genetic influences. In relation to both reading disability and conduct disorder there is evidence that genes may be involved in the comorbid condition that are different from pure ADHD. To date, progress with the investigation of endophenotypes for ADHD has been disappointing. It is suggested that extending such studies beyond cognitive underpinnings to include physiological and metabolic markers might facilitate progress. [source]


CLINICAL STUDY: A comparison of exposure to carcinogens among roll-your-own and factory-made cigarette smokers

ADDICTION BIOLOGY, Issue 3 2009
Lion Shahab
ABSTRACT Consumption of roll-your-own (RYO) tobacco is rising, but little is known about its in vivo delivery of toxins relative to factory-made (FM) cigarettes. To start to address this issue, this study compared the concentrations of metabolites of recognized human carcinogens in smokers of RYO tobacco and FM cigarettes. We opportunistically recruited 127 FM and 28 RYO cigarette smokers in central London and collected saliva and urine samples. Saliva samples were assayed for cotinine while urinary samples were assayed for 1-hydroxypyrene (1-HOP) and total 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL), metabolic markers of polycyclic aromatic hydrocarbons and tobacco-specific N -nitrosamines, respectively. Data on socio-demographic, anthropometric and puffing characteristics were also obtained. Both unadjusted and adjusted analyses (controlling for age, sex, body mass index, puff flow, puff duration and cotinine) showed no difference in metabolic markers between RYO and FM cigarette smokers. However, significant main effects for cotinine levels and sex were observed in adjusted analyses. Greater levels of cotinine were associated with a greater concentration of both 1-HOP (B = 0.002, P = 0.037) and NNAL (B = 0.002, P < 0.001). In addition, women had significantly greater concentrations of urinary 1-HOP (B = 0.679, P = 0.004) and total NNAL metabolites (B = 0.117, P = 0.024) than men, irrespective of the type of cigarettes smoked. More research is now needed to confirm these findings and gender-specific effects in a larger, representative sample. However, results do not support the common belief that RYO cigarettes are less harmful than manufactured cigarettes. [source]


High Oxidative Stress Is Correlated with Frailty in Elderly Chinese

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 9 2009
I-Chien Wu MD
OBJECTIVES: To evaluate the relationship between oxidative stress and frailty in elderly people. DESIGN: Cross-sectional study. SETTING: Community and hospital-based outpatient clinic. PARTICIPANTS: Ninety participants aged 65 and older. MEASUREMENTS: Frailty status was determined according to the presence of weak handgrip strength, weight loss, slow walking speed, exhaustion, and low activity level and was classified as frail (,3 criteria), prefrail (1 or 2 criteria), or robust (0 criteria). An oxidative stress marker (serum 8-hydroxy-2,-deoxyguanosine, 8-OHdG), metabolic markers (body mass index, waist,hip ratio, serum lipids, glucose, and albumin), an inflammatory marker (serum high-sensitivity C-reactive protein, hs-CRP), demographic information, and comorbidities (diabetes mellitus, hypertension, congestive heart failure, osteoarthritis, overweight or obesity, impaired fasting plasma glucose, renal insufficiency, and depression) were assessed. RESULTS: Of the 90 participants, 21 (23.3%) were frail, 56 (62.2%) were prefrail, and 13 (14.4%) were robust. Frail subjects had higher median (range) serum 8-OHdG (2.5 ng/mL (1.5,6.2 ng/mL) vs 2.3 ng/mL (0.5,8.1 ng/mL) and 1.0 ng/mL (0.5,5.3 ng/mL)) and serum hs-CRP (2.5 mg/L (0.3,32.1 mg/L) vs 1.8 mg/L (0.3,50.5 mg/L) and 1.7 mg/L (0.3,4.0 mg/L)) levels, lower mean±standard deviation serum albumin levels (4.1±0.4 g/dL vs 4.4±0.4 g/dL and 4.6±0.2 g/dL) and higher mean waist,hip ratios (0.96±0.11 vs 0.91±0.07 and 0.89±0.05)) than prefrail and robust subjects, respectively (P<.05 for all). In multivariable regression analysis, high serum 8-OHdG level was still significantly associated with frailty after adjusting for age, smoking status, comorbidities, waist,hip ratio, serum albumin level, and hs-CRP level. CONCLUSION: High oxidative stress, characterized by high serum 8-OHdG level, was independently associated with frailty in the selected sample of elderly Chinese. [source]


Metabolic Markers of Cobalamin Deficiency and Cognitive Function in Normal Older Adults

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 1 2004
Angeles A. Garcia MD, FRCPC
Objectives: To investigate the relationship between metabolic markers of cobalamin deficiency and cognitive function in normal older adults. Design: Cross-sectional study. Setting: Queen's University and St. Mary's of the Lake Hospital, Kingston, Ontario, Canada. Participants: Two hundred eighty-one cognitively normal, community-dwelling participants aged 65 and older. Measurements: Serum cobalamin, red blood cell folate, methylcitric acid, homocysteine, and methylmalonic acid were determined. Cognitive instruments included the California Verbal Learning Test, Mattis Dementia Rating Scale, and the Stroop Neuropsychological Screening Inventory (Stroop). Results: Serum levels of methylcitric acid had a significant negative correlation with recall, learning, and discriminability (factor 1) of the California Verbal Learning Test after adjusting for age and sex (,=,0.138, P=.019). Subjects with elevated methylcitric acid had significantly lower scores (factor 1) than subjects with normal methylcitric acid (P<.01). Bivariate analysis showed significant correlations between levels of homocysteine and the Stroop score and between cobalamin, methylmalonic acid, and homocysteine and some scores of the California Verbal Learning Test, but these relationships did not remain significant after multivariate analysis. Subjects with high homocysteine (tHcy) had lower Stroop scores than subjects with normal tHcy (P<.05). No biochemical parameters were associated with the Mattis Dementia Rating Scale scores. Conclusion: This study indicates that, in normal elderly subjects, some cognitive scores are related to serum methylcitric acid and possibly homocysteine. [source]


Positive Linear Growth and Bone Responses to Growth Hormone Treatment in Children With Types III and IV Osteogenesis Imperfecta: High Predictive Value of the Carboxyterminal Propeptide of Type I Procollagen,

JOURNAL OF BONE AND MINERAL RESEARCH, Issue 2 2003
Joan C Marini MD
Abstract Extreme short stature is a cardinal feature of severe osteogenesis imperfecta (OI), types III and IV. We conducted a treatment trial of growth hormone in children with OI and followed linear growth velocity, bone metabolism markers, histomorphometrics, and vertebral bone density. Twenty-six children with types III and IV OI, ages 4.5,12 years, were treated with recombinant growth hormone (rGH), 0.1,0.2 IU/kg per day for 6 days/week, for at least 1 year. Length, insulin-like growth factor (IGF-I), insulin-like growth factor binding protein (IGFBP-3), bone metabolic markers, and vertebral bone density by DXA were evaluated at 6-month intervals. An iliac crest biopsy was obtained at baseline and 12 months. Approximately one-half of the treated OI children sustained a 50% or more increase in linear growth over their baseline growth rate. Most responders (10 of 14) had moderate type IV OI. All participants had positive IGF-I, IGFBP-3, osteocalcin, and bone-specific alkaline phosphatase responses. Only the linear growth responders had a significant increase in vertebral DXA z-score and a significant decrease in long bone fractures. After 1 year of treatment, responders' iliac crest biopsy showed significant increases in cancellous bone volume, trabecular number, and bone formation rate. Responders were distinguished from nonresponders by higher baseline carboxyterminal propeptide (PICP) values (p < 0.05), suggesting they have an intrinsically higher capacity for collagen production. The results show that growth hormone can cause a sustained increase in the linear growth rate of children with OI, despite the abnormal collagen in their bone matrix. In the first year of treatment, growth responders achieve increased bone formation rate and density, and decreased fracture rates. The baseline plasma concentration of PICP was an excellent predictor of positive response. [source]


Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case,control study

JOURNAL OF CLINICAL PERIODONTOLOGY, Issue 11 2007
Luigi Nibali
Abstract Background and Aim: A cluster of metabolic factors defines a syndrome that predisposes to diabetes and cardiovascular disease. Chronic infections such as periodontitis might alter these individual metabolic factors and the systemic inflammatory burden. The aim of this study was to investigate the association between severe periodontitis and increase in inflammatory and metabolic risk factors for cardiovascular disease. Materials and Methods: We examined 302 patients with severe periodontitis and 183 healthy controls, and we collected a blood sample from each subject in order to investigate differences in inflammatory (leukocyte numbers and differential counts) and metabolic markers (lipids and glucose). Results: After correcting for differences in age, gender, smoking and ethnicity, periodontitis subjects exhibited a low-grade systemic inflammation (increased white cell counts, 1.10±1.02 × 109/l, 95%CI 1.05,1.15, p=0.0001), dyslipidemia [lower high-density lipoprotein cholesterol, 1.14±1.03 mmol/l, 95%CI 1.08,1.20, p<0.0001 and higher low-density lipoprotein cholesterol, 1.12±1.03, 95%CI 1.05,1.19, p<0.0001) and increased non-fasting serum glucose levels (1.04±1.01 mmol/l, 95%CI 1.02,1.06, p=0.01) when compared with controls. The associations were confirmed in a subpopulation of Caucasian non-smokers. A trend for a dose dependent effect of the number of periodontal pockets on the tested inflammatory and metabolic markers was observed. Conclusions: These data suggest a possible link between severe generalized periodontitis, systemic inflammation and a dysmetabolic state in otherwise healthy individuals. [source]


Chronic lithium administration attenuates up-regulated brain arachidonic acid metabolism in a rat model of neuroinflammation

JOURNAL OF NEUROCHEMISTRY, Issue 3 2007
Mireille Basselin
Abstract Neuroinflammation, caused by a 6-day intracerebroventricular infusion of lipopolysaccharide (LPS) in rats, is associated with the up-regulation of brain arachidonic acid (AA) metabolism markers. Because chronic LiCl down-regulates markers of brain AA metabolism, we hypothesized that it would attenuate increments of these markers in LPS-infused rats. Incorporation coefficients k* of AA from plasma into brain, and other brain AA metabolic markers, were measured in rats that had been fed a LiCl or control diet for 6 weeks, and subjected in the last 6 days on the diet to intracerebroventricular infusion of artificial CSF or of LPS. In rats on the control diet, LPS compared with CSF infusion increased k* significantly in 28 regions, whereas the LiCl diet prevented k* increments in 18 of these regions. LiCl in CSF infused rats increased k* in 14 regions, largely belonging to auditory and visual systems. Brain cytoplasmic phospholipase A2 activity, and prostaglandin E2 and thromboxane B2 concentrations, were increased significantly by LPS infusion in rats fed the control but not the LiCl diet. Chronic LiCl administration attenuates LPS-induced up-regulation of a number of brain AA metabolism markers. To the extent that this up-regulation has neuropathological consequences, lithium might be considered for treating human brain diseases accompanied by neuroinflammation. [source]


Weak and non-independent association between plasma TAFI antigen levels and the insulin resistance syndrome

JOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 4 2003
H. Aubert
Summary., Increased plasma thrombin-activatable fibrinolysis inhibitor (TAFI) levels were recently shown to be a part of the insulin resistance syndrome. We investigated the relationship between plasma TAFI antigen levels and insulin resistance markers and compared these results with those obtained for PAI-1 and fibrinogen which are known to be closely related to insulin resistance syndrome and fat mass, respectively. Eighty-nine obese females had 1.3-, 1.2-, and 3-fold higher circulating TAFI, fibrinogen and PAI-1, respectively, compared with 64 lean females. Univariate analysis showed that the significance level for association between TAFI or fibrinogen concentrations and insulin resistance markers was lower than the significance level for association between PAI-1 and insulin resistance markers. Nevertheless, TAFI, fibrinogen, and PAI-1 plasma levels were significantly associated to each other. In linear stepwise ascendant analysis, insulin resistance markers accounted for 50% of the interindividual variability of plasma PAI-1 and only for 10% of plasma TAFI and 13% of fibrinogen variability. The contribution of insulin resistance markers to plasma TAFI antigen levels variability disappeared when PAI-1 or fibrinogen was entered in the statistical model. TAFI mRNA was detected in the liver but not in adipose tissue and endothelial cells. No TAFI mRNA was detected in normal or atherosclerotic vessels either. These results suggest that elevated TAFI antigen levels found in obese subjects are not independently associated with the metabolic markers of the insulin resistance syndrome. Increased plasma TAFI antigen levels in obesity might reflect a specific pathway of regulation at the liver level. [source]


Prevalence of metabolic markers of insulin resistance in offspring of gestational diabetes pregnancies

PEDIATRIC DIABETES, Issue 1 2008
Erin J Keely
In utero hyperglycemia has been associated with insulin resistance (IR) in children; however, there are limited data in low-risk populations. The purpose of this study was to describe the prevalence of metabolic markers of IR in a primarily Caucasian cohort of gestational diabetes mellitus (GDM) offspring aged 7,11 yr (mean 9.1) and to correlate offspring with maternal indexes. Sixty-eight children were recruited through a follow-up study of women who participated in a randomized controlled trial of minimal intervention vs. tight glycemic control for GDM. All participants had a fasting plasma glucose (FPG), insulin, total cholesterol, high-density lipoprotein cholesterol (HDL-chol), triglyceride (TG) level, and a 2-h oral glucose tolerance test. We calculated homeostasis model assessment (HOMA) and recorded body mass index and waist circumference (WC). Criteria for metabolic syndrome for children included: FPG > 6.0 mmol/L, HDL-chol < 1.03 mmol/L, TG > 1.24 mmol/L, WC > 90% for age and gender, and 2-h glucose > 7.8 mmol/L. Among these children, 45 (66%), 17 (25%), 5 (7%), and 1 (1.5%) had zero, one, two, or three metabolic markers of IR, respectively. Hypertriglyceridemia (21%) was most prevalent, with no child having an elevated FPG. WC (p = 0.018) and TG (p = 0.005) were strong predictors of IR in the offspring after adjustment for age, gender, birthweight, family history, and maternal IR. Maternal and offspring HDL-chol, TG, WC, and HOMA but not fasting or 2-h glucose levels were significantly correlated. We conclude that metabolic markers of IR in children exposed to GDM may be present in the absence of abnormal fasting or 2-h glucose values. Screening strategies that focus on glucose levels may need to be reconsidered to institute early intervention with lifestyle changes for children at risk. [source]


cGMP-dependent cone photoreceptor degeneration in the cpfl1 mouse retina

THE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 17 2010
Dragana Trifunovi
Abstract Inherited retinal degeneration affecting both rod and cone photoreceptors constitutes one of the leading causes of blindness in the developed world. Such degeneration is at present untreatable, and the underlying neurodegenerative mechanisms are unknown, even though certain genetic causes have been established. The rd1 mouse is one of the best characterized animal models for rod photoreceptor degeneration, whereas the cpfl1 mouse is a recently discovered model for cone cell death. Because both animal models are affected by functionally similar mutations in the rod and cone phosphodiesterase 6 genes, respectively, we asked whether the mechanisms of photoreceptor degeneration in these two mouse lines share common pathways. In the present study, we followed the temporal progression of photoreceptor degeneration in the cpfl1 retina, correlated it with specific metabolic markers, and compared it with the wild-type and the rd1 situation. Similar to corresponding rd1 observations, cpfl1 cone photoreceptor cell death was associated with an accumulation of cyclic guanosine monophosphate (cGMP), activity of calpains, and phosphorylation of vasodilator-stimulated protein (VASP). Cone degeneration progressed rapidly, with a peak in cell death around postnatal day 24. Furthermore, cpfl1 cone photoreceptor migration during early postnatal development was delayed significantly compared with the corresponding wild-type retina. The finding that rod and cone photoreceptor degeneration was associated with the same metabolic markers suggests that in both cell types similar degenerative mechanisms are active. This raises the possibility that equivalent neuroprotective strategies may be used to prevent both rod and cone photoreceptor degeneration. J. Comp. Neurol. 518:3604,3617, 2010. © 2010 Wiley-Liss, Inc. [source]


Common Adiponectin Gene Variants Show Different Effects on Risk of Cardiovascular Disease and Type 2 Diabetes in European Subjects

ANNALS OF HUMAN GENETICS, Issue 4 2007
D. R. Gable
Summary Alterations in the secretion of adipokines may explain the link between obesity, type 2 diabetes (T2DM) and coronary artery disease (CAD). These conditions have been associated with variation in the adiponectin gene, although evidence for this relationship has been variable, with differences found even in similar samples. This study aims to clarify these inconsistencies by determining the impact of identified adiponectin gene (ADIPOQ) variants (,11391G>A,,1377C>G[promoter] and +45T>G[exon 2] and +276G>T[intron 2]) on the prospective risk of CAD and T2DM in healthy men, and on adverse metabolic markers, in myocardial infarct survivors and controls from different parts of Europe. The hazard ratio for cardiovascular disease varied across the ,11391GG/GA/AA(p = 0.03) and ,11371CC/CG/GG(p = 0.05) genotypes only. In contrast, only the +45T>G variant (3.80[1.76-8.24]) was associated with T2DM, while two haplotypes GCTT/GCGG (p < 0.05) and +276G>T(p = 0.01) increased risk in interaction with obesity. The variants were associated with a number of biomarkers in Southern but not Northern Europe (p = 0.01), despite no significant differences in allele or haplotype frequencies (p > 0.44). A risk haplotype could not be identified in either sample. Adiponectin gene variants are hence currently poor markers for the development of T2DM and CAD. Their influence on risk depends significantly on interactions that are not currently understood with either genetic variation elsewhere or the environment of the sample studied. [source]


Metabolic profiles of fat and glucose differ by gender in healthy 8-year-olds

ACTA PAEDIATRICA, Issue 1 2010
Susanne Eriksson
Abstract Objective:, The aim was to investigate if metabolic markers were associated with anthropometry and weight increase in healthy 8-year-olds. Methods:, Ninety-seven healthy children, 66 of whom had been examined at the age of 4 years, were investigated. Dual energy X-ray absorptiometry was performed to determine fat (FM) and lean body mass (LBM). Plasma glucose and serum levels of insulin, cholesterol, triglycerides, adiponectin and leptin were analysed and HOMA-indices were calculated. Results:, Despite similar anthropometry, metabolic markers differed by gender. Sixteen % of the children were overweight or obese. Body mass index (BMI) was strongly correlated to FM. Anthropometric measures except LBM correlated to metabolic markers in the girls. Boys had higher concentrations of plasma glucose than girls. In overweight children, insulin was negatively associated with LBM. Leptin and the ratio between leptin and adiponectin, but not adiponectin, were significantly associated with HOMA-IR and body composition. Conclusion:, The metabolic profile of plasma glucose, serum leptin, fasting insulin and related HOMA indices differed by gender, despite no difference in BMI or FM. LBM, but not FM correlated to the insulin concentration in the overweight children. Leptin was the best marker of overweight. [source]


Adiponectin levels are high in children with classic congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency

ACTA PAEDIATRICA, Issue 5 2009
Thomas MK Völkl
Abstract Objective: It has been shown that adiponectin serves as an insulin-sensitizing adipokine. Serum concentrations of adiponectin are low in children with obesity, and increase with fat mass loss, indicating that adiponectin can serve as a biomarker. Since the prevalence of overweight and obesity is increased in children with congenital adrenal hyperplasia (CAH), our study aimed to evaluate serum levels of adiponectin in a cohort of CAH children and adolescents, and their associations with clinical parameters such as chronological age (CA), body mass index (BMI), Tanner stage (TS), medication and metabolic control. Patients and methods: We studied 51 patients, aged between 5.6 and 19.6 years (median 11.8; 30 females, 21 males), cross-sectionally. All patients had genetically confirmed CAH and received standard steroid substitution therapy. Adiponectin was measured by an enzyme linked immunoassay. Since BMI SDS of the CAH cohort were significantly higher compared to the reference population, we built matched pairs with healthy Caucasian subjects from a normal representative cohort for sex, Tanner stage, chronologic age and BMI. Results: Adiponectin concentrations were significantly higher in CAH patients (median 11 ,g/L) compared to the matched controls (6.7 ,g/L, p < 0.0001). Correlation analyses in CAH patients revealed a significant inverse relationship between adiponectin and CA, TS, BMI, serum DHEAS and serum testosterone, but no correlation with hydrocortisone and fludrocortisone dosage. Conclusion: Currently, the importance of the elevated adiponectin concentrations in CAH children for risk assessment is not clear. However, our data imply that besides adequate metabolic control of glucocorticoid substitution, a long-term follow-up of other metabolic markers of insulin resistance should be conducted in CAH patients. [source]


Low-carbohydrate (low & high-fat) versus high-carbohydrate low-fat diets in the treatment of obesity in adolescents

ACTA PAEDIATRICA, Issue 2 2009
S Demol
Abstract Aim: To compare the impact of low-carbohydrate diets of different fat content to high-carbohydrate low-fat diet on weight and metabolic parameters in obese adolescents. Methods: Fifty-five patients aged 12,18 years with a body mass index (BMI) above the 95th percentile were randomly allocated to one of three isoenergetic diet regimens. Anthropometric and metabolic measurements were taken after overnight fast, at baseline, after the 12-week intervention and after nine month of follow-up. Results: No significant differences were found among the groups in changes in BMI, BMI-percentile, fat percentage, or metabolic markers at the end of the intervention and at the end of follow-up. Insulin level and homeostasis model assessment (HOMA) level decreased significantly at both time points only in the two low carbohydrate diet groups. Conclusion: All diet regimens are associated with a significant reduction in BMI and improvement of some metabolic parameters in obese adolescents. Low-carbohydrate diets apparently have no advantage over high-carbohydrate low-fat diets. The significant drop in insulin level and HOMA in the low carbohydrate diet groups is noteworthy given the increasing frequency of type-2 diabetes as part of metabolic syndrome in children and youth. The impact of low carbohydrate diets in obese and insulin-resistant youth warrants further investigation. [source]