Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.6.1.2 (alanine aminotransferase)
 26,722 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

While obesity has a high prevalence in developed countries, the routine abnormalities seen from the clinical biochemistry laboratory that may be caused by obesity related pathology do not seem to be as common. Insulin resistance, which is often associated with obesity, is difficult to assess as formal procedures are too complex for clinical practice. Furthermore the interpretation of insulin levels is hampered by their in vivo variability, assay differences and the lack of reference intervals from an unaffected reference population. Interpretation of fasting glucose levels between 5.5 and 6.0mmol/L are also being debated however, it is useful to understand the age related changes in this parameter, which may also be due to increasing obesity in the reference population. The association of obesity and dyslipidaemia in the metabolic syndrome should focus on elevated triglycerides (>1.5mmol/L), which is associated with low HDLC and correlates with atherogenic small dense LDL. High triglycerides are also predictive of fatty liver and the common abnormality of an elevated ALT may not be appreciated if laboratories allow their reference intervals to increase as the population gets more obese with aging. SHBG levels fall with insulin resistance/hyperinsulinaemia and this needs to be taken into account when testosterone is measured. However, low SHBG is showing huge potential as a disease and prognostic marker in obesity. These commonly available tests provide useful insights for the obese patient and their utility may improve with future research into the growing problem of obesity.
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PMID:The clinical biochemistry of obesity-more than skin deep. 1761 Nov 53

Biochemical traits such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), gamma glutamyltransferase (GGT) and uric acid are associated with obesity, and with risk of cardiovascular disease, metabolic syndrome and diabetes. Each is subject to genetic influences, but little is known about changes in genetic and environmental influences on these traits over time. We investigated the contribution of genetic and environmental influences to variation in these biochemical traits in adolescent twins and their nontwin siblings from 965 twin families. Twins were studied at ages 12, 14 and 16 years. Multivariate genetic models that included effects of age and sex were fitted to determine whether the same or different genetic or environmental factors influence each trait at different ages. Results showed that the genetic factors influencing AST, ALT, GGT and uric acid change over time during adolescence, and that the magnitude of these effects differs between males and females. The nonshared environment effects were generally time specific. There are developmental changes in genes affecting these traits during adolescence.
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PMID:A longitudinal genetic study of uric acid and liver enzymes in adolescent twins. 1790 17

Evidence suggesting an effect of fetal growth on liver development and function stems from both animal and human studies. The association of birthweight with adult markers of liver damage and function was examined in a random sample of 2101 British women aged 60-79 years. Age-adjusted natural logged levels of alanine aminotransferase (ALT) and gamma glutamyltransferase (GGT) decreased linearly across increasing thirds of birthweight. Alkaline phosphatase (ALP) levels were higher in women of the lowest third of the birthweight distribution compared with other women. No evidence was found for associations of birthweight with aspartate aminotransferase (AST), total bilirubin and albumin. After full adjustment for social class, physical activity, smoking and alcohol consumption, an increase in one standard deviation of birthweight (691 g) was associated with a 2% ([95% CI 0%, 4%], P = 0.021) decrease in the geometric mean of ALT, a 4% decrease in GGT ([95% CI 1%, 6%], P = 0.008) and a 2% decrease in ALP ([95% CI 0%, 3%], P = 0.001). Associations of birthweight with ALT and GGT, but not with ALP, were attenuated when adjusting for components of the metabolic syndrome. These findings suggest that factors affecting intrauterine growth may increase the propensity for adult liver damage. The attenuation of associations with adjustment for components of the metabolic syndrome is in line with non-alcoholic fatty liver disease, indicated by elevated ALT and GGT, being the hepatic manifestation of the metabolic syndrome, and of the influence of perinatal factors on this syndrome.
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PMID:The associations between birthweight and adult markers of liver damage and function. 1817 79

The present study was performed to determine the prevalence of metabolic syndrome (MS) and its risk factors in obese children and adolescents. The study included 352 obese children and adolescents (body mass index [BMI] > or = 95th percentile) aged between 2 and 19 years. The diagnosis of MS was made according to the criteria adapted from the World Health Organization (WHO) and the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) guidelines. BMI z-scores were calculated to assess the degree of obesity. The prevalence of MS and risk factors were determined. Determinants of MS were examined using regression analysis. The prevalence of MS was 41.8%. The age at onset of obesity, sedentary life-span, fasting blood levels of glucose, insulin, triglyceride, very-low-density lipoprotein (VLDL) cholesterol, and alanine aminotransferase (ALT) were higher, while levels of high-density lipoprotein (HDL) cholesterol and the number of actively spent hours were lower in cases with MS (p < 0.05). The most important determinant of MS was BMI z-score (r = 0.31, p < 0.0001). A one-point increase in BMI z-score yielded a 2-fold increase in the prevalence of MS. The prevalence of MS increased from 27.6% to 60.7% when the BMI z-score increased from 2.3 to 3.3. The risk of developing MS was 2.6-fold higher in cases with BMI z-score > 3 when compared to those with z-scores between 2 and 3. The results from this study indicate that, although the correlation between MS and the BMI z-score was weak, the BMI z-score may be an effective parameter in identifying obese children and adolescents at risk for MS. Screening the cases with BMI z-scores > or = 2 for MS is important for establishing an early diagnosis.
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PMID:Prevalence and risk factors of metabolic syndrome in obese children and adolescents: the role of the severity of obesity. 1820 11

1. The worldwide epidemic of obesity in adults has been mirrored in children in developed and developing countries. 2. Central obesity appears to be driving a cluster of abnormalities often referred to as the metabolic syndrome. 3. The definition of the metabolic syndrome in children is not suited to arbitrary cut-offs and a definition using the significant clustering of risk factors that is already evident in childhood and adolescent populations may be preferable. 4. An Australian population study showed that 25% of 8-year-olds and 29% of 14-year-olds could be described by the high risk cluster with features similar to adult metabolic syndrome. 5. The high risk cluster was significantly linked to high and low birthweight, shorter duration of breast-feeding, larger postnatal weight gains after 12 months of age and raised C-reactive protein, gamma glutamyl transferase and alanine transaminase levels. At-risk young adults have also been shown to have macroscopic atherosclerosis in post-mortem studies. 6. Identification of at-risk children has obvious benefits for the individual and as well, for prevention of a future cohort with raised cardiovascular morbidity and mortality; however, complexities and controversies exist in doing so. Familial, genetic and lifestyle risk factors aggregate and labelling children with predisease may be problematic. Committed political and societal changes are necessary to reduce childhood obesity and subsequent adult cardiovascular disease.
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PMID:Childhood obesity, hypertension, the metabolic syndrome and adult cardiovascular disease. 1830 30

The occurrence of liver disease and raised liver enzymes is common in Type 2 diabetes, and may be multifactorial in origin. Very few studies are available on the exact prevalence of the phenomenon, however. We carried out an observational point-prevalence study of elevated liver enzymes in eight hospital-based Italian diabetes units. Data of 9621 consecutive Type 2 diabetes patients (males, 52.4%; median age, 65 yr) were analyzed, and alanine and aspartate aminotransferase (ALT, AST) and gamma-glutamyltransferase (GGT) levels were related to body mass index (BMI), metabolic control and the presence of the metabolic syndrome. ALT, AST, and GGT levels exceeding the upper limit of normal were present in 16.0%, 8.8%, 23.1%, respectively, the prevalence being higher in males, increasing with obesity class and poor metabolic control, and decreasing with age. Elevated enzymes were systematically associated with most parameters of the metabolic syndrome. After correction for age, gender, BMI, and differences across centers, elevated triglyceride levels/fibrate treatment [odds ratio (OR), 1.57; 95% confidence interval (CI), 1.34- 1.84] and an enlarged waist circumference (OR, 1.47; 95% CI, 1.17-1.85) were the only parameters independently associated with high ALT. In a separate analysis, the presence of metabolic syndrome (Adult Treatment Panel III criteria) was highly predictive of raised liver enzymes. After exclusion of hepatitis B and C positive cases, tested in 2 centers, the prevalence of raised enzymes decreased by approximately 4%, but the association with the metabolic syndrome did not change significantly. In conclusion, the high prevalence of elevated liver enzymes in Type 2 diabetes is in keeping with the well-demonstrated risk of progressive liver disease. A large amount of diabetes patients may require a thorough clinical, laboratory and histological investigation.
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PMID:Prevalence of elevated liver enzymes in Type 2 diabetes mellitus and its association with the metabolic syndrome. 1836 6

Emerging scientific evidence suggests that increases in body iron represent a risk factor for the development of metabolic syndrome and diabetes. The aim of our study was to determine the body iron stores in patients with metabolic syndrome, and to evaluate the potential relationship of iron overload with specific features of the metabolic syndrome, such as fatty liver. A total of 490 individuals were enrolled. The diagnosis of metabolic syndrome was based on National Cholesterol Education Program-Adult Treatment Panel III (ATPIII) criteria. The metabolic syndrome group was consisted of 185 patients having three or more criteria, whereas individuals with less than three criteria constituted the control group. Metabolic syndrome patients displayed higher ferritin concentration as compared to control individuals. Ferritin levels were positively correlated with insulin concentration, as well as with Homeostasis Model Assessment (HOMA) index values. Multiple regression analysis revealed that ferritin was the most important independent determinant of insulin resistance indices. Patients with metabolic syndrome also exhibited increased concentrations of alanine aminotransferase and gamma-glutamyltranspeptidase compared to controls. Multiple regression analysis revealed that ferritin concentration was the most important determinant of gamma-glutamyltranspeptidase levels. Patients with the metabolic syndrome exhibit an increase in body iron stores as well as elevated concentrations of liver enzymes compared to the individuals who do not fulfill the criteria for the diagnosis of this syndrome. Our data support a direct role of increased body iron in the pathogenesis of insulin resistance, whereas iron overload may also contribute to the development of specific features of the metabolic syndrome, such as fatty liver.
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PMID:Increased serum ferritin concentrations and liver enzyme activities in patients with metabolic syndrome. 1837 Jul 38

Lipocalin-2 (also known as neutrophil gelatinase-associated lipocalin [NGAL]) has been described as a promising marker of metabolic syndrome associated with inflammation. The aim of our work was to develop an assay for the determination of lipocalin-2 in human serum and to investigate its levels in healthy volunteers and donors suffering from metabolic syndrome. We also conducted a pilot study on individuals with metabolic syndrome and on healthy probands and measured lipocalin-2 in these individuals. We developed and evaluated the sandwich ELISA method for the quantitative determination of human lipocalin-2 in serum samples. We measured blood pressure, waist circumference, serum cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, insulin, glucose, creatinine, hs-CRP, and adiponectin and calculated the BMI and Quicki insulin sensitivity index. In the study on 153 healthy volunteers, we showed that sex and age are not determinative for lipocalin-2 serum values. Furthermore, we tested 45 individuals with metabolic syndrome; values of lipocalin-2 did not differ (78.8 vs. 80.0 microg/l, p =0.56) from the data of healthy individuals from the first study. Neither group differed with regard to sex or age. Lipocalin-2 correlated with alanine aminotransferase (ALT) (r=-0.3, p<0.01) aspartate aminotransferase (AST) (r=-0.3, p<0.01), cholesterol (r=-0.21, p=0.047), creatinine (r=0.19, p=0.05), and high-sensitivity C-reactive protein (hs-CRP) (r=0.22, p=0.036). No significant correlation was found between serum lipocalin-2 and BMI, waist circumference, blood pressure, triglycerides, HDL, Quicki, or the number of metabolic syndrome components. When study patients with metabolic syndrome were further stratified according to the number of components of metabolic syndrome, serum concentrations of lipocalin-2 did not differ. The results presented demonstrate the analytical competence of the lipocalin-2 assay. However, we assumed that lipocalin-2 is not a routinely usable marker of metabolic syndrome or obesity. The association between serum lipocalin-2 and obesity or metabolic syndrome was not validated in our study.
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PMID:Lipocalin-2: development, analytical characterization, and clinical testing of a new ELISA. 1839 69

Non-alcoholic steatohepatitis (NASH) is a hepatic manifestation of the metabolic syndrome that can progress to liver cirrhosis. The major aim of this study was to establish a novel NASH mouse model accompanied by obesity and insulin resistance, then explore the molecular mechanisms of NASH and evaluate the effects of both the peroxisome proliferator-activated receptor alpha (PPARalpha) agonist fenofibrate and the PPARgamma agonist rosiglitazone in this established NASH model. The novel model was induced in C57BL/6 mice by 23 weeks of ad libitum feeding of a modified high-fat diet (mHFD), with lower methinione and choline and higher fat content. In comparison to the controls, the model animals developed pronounced obesity, dyslipidemia and insulin resistance. Marked liver lesions characterized by severe steatosis, inflammation, fibrosis, increased hepatic triglyceride content, and elevated serum alanine aminotransferase (ALT) levels were observed in the models. In this novel model, treatment with fenofibrate or rosiglitazone significantly improved insulin sensitivity and corrected dyslipidemia; however, fenofibrate was more effective than rosiglitazone in improving hepatic morphology and ALT levels. Further study showed that long-term feeding of mHFD significantly increased expression of mRNA for hepatic PPARgamma, adipose fatty acid binding protein (ap2) and CD36 and suppressed expression of mRNA for hepatic PPARalpha and carnitine palmitoyl transferase-1a (CPT-1a). These results showed the successful establishment of the combined NASH and obese-insulin resistance mouse model. Additionally, aberrant expressions of hepatic PPARalpha and PPARgamma may play a major role in the pathogenesis of NASH by affecting hepatic lipogenesis and fatty acid oxidation in this novel model.
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PMID:The establishment of a novel non-alcoholic steatohepatitis model accompanied with obesity and insulin resistance in mice. 1841 55

We studied the association between alanine aminotransferase (ALT) and features of the metabolic syndrome in a cohort of overweight and obese children aged 3-18 years. An oral glucose tolerance test was performed in 443 consecutive children from an obesity out-patient clinic (median age 11.2, range 3.1-18.0 years; n=240 boys) of multi-ethnic origin. The prevalence of the metabolic syndrome, insulin resistance, elevated ALT (>30 IU/L), and the association of ALT with (components of) the metabolic syndrome was assessed. The metabolic syndrome was present in 26.9%. Elevated ALT levels were found in 20.3%, with a higher prevalence in boys than in girls (25.8% versus 13.8%, P<0.001). ALT was associated with the prevalence of the metabolic syndrome, insulin resistance, high triglycerides, and low HDL-cholesterol after adjustment for gender, age, and BMI. In conclusion, elevated ALT levels were highly prevalent and associated with the metabolic syndrome, insulin resistance, high triglycerides, and low HDL-cholesterol in an obese multiethnic pediatric population.
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PMID:The association of elevated alanine aminotransferase and the metabolic syndrome in an overweight and obese pediatric population of multi-ethnic origin. 1869 12


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