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ObjectiveThe prevalence of obesity increases with age and is higher in each younger generation (unfavorable generation shift). This may influence patterns of oxidative stress and inflammation. Age-related changes and generation shifts in markers of oxidative stress and inflammation were investigated, specifically addressing the role of body mass index (BMI).MethodsFour generations (aged 26-35, 36-45, 46-55, and 56-65 at baseline) (N = 5,155) were examined every 5 years for 15 years between 1993 and 2012. Random coefficient analyses were used to study age-related changes and generation shifts in BMI, -glutamyltransferase (GGT), uric acid (UA), and C-reactive protein (CRP).ResultsLevels of BMI, UA, and CRP increased in all generations up to age 75, whereas GGT increased up to age 55. No consistent generation shifts were observed for GGT, UA, and CRP (P 0.05). Participants with a stable BMI (change 1 kg/m(2)/15 years) had either no or small increases with age in GGT, UA, and CRP, whereas participants with increasing BMI (increase >1 kg/m(2)/15 years) had much larger increases (P ConclusionsThe unfavorable age-related changes in obesity-related biochemical markers, particularly among individuals with increasing BMI, show the importance of maintaining a healthy weight to improve population levels of oxidative stress and inflammation.

[Aim]: Our aim is to demonstrate that a healthy diet might reduce the relation between adiposity and inflammation, whereas an unhealthy diet may increase the effect of adiposity on inflammatory biomarkers., [Methods]: In 618 adolescents (13–17 years) of the European HELENA study, data were available on body composition, a set of inflammation markers, and food intake determined by a self-administered computerized 24-h recall. A 9-point Mediterranean diet score and an antioxidant-rich diet score were used as dietary parameters and tested as moderator. Total body fat was represented by the sum of six skinfold thicknesses and central adiposity by waist circumference. A set of inflammation-related biomarkers was used as outcome: a pro/anti-inflammatory interleukins ratio, TGFβ-1, C-reactive protein, TNF-α, 3 cell adhesion molecules, and 3 types of immune cells; gamma-glutamyltransferase (GGT) and homocysteine were used as cardiovascular disease risk biomarkers, and alanine transaminase (ALT) as liver dysfunction biomarker. Multiple linear regression analyses tested moderation by diet in the adiposity-inflammation association and were adjusted for age, sex, country, puberty, socioeconomic status., [Results]: Both the Mediterranean and antioxidant-rich diet, and overall and central adiposity, were important in the moderation. Diet was a significant protective moderator in the effect of adiposity on the pro/anti-inflammatory interleukins ratio, TGFβ-1, GGT, and ALT., [Conclusion]: In conclusion, in some cases, a diet rich in antioxidants and essential nutrients may attenuate the concentration of inflammatory biomarkers caused by adiposity, whereas a poor diet appears to contribute to the onset of early oxidative stress signs., The HELENA Study was carried out with the financial support of the European Community Sixth RTD Framework Programme (Contract FOODCT-2005-007034).

Background Moderate alcohol consumption has been associated with a lower risk of cardiovascular disease (CVD) and all‐cause mortality compared with heavy drinkers and abstainers. To date, studies have relied on self‐reported consumption, which may be prone to misclassification. Urinary ethyl glucuronide (EtG) is an alcohol metabolite and validated biomarker for recent alcohol consumption. We aimed to examine and compare the associations of self‐reported alcohol consumption and EtG with CVD and all‐cause mortality. Methods and Results In 5676 participants of the PREVEND (Prevention of Renal and Vascular End‐Stage Disease) study cohort, EtG was measured in 24‐hour urine samples and alcohol consumption questionnaires were administered. Participants were followed up for occurrence of first CVD and all‐cause mortality. Cox proportional hazards regression models, adjusted for age, sex, and CVD risk factors, were fitted for self‐reported consumption, divided into 5 categories: abstention, 1 to 4 units/month (reference), 2 to 7 units/week, 1 to 3 units/day, and ≥4 units/day. Similar models were fitted for EtG, analyzed as both continuous and categorical variables. Follow‐up times differed for CVD (8 years; 385 CVD events) and all‐cause mortality (14 years; 724 deaths). For both self‐reported alcohol consumption and EtG, nonsignificant trends were found toward J‐shaped associations between alcohol consumption and CVD, with higher risk in the lowest (hazard ratio for abstention versus 1–4 units/month, 1.42; 95% CI, 1.02–1.98) and highest drinking categories (hazard ratio for ≥4 units/day versus 1–4 units/month, 1.11; 95% CI, 0.68–1.84). Neither self‐report nor EtG was associated with all‐cause mortality. Conclusions Comparable associations with CVD events and all‐cause mortality were found for self‐report and EtG. This argues for the validity of self‐reported alcohol consumption in epidemiologic research.

Background The role of dietary antioxidants and plasma oxidant-antioxidant status in low-grade chronic inflammation and adipocytokine levels is not established yet. Objectives We aimed to evaluate whether total dietary antioxidant capacity (assessed by dietary ferric reducing antioxidant potential (FRAP)), serum uric acid (UA) and gamma glutamyltransferase (GGT) were associated with low-grade chronic inflammation and circulating adipocytokines. Methods Data of 4506 participants aged ≥ 55 years from the Rotterdam Study were analyzed. Baseline (1990–1993) FRAP score was assessed by a food frequency questionnaire. Baseline UA and GGT levels were assessed in non-fasting serum samples. Serum high sensitivity C-reactive protein (hs-CRP) was measured at baseline and 10 years later. Plasma leptin, adiponectin, plasminogen activator inhibitor-1 (PAI-1) and resistin levels were assessed 10 years later.Results A high FRAP score was associated with lower levels of UA and GGT. Overall, no association was found between FRAP and hs-CRP levels. FRAP score was associated with lower levels of leptin and PAI-1, higher levels of adiponectin, and no difference in resistin levels. Increased levels of UA were associated with higher levels of hs-CRP, PAI-1 and leptin; lower levels of adiponectin and no difference in resistin levels. Similarly, GGT was associated with higher levels of hs-CRP whereas no association was observed between GGT and adipocytokines. Conclusion These findings suggest that overall antioxidant capacity of diet and low levels of UA are associated with circulating adipocytokines whereas no consistent association was found with hs-CRP.

Objective To quantify the dose-response relation between consumption of whole grain and specific types of grains and the risk of cardiovascular disease, total cancer, and all cause and cause specific mortality. Data sources PubMed and Embase searched up to 3 April 2016. Study selection Prospective studies reporting adjusted relative risk estimates for the association between intake of whole grains or specific types of grains and cardiovascular disease, total cancer, all cause or cause specific mortality. Data synthesis Summary relative risks and 95% confidence intervals calculated with a random effects model. Results 45 studies (64 publications) were included. The summary relative risks per 90 g/day increase in whole grain intake (90 g is equivalent to three servings—for example, two slices of bread and one bowl of cereal or one and a half pieces of pita bread made from whole grains) was 0.81 (95% confidence interval 0.75 to 0.87; I 2 =9%, n=7 studies) for coronary heart disease, 0.88 (0.75 to 1.03; I 2 =56%, n=6) for stroke, and 0.78 (0.73 to 0.85; I 2 =40%, n=10) for cardiovascular disease, with similar results when studies were stratified by whether the outcome was incidence or mortality. The relative risks for morality were 0.85 (0.80 to 0.91; I 2 =37%, n=6) for total cancer, 0.83 (0.77 to 0.90; I 2 =83%, n=11) for all causes, 0.78 (0.70 to 0.87; I 2 =0%, n=4) for respiratory disease, 0.49 (0.23 to 1.05; I 2 =85%, n=4) for diabetes, 0.74 (0.56 to 0.96; I 2 =0%, n=3) for infectious diseases, 1.15 (0.66 to 2.02; I 2 =79%, n=2) for diseases of the nervous system disease, and 0.78 (0.75 to 0.82; I 2 =0%, n=5) for all non-cardiovascular, non-cancer causes. Reductions in risk were observed up to an intake of 210-225 g/day (seven to seven and a half servings per day) for most of the outcomes. Intakes of specific types of whole grains including whole grain bread, whole grain breakfast cereals, and added bran, as well as total bread and total breakfast cereals were also associated with reduced risks of cardiovascular disease and/or all cause mortality, but there was little evidence of an association with refined grains, white rice, total rice, or total grains. Conclusions This meta-analysis provides further evidence that whole grain intake is associated with a reduced risk of coronary heart disease, cardiovascular disease, and total cancer, and mortality from all causes, respiratory diseases, infectious diseases, diabetes, and all non-cardiovascular, non-cancer causes. These findings support dietary guidelines that recommend increased intake of whole grain to reduce the risk of chronic diseases and premature mortality.

INTRODUCTION: Serum liver biomarkers (gamma-glutamyl transferase, GGT; alanine aminotransferase, ALT; aspartate aminotransferase, AST; alkaline phosphatase, ALP; total bilirubin) are used as indicators of liver disease, but there is currently little data on their prospective association with risk of hepatobiliary cancers.METHODS: A nested-case control study was conducted within the prospective EPIC cohort (>520,000 participants, 10 European countries). After a mean 7.5 mean years of follow-up, 121 hepatocellular carcinoma (HCC), 34 intrahepatic bile duct (IHBC) and 131 gallbladder and biliary tract (GBTC) cases were identified and matched to 2 controls each. Circulating biomarkers were measured in serum taken at recruitment into the cohort, prior to cancer diagnosis. Multivariable adjusted conditional logistic regression was used to calculate odds ratios and 95% confidence intervals (OR; 95%CI).RESULTS: In multivariable models, 1SD increase of each log-transformed biomarker was positively associated with HCC risk (OR(GGT)=4.23, 95%CI:2.72-6.59; OR(ALP)=3.43, 95%CI:2.31-5.10;OR(AST)=3.00, 95%CI:2.04-4.42; OR(ALT)=2.69, 95%CI:1.89-3.84; OR(Bilirubin)=2.25, 95%CI:1.58-3.20). Each liver enzyme (OR(GGT)=4.98; 95%CI:1.75-14.17; OR(AST)=3.10, 95%CI:1.04-9.30; OR(ALT)=2.86, 95%CI:1.26-6.48, OR(ALP)=2.31, 95%CI:1.10-4.86) but not bilirubin (OR(Bilirubin)=1.46,95%CI:0.85-2.51) showed a significant association with IHBC. Only ALP was significantly associated with GBTC risk (OR(ALP)=1.59, 95%CI:1.20-2.09).CONCLUSION: This study shows positive associations between circulating liver biomarkers in sera collected prior to cancer diagnoses and the risks of developing HCC or IHBC, but not GBTC.

BACKGROUND: Higher coffee intake has been purportedly related to a lower risk of liver cancer. However, it remains unclear whether this association may be accounted for by specific biological mechanisms.OBJECTIVE: We aimed to evaluate the potential mediating roles of inflammatory, metabolic, liver injury, and iron metabolism biomarkers on the association between coffee intake and the primary form of liver cancer-hepatocellular carcinoma (HCC).DESIGN: We conducted a prospective nested case-control study within the European Prospective Investigation into Cancer and Nutrition among 125 incident HCC cases matched to 250 controls using an incidence-density sampling procedure. The association of coffee intake with HCC risk was evaluated by using multivariable-adjusted conditional logistic regression that accounted for smoking, alcohol consumption, hepatitis infection, and other established liver cancer risk factors. The mediating effects of 21 biomarkers were evaluated on the basis of percentage changes and associated 95% CIs in the estimated regression coefficients of models with and without adjustment for biomarkers individually and in combination.RESULTS: The multivariable-adjusted RR of having ≥4 cups (600 mL) coffee/d compared with CONCLUSION: These data suggest that the inverse association of coffee intake with HCC risk was partly accounted for by biomarkers of inflammation and hepatocellular injury.

1 Dipartimento di Agronomia Animali Alimenti Risorse Naturali e Ambiente (DAFNAE), University of Padova, Legnaro, Italy, 2 Research Laboratory for Biotechnology and Biochemistry, Kathmandu, Nepal, 3 GRADE (Global Research Arch for Developing Education) Academy Private Limited, Birgunj, Nepal, 4 Organization for Educational Initiatives, University of Tsukuba, Tsukuba, Japan, 5 Department of Anatomy I, Showa University School of Medicine, Shinagawa, Japan

Renal cell carcinoma (RCC) diagnosis is mostly achieved incidentally by imaging provided for unrelated clinical reasons. The surgical management of localized tumors has reported excellent results. The therapy of advanced RCC has evolved considerably over recent years with the widespread use of the so-called “targeted therapies.” The identification of molecular markers in body fluids (e.g., sera and urine), which can be used for screening, diagnosis, follow-up, and monitoring of drug-based therapy in RCC patients, is one of the most ambitious challenges in oncologic research. Although there are some promising reports about potential biomarkers in sera, there is limited available data regarding urine markers for RCC. The following review reports some of the most promising biomarkers identified in the biological fluids of RCC patients.

Background: A chemometric class modeling strategy (unequal dispersed classes [UNEQ]) is applied for the first time to evaluate harmful alcohol drinking within large population screening programs, in comparison with traditional strategies of data interpretation. Five inexpensive indirect biomarkers (aspartate aminotransferase, alanine aminotransferase, γ-glutamyltransferase, mean corpuscular volume and carbohydrate-deficient transferrin) were determined in blood samples from 423 patients, classified as low-risk or harmful drinkers, according to their ethanol consumption. Results: The multivariate UNEQ approach remarkably improves the diagnostic performances of indirect biomarkers in harmful drinking evaluation, leading to reliable decision rules, with few doubtful classifications to be reviewed through complex confirmation procedures. Conclusion: This UNEQ model represents an innovative general approach for clinical evaluation that efficiently extracts the information content present in each biomarker to provide a new synthetic multivariate parameter, to be directly used in diagnostic protocols.

OBJECTIVE Nonalcoholic fatty liver disease (NAFLD) coexists with insulin resistance (IR), but it is uncertain whether NAFLD and IR contribute independently to atherosclerosis. We tested whether fatty liver, IR, and metabolic syndrome (MetS) features (waist, glucose, triglyceride, HDL cholesterol [HDL-C], and blood pressure) were associated with a marker of atherosclerosis (coronary artery calcium [CAC] score > 0), independently of cardiovascular risk factors and cardiovascular disease (CVD). RESEARCH DESIGN AND METHODS Data were analyzed from a South Korean occupational cohort of 10,153 people who all received ultrasound measurements of fatty liver and a cardiac computed tomography CAC score. IR was defined by homeostasis model assessment of IR (HOMA-IR) >= 75th percentile. Odds ratios (ORs) (95% CIs) for the presence of a CAC score > 0 were estimated using logistic regression. RESULTS There were 915 people with a CAC score > 0. MetS features were increased (glucose, blood pressure, triglyceride, and waist) or decreased (HDL-C) among people with a CAC score > 0 (all comparisons against CAC score 0, 55% had fatty liver and 33.7% were insulin resistant. Fatty liver (OR 1.21 [95% CI 1.01-1.45]; P = 0.04) and HOMA-IR (1.10 [1.02-1.18]; P = 0.02) were associated with CAC score > 0, independently of all MetS features, conventional cardiovascular risk factors, and prior evidence of CVD. The presence of IR and fatty liver combined was associated with CAC score > 0 (1.53 [1.20-1.95]; P = 0.001). CONCLUSIONS Fatty liver and HOMA-IR are both associated with a CAC score > 0 (independently of each other), features of MetS, conventional cardiovascular risk factors, and existing CVD.

Background: Parenteral nutrition-associated liver dysfunction can be progressive and irreversible, particularly in children and patients with long-term treatment. This study has assessed the incidence of abnormal liver function tests in hospitalized adults during short term parenteral nutrition (PN) and has investigated risk factors for developing alterations of each parameter. Methods: A prospective cohort study of parenteral nutrition treated patients with preserved liver function at baseline. Variables examined included nutritional and clinical data and laboratory parameters. Determinations were performed before starting PN and weekly until liver function test alteration was observed. Risk factors were investigated by four stepwise forward logistical regressions. Results: Eighty patients were included, 57.5% had liver function test alterations. PN mean duration was 15.9 (8-54) days. Mean days with PN and additional enteral/ oral nutrition were 1.5 (0-20). The following associations were found: gamma-glutamyl-transferase increased with soybean lipid intake and absolute diet; alkaline phosphatase increased with septic shock; alanine transaminase increased with septic shock, hyperglycemia and elevated creatinine; total bilirubin increased with septic shock, absolute diet, low prealbumin and glucose, and high creatinine. Conclusions: The incidence of altered liver function tests is high in adult hospitalized patients treated with short-term PN. However, the effect of nutritional factors in this alteration is low. Oral/enteral nutrition and reduction of soybean lipid supply can reduce increases in some liver function tests such as gamma-glutamyl-transferase and total bilirubin. The high association between all liver function tests and clinical systemic-hypermetabolic variables suggest the importance of specific nutritional strategies for this condition. Introducción: La alteración hepática asociada a la nutrición parenteral (NP) puede ser progresiva e irreversible particularmente en niños y en tratamientos de larga duración. El objetivo de este estudio es establecer la incidencia de las alteraciones de los parámetros hepáticos en pacientes adultos hospitalizados en tratamiento con NP y estudiar los factores de riesgo asociados al desarrollo de las alteraciones de cada uno de los parámetros hepáticos. Métodos: Estudio prospectivo de cohortes de los pacientes tratados con NP con función hepática normal al inicio del tratamiento. Se estudiaron parámetros clínicos, nutricionales y analíticos. Las determinaciones se hicieron antes de iniciar la nutrición y semanalmente hasta que se detectó la alteración de algún parámetro hepático. Los factores de riesgo asociados a la alteración hepática se estudiaron con 4 regresiones logísticas. Resultados: Se incluyeron 80 pacientes y 57,5% mostraron alteraciones hepáticas. La media de duración de la NP fue 15,9 días (8-54) y la media de días con nutrición enteral u oral concomitantes fue de 1,5 (0-20). Se encontraron las siguientes asociaciones: la gamma-glutamil-transferasa aumentaba con la cantidad de lípidos de soja administrados y los días en dieta absoluta; la fosfatasa alcalina con el shock séptico, la alanina-aminotransferasa con el shock séptico, la hiperglucemia y los valores elevados de creatinina; la bilirrubina total con el shock séptico, la dieta absoluta, valores bajos de prealbúmina y glucosa; y valores altos de creatinina. Conclusiones: La incidencia de alteraciones de los parámetros hepáticos es elevada en pacientes adultos hospitalizados tratados con NP, aunque el efecto de los factores nutricionales en esta alteración es bajo. La nutrición oral/enteral y la reducción de los lípidos en forma de soja pueden reducir el aumento de algunos parámetros hepáticos como la gamma-glutamiltransferasa y la bilirrubina total. La gran asociación entre todos los parámetros hepáticos y las variables sistémicas indicadoras de hiper-metabolismo apuntan a la importancia de las estrategias nutricionales específicas en esta situación.

Background: Liver function tests might predict the risk of type 2 diabetes. An independent study evaluating utility of these markers compared with an existing prediction model is yet lacking. Methods and Findings: We performed a case-cohort study, including random subcohort (6.5%) from 38,379 participants with 924 incident diabetes cases (the Dutch contribution to the European Prospective Investigation Into Cancer and Nutrition, EPIC-NL, the Netherlands), and another population-based cohort study including 7,952 participants with 503 incident cases (the Prevention of Renal and Vascular End-stage Disease, PREVEND, Groningen, the Netherlands). We examined predictive value of combination of the Liver function tests (gamma-glutamyltransferase, alanine aminotransferase, aspartate aminotransferase and albumin) above validated models for 7.5-year risk of diabetes (the Cooperative Health Research in the Region of Augsburg, the KORA study). Basic model includes age, sex, BMI, smoking, hypertension and parental diabetes. Clinical models additionally include glucose and uric acid (model1) and HbA1c (model2). In both studies, addition of Liver function tests to the basic model improved the prediction (C-statistic by~0.020; NRI by~9.0%; P

OBJECTIVE The pathophysiological mechanisms to explain the association between risk of type 2 diabetes and elevated concentrations of γ-glutamyltransferase (GGT) and alanineaminotransferase (ALT) remain poorly characterized. We explored the association of liver enzymes with peripheral and hepatic insulin resistance, insulin secretion, insulin clearance, and glucagon concentration. RESEARCH DESIGN AND METHODS We studied 1,309 nondiabetic individuals from the Relationship between Insulin Sensitivity and Cardiovascular disease (RISC) study; all had a euglycemic-hyperinsulinemic clamp and an oral glucose tolerance test (OGTT) with assessment of insulin secretion and hepatic insulin extraction. The hepatic insulin resistance index was calculated in 393 individuals. RESULTS In both men and women, plasma concentrations of GGT and ALT were inversely related with insulin sensitivity (M/I) (all P < 0.01). Likewise, the hepatic insulin resistance index was positively correlated with both GGT (r = 0.37, P < 0.0001, men; r = 0.36, P < 0.0001, women) and ALT (r = 0.25, P = 0.0005, men; r = 0.18, P = 0.01, women). These associations persisted in multivariable models. Increased GGT and ALT were significantly associated with higher insulin secretion rates and with both reduced endogenous clearance of insulin and hepatic insulin extraction during the OGTT (P = 0.0005 in men; P = 0.003 in women). Plasma fasting glucagon levels increased over ALT quartiles (men, quartile 4 vs. quartile 1 11.2 ± 5.1 vs. 9.3 ± 3.8 pmol/L, respectively, P = 0.0002; women, 9.0 ± 4.3 vs. 7.6 ± 3.1, P = 0.001). CONCLUSIONS In healthy individuals, increased GGT and ALT were biomarkers of both systemic and hepatic insulin resistance with concomitant increased insulin secretion and decreased hepatic insulin clearance. The novel finding of a positive correlation between ALT and fasting glucagon level concentrations warrants confirmation in type 2 diabetes.

OBJECTIVE: To investigate whether the elevated liver enzymes gamma-glutamyltransferase (GGT), glutamate-pyruvate transaminase (GPT), glutamate-oxalacetate transaminase (GOT) and alkaline phosphatase (AP) and non-alcoholic fatty liver disease (NAFLD) respectively are independently associated with pre-diabetic states, namely impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) or known and newly diagnosed diabetes (NDD), in men and women from the general German population. METHODS: The study was based on 3009 subjects (1556 females, 1453 males) aged 32 to 81 years who participated in the KORA-F4-Study in 2006/2008 in Augsburg, Southern Germany. All non-diabetic participants underwent an oral glucose tolerance test to assess disturbances in glucose metabolism. NAFLD was estimated by liver enzyme concentrations and the Bedogni Fatty Liver Index (FLI). RESULTS: 229 participants (7.6%) reported known diabetes, 106 had NDD (3.5%), 107 (3.6%) had IFG, 309 (10.3%) had IGT, 69 (2.3%) were affected with both metabolic disorders (IFG/IGT) and 74 (2.5%) could not be classified. GGT and GPT were significantly elevated in persons with pre-diabetes and diabetes (GGT in diabetic persons OR = 1.76, [1.47-2.09], in IFG OR = 1.79 [1.50-2.13], GPT in diabetic persons OR = 1.51, [1.30-1.74], in NDD OR = 1.77 [1.52-2.06]), GOT and AP only inconsistently in some pre-diabetes groups. The effects were sharpened in models using an increase of two or three out of three enzymes as an estimate of fatty liver and especially in models using the FLI. Overall frequency of NAFLD applying the index was 39.8% (women: 27.3% and men: 53.2%). In participants with fatty liver disease, the OR for NDD adjusted for sex and age was 8.48 [5.13-14.00], 6.70 [3.74-12.01] for combined IFG and IGT and 4.78 [3.47-6.59] for known diabetes respectively. CONCLUSIONS: Elevated GGT and GPT-values as well as estimates of fatty liver disease are significantly associated with pre-diabetes and diabetes and thus very useful first indicators of a disturbed glucose metabolism.

Cardiovascular disease (CVD) is a leading cause of mortality in renal transplant recipients (RTRs). Metabolic syndrome (MS) is highly prevalent in RTRs. Nonalcoholic fatty liver disease (NAFLD) is considered the hepatic component of MS. We investigated associations of NAFLD markers with MS and mortality. RTRs were investigated between 2001 and 2003. NAFLD markers, alanine aminotransferase (ALT), gamma-glutamyl transferase (GGT) and alkaline phosphatase (AP) were measured. Bone and nonbone fractions of AP were also determined. Death was recorded until August 2007. Six hundred and two RTRs were studied (age 52 +/- 12 years, 55% men). At baseline 388 RTRs had MS. Prevalence of MS was positively associated with liver enzymes. During follow-up for 5.3[4.5-5.7] years, 95 recipients died (49 cardiovascular). In univariate Cox regression analyses, GGT (HR = 1.43[1.21-1.69], p

Background and aims: To investigate the effect of moderate alcohol consumption on lipoprotein-associated phospholipase A2 activity, markers of inflammation and oxidative stress and whether these effects are modified by BMI. Methods and results: Eleven lean (BMI: 18.5-25 kg/m2) and 9 overweight (BMI > 27 kg/m2) men participated in a randomized controlled crossover trial. After consuming 3 cans of beer (40 g ethanol) or alcohol-free beer daily during 3 weeks, fasting blood samples were taken. HDL cholesterol increased by 18.2% (p < 0.001) after beer compared to alcohol-free beer, while LDL cholesterol decreased by 7.8% (p = 0.008). Lipoprotein-associated phospholipase A2 activity was not different (p = 0.23) between beer (47.5 ± 0.8) and alcohol-free beer (48.9 ± 0.8). High-sensitive C-reactive protein was unaffected, but urinary isoprostanes tended to increase (p = 0.09) after beer (114.0 ± 6.9) compared to alcohol-free beer (96.9 ± 6.5). An interaction between BMI and treatment (p < 0.05) on liver enzymes was observed, indicating an increase of liver enzymes after moderate alcohol consumption in overweight men only. Conclusion: Despite profound effects on HDL and LDL cholesterol, moderate alcohol consumption did not affect lipoprotein-associated phospholipase A2 activity. Liver enzymes increased after alcohol consumption in overweight men only, suggesting a less favorable response to moderate alcohol consumption in overweight people.

Background: There are only limited data obtained under well controlled conditions on the effects of moderate drinking on markers of alcohol use disorders. The aim of this study was to investigate the effects of moderate intake of different alcoholic beverages on these markers, including carbohydrate-deficient transferrin (CDT), sialic acid (SA), and the liver enzymes γ-glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase. Methods: Eleven apparently healthy, nonsmoking middle-aged men were included in a 12-week randomized, diet-controlled crossover trial according to a 4 x 4 Latin-square design. Changes in CDT, SA, γ-glutamyltransferase, aspartate aminotransferase, and alanine aminotransferase were analyzed after 3 weeks of daily intake of four glasses (40 g of alcohol) of red wine, beer, spirits (Dutch gin), or water (control). Results: After 3 weeks' daily consumption of red wine, a significant decrease of serum CDT concentration was observed compared with water consumption. There was no effect of any alcoholic beverage on the other outcome measures. Conclusions: Daily consumption of 40 g of alcohol from different types of alcoholic beverages with dinner did not affect SA or liver enzymes. Further investigations to explore the mechanisms for the red wine-induced decreases of CDT, including changes in iron metabolism, are clearly needed.

Biochemical, histopathological and cell culture evaluations compared the nephrotoxicity of cefazolin with that of gentamicin. New Zealand rabbits were dosed with 250 mg cefazolin/animal im twice daily, 3 mg gentamicin/kg im twice daily, or 0.9% NaCl solution for 10 d. The rabbits in drug-treated groups had necrosis of proximal kidney tubules and elevated urinary-gamma glutamyl transferase (uGGT) levels. The results of the histopathological examinations, uGGT analyses and effects in cell culture indicated the nephrotoxicities of both antibiotics were similar.