Does overfeeding enhance genotype effects on liver ability for lipogenesis and lipid secretion in ducks?

We evaluated the effects of genotype (Muscovy, Pekin and their crossbreed hinny and mule ducks) and feeding levels (overfeeding between 12 and 14 weeks of age vs ad libitum feeding) on liver ability for lipogenesis and lipid secretion in ducks. Samples of liver and blood were collected at 14 weeks of age from 8 birds per group. Plasma levels of insulin was considerably increased in overfed ducks (1.9-fold), stimulating the hepatic activity of the main enzymes involved in lipogenesis from glucose (glucokinase, GK, glucose-6-phosphate dehydrogenase, G6PDH, malic enzyme, ME, acetyl CoA carboxylase, ACX), while cytochrome-c oxidase (COX) activity, indicating overall oxidation ability of energy-yielding substrates, remained unchanged. Plasma levels of triglycerides, phospholipids and total cholesterol were therefore increased (1.9, 3.7, 1.6 and 1.6-fold, respectively). Glycaemia also significantly increased (+8%). Pekin ducks exhibited higher levels of GK and G6PDH activity in the liver than Muscovy ducks, suggesting a greater ability to use glucose consistent with their lower glycaemia. Muscovy ducks had greater ACX activity, suggesting greater ability to synthesise lipids. However, plasma lipid levels were much higher in Pekin ducks than in Muscovy ducks, suggesting a greater ability to export lipids from the liver. Values for the different criteria measured in this study were intermediate or similar in hinny and mule ducks to those of parental species. The high values for GK, G6PDH, ME and ACX activity in hybrid ducks enabled them to produce heavy fatty livers with the same chemical and lipid composition as Muscovy ducks and characterised by high amounts of triglycerides (around 96% of total lipids), and saturated and mono-unsaturated fatty acids.     

Genes involved in the establishment of hepatic steatosis in Muscovy,Pekin and mule ducks

Our main objectives were to determine the genes involved in the establishment of hepatic steatosis in three genotypes of palmipeds. To respond to this question, we have compared Muscovy ducks, Pekin ducks and their crossbreed the mule duck fed ad libitum or overfed. We have shown a hepatic overexpression of fatty acid synthase (FAS) and di-acyl glycerol acyl transferase 2 (DGAT2) in overfed individuals, where DGAT2 seemed to be more regulated. This increase in lipogenesis genes is associated with a decrease of lipoprotein formation in Muscovy and mule ducks, especially apolipoprotein B (ApoB) and Microsomal Triglyceride Transfer Protein (MTTP), leading to lipid accumulation in liver. In Pekin ducks, MTTP expression is upregulated suggesting a better hepatic lipids exportation. Regarding lipids re-uptake, fatty acid-binding protein 4 and very-low-density-lipoprotein receptor are overexpressed in liver of mule ducks at the end of the overfeeding period. This phenomenon puts light on a mechanism unknown until today. In fact, mule can incorporate more lipids in liver than the two other genotypes leading to an intensified hepatic steatosis. To conclude, our results confirmed the genotype variability to overfeeding. Furthermore, similar observations are already described in non-alcoholic fatty liver disease in human, and ask if ducks could be an animal model to study hepatic triglyceride accumulation.     

Does overfeeding enhance genotype effects on energy metabolism and lipid deposition in breast muscle of ducks?

We evaluated the effects of genotype (Muscovy, Pekin and their crossbreed hinny and mule ducks) and feeding levels (overfeeding between 12 and 14 weeks of age vs ad libitum feeding) on energy metabolism and lipid deposition in breast muscle of ducks. Samples of breast muscle (Pectoralis major) were collected at 14 weeks of age from 8 birds per group. Overfeeding induced an accumulation of lipids in breast muscle (1.5- to 1.7-fold, depending on genotype) mainly induced by triglyceride deposition. It also induced a considerable increase in the amounts (expressed as g/100 g of tissue) of saturated and mono-unsaturated fatty acids (SFA, MUFA), while the amounts of poly-unsaturated fatty acids (PUFA) remained unchanged in hinny and Muscovy ducks or slightly increased in Pekin and mule ducks. In breast muscle, overfeeding decreased the activity of the main enzymes involved in lipogenesis from glucose (glucose-6-phosphate dehydrogenase, G6PDH, malic enzyme, ME, acetyl CoA carboxylase, ACX). Lipoprotein lipase (LPL) activity in Pectoralis major muscle was also significantly decreased (-21%). The ability of muscle tissues to catabolize long-chain fatty acids, as assessed by beta-hydroxyacyl CoA dehydrogenase (HAD) activity, was increased in Pectoralis major muscle, as was cytochrome-c oxidase (COX) activity. Hybrid and Pekin ducks exhibited higher levels of ACX and LPL activity in Pectoralis major muscle than Muscovy ducks, suggesting a greater ability to synthesise lipids in situ, and to take up circulating lipids. Total lipid content in breast muscle of hybrid and Pekin ducks was higher than in that of Muscovy ducks. In hybrid and Pekin ducks, lipid composition of breast muscle was characterized by higher amounts of triglycerides, SFA and MUFA than in Muscovy ducks. Finally, oxidative metabolism was greater in Pectoralis major muscles of hybrid and Pekin ducks than in Muscovy ducks, suggesting an adaptative strategy of muscle energy metabolism according to lipid level.     

Is ability to hepatic steatosis influenced by age at the beginning of the overfeeding period in Muscovy and Pekin ducks?

The aim of this study was to analyse the effects of species (Muscovy and Pekin ducks) and age at the beginning of the overfeeding period on fatty liver production, carcass composition and lipid and moisture content of the liver and breast muscle. We reared four groups of 40 ducks per species for the study, starting at 2-week intervals in order to have four different ages together at the beginning of the overfeeding period (10, 12, 14 and 16 weeks). At the end of the overfeeding period, all ducks were slaughtered. Our results confirmed the high levels of difference in carcass composition and lipid content in the plasma, liver and breast muscle between Muscovy and Pekin ducks at all ages. Pekin ducks were not able to develop a high degree of hepatic steatosis, but had increased lipid storage in peripheral adipose and muscle tissues than Muscovy ducks. However, the fatty liver weight of Pekin ducks increased with age, with lipid deposition in the liver and peripheral tissues. The ability of Muscovy ducks to produce fatty livers remained unchanged with age in line, with lipid deposition in the liver and peripheral tissues. The sites of lipid deposition thus depend on species and not on the physiological maturity of ducks.     

Influence of lipoprotein-lipase activity on plasma triacylglycerol concentration and lipid storage in three genotypes of ducks

The lipoprotein-lipase (LPL) hydrolyses the triacylglycerols (TG) secreted by the liver and, thus, allows the storage of lipids onto the extrahepatic tissues. The LPL activity has been studied by injection of LPL antibodies in three genotypes of ducks (Muscovy (Cairina moschat), Pekin (Anas plathyrhynchos) and Mule (hybrids of male Muscovy ducks and female Pekin ducks)) under overfeeding condition. The results show a similar weight gain between injected and control animals. A higher liver steatosis is observed in Mule ducks (616 ± 18 g; 8.79% of body mass (BW)) and Muscovy ducks (514 ± 13 g; 7.05% BW) compared to Pekin ducks (353 ± 21 g; 5.89% BW, p < 0.05). Pekin ducks showed a much marked extrahepatic fattening of abdominal and subcutaneous adipose tissues. The LPL activity was evaluated by comparing the evolution of the plasma TG concentrations after injections of saline (control animals) or injections of specific LPL-antibodies. Inhibition of LPL activity performed by intravenous injections of LPL-antibodies showed a spectacular increase in the plasma TG concentrations in the three genotypes. That increase was considerably higher in Pekin ducks (98 ± 10 g/L) compared to Muscovy ducks (35 ± 2 g/L, p < 0.01) and Mule ducks (30 ± 4 g/L, p < 0.01). Those data suggest that a high export of lipids synthesized in liver and a high LPL activity occur in overfed Pekin ducks, which can favour the extrahepatic fattening to the detriment of the liver steatosis, and conversely in overfed Muscovy and Mule ducks.     

Oxidative stress programming in a rat model of postnatal early overnutrition — role of insulin resistance

Postnatal early overfeeding (EO) is related to later development of overweight and other metabolic disorders. As oxidative stress is implicated in most human diseases, as obesity and diabetes, we decided to study some parameters related to oxidative stress and insulin signaling in liver from EO animals in adult life. To induce EO, litter size was reduced to three pups per litter (SL: small litter) and groups with normal litter size (NL:10 pups per litter) were used as control. After weaning, rats had free access to standard diet and water. Body weight and food intake were monitored daily and offspring were killed at 180 days-old. Significant differences had P<.05 or less. As expected, SL rats had hyperphagia, higher body weight and higher visceral fat mass at weaning and adulthood. In liver, postnatal EO programmed for lower catalase (? 42%), superoxide dismutase (? 45%) and glutathione peroxidase (? 65%) activities. The evaluation of liver injury in adult SL group showed lower nitrite content (? 10%), higher liver and plasma malondialdehyde content (+ 25% and 1.1-fold increase, respectively). No changes of total protein bound carbonyl or Cu/Zn superoxide dismutase protein expression in liver were detected between the groups. Regarding insulin signaling pathway in liver, SL offspring showed lower IRβ (? 66%), IRS1 (? 50%), phospho-IRS1 (? 73%), PI3-K (? 30%) and Akt1 (? 58%). Indeed, morphological analysis showed that SL rats presented focal areas of inflammatory cell infiltrate and lipid drops in their cytoplasm characterizing a microsteatosis. Thus, we evidenced that postnatal EO can program the oxidative stress in liver, maybe contributing for impairment of the insulin signaling.     

Is the hepatic metabolism of glucose and linoleic acid influenced by species in overfed ducks?

There are genetic differences in the hepatic glucose and linoleic acid metabolisms between Muscovy and Pekin ducks ad libitum-fed. To understand the effect of overfeeding on the hepatic metabolisms in these two species of ducks, we compared the different pathways of glucose and linoleic acid reaching the liver of Muscovy (Cairina moschata) (n = 6) and Pekin (Anas platyrhynchos) (n = 6) ducks overfed for 1 week and sacrificed 2–4 h after their last meal by using the ex vivo method of liver slices incubated for 16 h with [U-¹⁴C]-glucose, [1-¹⁴C]-linoleic acid and [³⁵S]-methionine added to the survival medium. The glucose was the main precursor of triacylglycerol synthesis in the liver of these two species and its hepatic metabolism was similar between species. The hepatic uptake of linoleic acid was 1.7-fold higher (P = 0.020) in the Muscovy duck than in the Pekin duck leading to a 1.9-fold higher (P = 0.017) esterification of this fatty acid in the liver of the Muscovy duck than in that of the Pekin duck. Finally, both species after 1 week of overfeeding exhibited the same capacity to secrete VLDL remaining insufficient to avoid hepatic steatosis.     

Factors affecting nest choice by Pekin ducks

To encourage nest use in breeder poultry flocks, it is important that nest boxes are attractive. Few studies have evaluated factors affecting nest attractiveness to ducks. We assessed the effects of nest box experience (Experiments 1 and 2) and features of nests, including degree of enclosure (Experiments 1 and 2) and the presence of an egg (Experiment 3), on nest site selection by sexually mature Pekin ducks. The hens were tested individually in pens containing different nest box choices. Nest preferences were determined based on the locations of 14 successively laid eggs. Ducks in Experiment 1 were provided with nest box access prior to the onset of lay (20 weeks of age, EXP group, N = 12) or at the time of preference testing (35 weeks of age, DELAYED-EXP group, N = 12). Delaying nest box access by 15 weeks did not significantly affect the proportion of eggs laid in nest boxes rather than on the floor (P = 0.40). Regardless of experience ducks laid more than 66% of their eggs in nest boxes offering a higher degree of enclosure. Ducks in Experiment 2 were reared with either open-top (OP, N = 12) or closed-top (CL, N = 12) boxes. Regardless of rearing condition, ducks preferred boxes with the highest level of enclosure offered. Ducks laid twice the expected proportion (25%) of eggs in CL boxes with curtains (P = 0.0004). CL boxes without curtains were used as predicted by chance, 25% (P = 0.746), while OP boxes with (P = 0.009) and without (P = 0.015) curtains each contained only half the expected number of eggs. Ducks in Experiment 3 were provided with two nest boxes, one of which contained the egg laid the previous day. Each day, the newly laid egg was marked and either placed back in the nest box where it was found (HANDLED, N = 12) or moved into the adjacent nest box (MOVED, N = 12). Ducks in HANDLED and MOVED laid 97.6% and 79.8%, respectively, of their eggs in boxes containing the previous day's egg. While ducks in HANDLED were consistent in their choice throughout the test, those in MOVED developed the preference over time (P = 0.039), suggesting that the preference for laying in a nest containing an egg may be influenced by experience. These results indicate that nest box enclosure and the presence of an egg are important in determining the nesting choices of Pekin ducks. Incorporating these features into nest boxes may be useful for increasing consistency of nest use in breeder duck flocks.     

Hormonal and metabolic responses to overfeeding in three genotypes of ducks

Muscovy, Pekin and Mule duck are different in their body weight. To make a valid comparison in the lipid metabolism between these three genotypes, overfeeding was carried out by providing the animals with amounts of food in proportion to their body weight. Under these conditions, Muscovy ducks developed a strong liver steatosis, whereas it was not very pronounced in the Mule ducks and even less in the Pekin ducks. On the contrary, Pekin ducks showed a much marked extrahepatic fattening. At the beginning of overfeeding, there was a similarity in the three genotypes as regards the post-heparin lipoprotein-lipase (LPL) activity and the insulin and glucagon concentrations. After 10 days of overfeeding, the LPL activity dramatically fell in Muscovy and in Mule ducks, whereas it remained steady in Pekin ducks. Compared to values found at the beginning of the overfeeding period, plasma glucagon and insulin shown no evolution, except for the insulin of Pekin ducks which was dramatically higher. Those data suggest that high plasma insulin concentrations measured in Pekin ducks after 10 days of overfeeding can be responsible for the maintenance of the LPL activity, which favors the extrahepatic fattening to the detriment of liver steatosis.     

Behavioural and physiological fear responses in ducks: genetic cross effects

Mule duck, a cross between a Muscovy drake and a Pekin female, is reported by the farmers to frequently express fear behaviours, such as man avoidance. The genetic basis of fear responses in mule ducks was therefore investigated in this study. According to a previous experiment, the dominant effect of Pekin genotype was hypothesised; however, due to the absence of birds from the reciprocal cross, a superiority of the Pekin in additive effect could not be distinguished from a direct maternal additive effect. In order to clarify this, ducks from the mule genotype, the two parental genotypes (Pekin and Muscovy) and the reciprocal intercross (hinny) underwent a set of physiological and individual behavioural tests of fear. Both parental genotypes were highly fearful but exhibited responses of different patterns: Pekin ducks manifested a higher locomotor activity, whereas the Muscovy ducks showed a higher avoidance to man. Hybrids expressed higher panic responses and specific fear of man than the two parent breeds. Both hybrids expressed similar patterns and the maternal effects were not significant. Significant heterosis effects were found for most of the behavioural responses, in agreement with the fact that higher fear responses were expressed by the hybrids compared to the parental genotypes. A significant heterosis effect was also found for basal adrenal activity; hybrids having higher basal level than parental genotypes. Maximum capacity of adrenal response appeared to be determined by direct additive effects with a superiority of the Pekin genotype.     

Heat shock protein-27 attenuates foam cell formation and atherogenesis by down-regulating scavenger receptor-A expression via NF-κB signaling

Previously, we showed an inverse correlation between HSP27 serum levels and experimental atherogenesis in ApoE^?/? mice that over-express HSP27 and speculated that the apparent binding of HSP27 to scavenger receptor-A (SR-A) was of mechanistic importance in attenuating foam cell formation. However, the nature and importance of the interplay between HSP27 and SR-A in atheroprotection remained unclear. Treatment of THP-1 macrophages with recombinant HSP27 (rHSP27) inhibited acLDL binding (? 34%; p < 0.005) and uptake (? 38%, p < 0.05). rHSP27 reduced SR-A mRNA (? 39%, p = 0.02), total protein (? 56%, p = 0.01) and cell surface (? 53%, p < 0.001) expression. The reduction in SR-A expression by rHSP27 was associated with a 4-fold increase in nuclear factor-kappa B (NF-κB) signaling (p < 0.001 versus control), while an inhibitor of NF-κB signaling, BAY11-7082, attenuated the negative effects of rHSP27 on both SR-A expression and lipid uptake. To determine if SR-A is required for HSP27 mediated atheroprotection in vivo, ApoE^?/? and ApoE^?/? SR-A^?/? mice fed with a high fat diet were treated for 3 weeks with rHSP25. Compared to controls, rHSP25 therapy reduced aortic en face and aortic sinus atherosclerotic lesion size in ApoE^?/? mice by 39% and 36% (p < 0.05), respectively, but not in ApoE^?/?SR-A^?/? mice. In conclusion, rHSP27 diminishes SR-A expression, resulting in attenuated foam cell formation in vitro. Regulation of SR-A by HSP27 may involve the participation of NF-κB signaling. Lastly, SR-A is required for HSP27-mediated atheroprotection in vivo.     

Influence of lipoprotein-lipase activity on plasma triacylglycerol concentration and lipid storage in three genotypes of ducks.

The lipoprotein-lipase (LPL) hydrolyses the triacylglycerols (TG) secreted by the liver and, thus, allows the storage of lipids onto the extrahepatic tissues. The LPL activity has been studied by injection of LPL antibodies in three genotypes of ducks (Muscovy (Cairina moschat), Pekin (Anas plathyrhynchos) and Mule (hybrids of male Muscovy ducks and female Pekin ducks)) under overfeeding condition. The results show a similar weight gain between injected and control animals. A higher liver steatosis is observed in Mule ducks (616+/-18 g; 8.79% of body mass (BW)) and Muscovy ducks (514+/-13 g; 7.05% BW) compared to Pekin ducks (353+/-21 g; 5.89% BW, p<0.05). Pekin ducks showed a much marked extrahepatic fattening of abdominal and subcutaneous adipose tissues. The LPL activity was evaluated by comparing the evolution of the plasma TG concentrations after injections of saline (control animals) or injections of specific LPL-antibodies. Inhibition of LPL activity performed by intravenous injections of LPL-antibodies showed a spectacular increase in the plasma TG concentrations in the three genotypes. That increase was considerably higher in Pekin ducks (98+/-10 g/L) compared to Muscovy ducks (35+/-2 g/L, p<0.01) and Mule ducks (30+/-4 g/L, p<0.01). Those data suggest that a high export of lipids synthesized in liver and a high LPL activity occur in overfed Pekin ducks, which can favour the extrahepatic fattening to the detriment of the liver steatosis, and conversely in overfed Muscovy and Mule ducks.     

δ15N and δ13C diet–tissue discrimination factors for large sharks under semi-controlled conditions

Stable isotopes (δ¹⁵N and δ¹³C) are being widely applied in ecological research but there has been a call for ecologists to determine species- and tissue-specific diet discrimination factors (?¹³C and ?¹⁵N) for their study animals. For large sharks stable isotopes may provide an important tool to elucidate aspects of their ecological roles in marine systems, but laboratory based controlled feeding experiments are impractical. By utilizing commercial aquaria, we estimated ?¹⁵N and ?¹³C of muscle, liver, vertebral cartilage and a number of organs of three large sand tiger (Carcharias taurus) and one large lemon shark (Negaprion brevirostris) under a controlled feeding regime. For all sharks mean ± SD for ?¹⁵N and ?¹³C in lipid extracted muscle using lipid extracted prey data were 2.29‰ ± 0.22 and 0.90‰ ± 0.33, respectively. The use of non-lipid extracted muscle and prey resulted in very similar ?¹⁵N and ?¹³C values but mixing of lipid and non-lipid extracted data produced variable estimates. Values of ?¹⁵N and ?¹³C in lipid extracted liver and prey were 1.50‰ ± 0.54 and 0.22‰ ± 1.18, respectively. Non-lipid extracted diet discrimination factors in liver were highly influenced by lipid content and studies that examine stable isotopes in shark liver, and likely any high lipid tissue, should strive to remove lipid effects through standardising C:N ratios, prior to isotope analysis. Mean vertebral cartilage ?¹⁵N and ?¹³C values were 1.45‰ ± 0.61 and 3.75‰ ± 0.44, respectively. Organ ?¹⁵N and ?¹³C values were more variable among individual sharks but heart tissue was consistently enriched by ~ 1–2.5‰. Minimal variability in muscle and liver δ¹⁵N and δ¹³C sampled at different intervals along the length of individual sharks and between liver lobes suggests that stable isotope values are consistent within tissues of individual animals. To our knowledge, these are the first reported diet–tissue discrimination factors for large sharks under semi-controlled conditions, and are lower than those reported for teleost fish.     

Zinc and glycemic control: A meta-analysis of randomised placebo controlled supplementation trials in humans

BackgroundImpaired zinc metabolism is prominent in chronic disorders including cardiovascular disease and diabetes. Zinc has the potential to affect glucose homeostasis in animals and humans and hence impact the risk of type 2 diabetes mellitus.MethodsA systematic review and meta-analysis of randomised placebo controlled trials was conducted to determine the effect of zinc supplementation on fasting blood glucose, HbA1c, serum insulin and serum zinc concentrations. Relevant studies for inclusion were identified from a literature search of electronic databases up to July 2011.ResultsFourteen reports (n = 3978 subjects) were included in the meta-analysis. In the overall analysis, a small but statistically significant reduction in fasting glucose concentrations was observed (?0.19 ± 0.08 mmol/L, P = 0.013) after zinc supplementation. HbA1c tended to decrease in zinc-supplemented individuals (?0.64 ± 0.36%, P = 0.072). No significant effect was observed for serum insulin concentrations. Plasma zinc concentrations increased significantly following supplementation (+4.03 ± 0.81 μmol/L, P = 0.001). In secondary analyses of participants with chronic metabolic disease (types 1 and 2 diabetes mellitus, metabolic syndrome and obesity), zinc supplementation produced a greater reduction in glucose concentrations (?0.49 ± 0.11 mmol/L, P = 0.001) compared to the effect that was observed in healthy participants.ConclusionThe significant albeit modest reduction in glucose concentrations and tendency for a decrease in HbA1c following zinc supplementation suggest that zinc may contribute to the management of hyperglycemia in individuals with chronic metabolic disease.     

Tumor Necrosis Factor gene polymorphism results in high TNF level in sepsis and septic shock

IntroductionSystemic sepsis releases several cytokines among which tumor necrosis factor alfa (TNFα) has emerged as key cytokine causing septic shock. Single Nucleotide Polymorphisms (SNPs) at positions ?238, ?308, ?376 and +489 in the promoter region of TNF gene exhibit differential association to inflammation and increased TNF production in sepsis.Materials and MethodsThis research work was carried out in 278 critically ill patients and 115 controls. The patients were divided into four groups: Healthy controls, SIRS, Sepsis and Septic shock. Plasma cytokine level was evaluated by ELISA. Specific sequences of TNF gene (?238, ?308, ?376, +489) were amplified using polychromase chain reaction (PCR). SNP detected by BamHiI, NcoI, FokI, TaiI restriction enzymes.ResultsMean plasma TNFα level in healthy Control group was 8.37 ± 2.23 pg/ml, in SIRS group, the mean plasma TNFα level was 77.99 ± 5.51 pg/ml, in Sepsis patients 187.1 ± 14.33 pg/ml and in septic shock 202.2 ± 14.85 pg/ml; range 56.17–417.1 pg/ml. SNP was studied among different patient groups, which showed a higher frequency of mutants among sepsis and shock patients as compared to control.ConclusionPlasma TNF alpha level was significantly high in patients with sepsis and septic shock. SNP of TNF gene showed significant association between polymorphism and development of severe sepsis and septic shock, this would help us in evaluating patients at high risk for septic shock and such patients needed to obtain a rational basis for therapy.     

Hígado graso no alcohólico y su asociación con variables clínicas y bioquímicas en niños y adolescentes obesos: efecto de un año de intervención en el estilo de vida

ObjectiveTo study the frequency of non-alcoholic fatty liver disease (NAFLD), its relationship to clinical and biochemical variables, and the effect 12-month's lifestyle intervention in obese children and adolescents.MethodsThirty-six obese patients aged 7 to 18 years, 42% female and 58% male, 72.2% prepubertal and 27.8% pubertal, were selected. Anthropometric measurements and glucose, insulin (baseline and after a glucose load), lipid profile, C-reactive protein, and aminotransferase tests were performed before and 12 months after dietary and physical activity intervention. Liver ultrasound was performed to determine the presence of NAFLD.ResultsNAFLD was found in 66.7% (n = 24), and was mild in 30.6%, moderate in 27.8%, and severe in 8.3%. Subjects with NAFLD had higher body mass index (BMI, p = 0.007), waist (p = 0.005), fat area (p = 0.002), basal insulin (p = 0.01), and HOMA-IR (p = 0.008) values and lower QUICKI (p = 0.02) values than those with no NAFLD. After intervention, physical activity increased (p = 0.0001) and calorie intake remained unchanged. NAFLD disappeared in 9 patients (37.5%, p = 0.02) and disease severity decreased in 3 patients (12.5%). In addition, BMI Z-score (p = 0.005), fat area (p = 0.0001), basal insulin (p < 0.05), insulin resistance (p < 0.005), lipid profile (p < 0.03), and transaminases decreased. Weight loss was the main variable accounting for NAFLD improvement.ConclusionThis group of obese children and adolescents showed a high frequency of NAFLD. The lifestyle intervention with weight reduction is effective for the treatment of NAFLD.     

Does access to open water affect the behaviour of Pekin ducks (Anas platyrhynchos)?

Ducks show a wide range of water-related behaviours but commercial production often involves access to water that allows drinking only. In this study we evaluated effects of four water resource (WR) treatments on water related behaviours of Pekin ducks. Ducks (n = 2800) were kept in one of four water provision treatments (7 replicate groups of 100 ducks per treatment) from 20 days of age: a bath that allowed full access to water; a trough in which the head could be dipped but without body access; turkey bell drinkers; chicken bell drinkers. The turkey and chicken bells provided easy access for drinking but less opportunity for interaction with the water. The behaviour of the ducks was video recorded, then analysed using scan sampling at 7.5 min intervals between 10:00 and 22:00 at 21, 32, 42 and 45 days. As might be expected, as birds grew, fewer were observed in the bath and over all treatments the amount of preening behaviour increased as ducks aged. Although ducks with access to a bath spent less time in or near the bath, this does not indicate lack of importance to the birds. Fewer ducks were observed standing or resting idle at the bath, and they performed proportionately more water-related preening behaviours than ducks in the other treatments. Moreover, as access to water increased (i.e. from beak only, through to entire body access) higher proportion of preening ducks performed head-dipping behaviour, and a lower proportion performed feather manipulation. This work shows that provision of a water resource that permits full body access appears to promote efficiency of drinking-related behaviours and preening behaviour. This helps to explain improvements in feather hygiene reported in other studies where the birds had full access to, or greater access to water.     

High urinary excretion of lipid peroxidation-derived DNA damage in patients with cancer-prone liver diseases

Chronic inflammatory processes induce oxidative and nitrative stress that trigger lipid peroxidation (LPO), whereby DNA-reactive aldehydes such as trans-4-hydroxy-2-nonenal (HNE) are generated. Miscoding etheno-modified DNA adducts including 1,N⁶-etheno-2′-deoxyadenosine (?dA) are formed by reaction of HNE with DNA-bases which are excreted in urine, following elimination from tissue DNA. An ultrasensitive and specific immunoprecipitation/HPLC-fluorescence detection method was developed for quantifying ?dA excreted in urine. Levels in urine of Thai and European liver disease-free subjects were in the range of 3–6 fmol ?dA/μmol creatinine. Subjects with inflammatory cancer-prone liver diseases caused by viral infection or alcohol abuse excreted massively increased and highly variable ?dA-levels. Groups of Thai subjects (N = 21) with chronic hepatitis, liver cirrhosis, or hepatocellular carcinoma (HCC) due to HBV infection had 20, 73 and 39 times higher urinary ?dA levels, respectively when compared to asymptomatic HBsAg carriers. In over two thirds of European patients (N = 38) with HBV-, HCV- and alcohol-related liver disease, urinary ?dA levels were increased 7–10-fold compared to healthy controls. Based on this pilot study we conclude: (i) high urinary ?dA-levels, reflecting massive LPO-derived DNA damage in vivo may contribute to the development of HCC; (ii) ?dA-measurements in urine and target tissues should thus be further explored as a putative risk marker to follow malignant progression of inflammatory liver diseases in affected patients; (iii) etheno adducts may serve as biomarkers to assess the efficacy of (chemo-)preventive and therapeutic interventions.     

Switching to basal-bolus insulin therapy is effective and safe in long-term type 2 diabetes patients inadequately controlled with other insulin regimens

AimTo assess in standard clinical practice the feasibility, efficacy, and safety of switching patients with long-standing type 2 diabetes (T2DM) and poor or unstable blood glucose control to basal-bolus insulin therapy.Material and methodsThis was a prospective, single center study including 37 patients with T2DM (age 65 ± 8 years, 62.2% men, body mass index 28.8 ± 6.2 kg/m², diabetes duration 18 ± 8 years) with poor or unstable glycemic control, who were switched to a basal-bolus insulin regimen with glargine and rapid-acting insulin analogue at the discretion of their physicians. After a group-structured outpatient diabetes training program, patients were followed in a clinical practice setting for 6 months. Clinical and biochemical variables were collected before switching and at 3 and 6 months.ResultsAfter switching to basal-bolus therapy, glycosylated hemoglobin (HbA1c) decreased from 9 ± 1.2% to 8.1 ± 1.2% (p < 0.001) at 3 months and to 8.0 ± 1.2% at 6 months (p < 0.001) without changing total daily insulin dose. The proportion of patients with HbA1c ≥ 9% decreased from 51% to 13.8% at 3 months and to 18.9% at 6 months respectively. There was a single episode of severe hypoglycemia. No changes were seen in body weight and quality of life. The size of LDL (low density lipoprotein) particles significantly increased at 3 and 6 months, while all other lipid parameters remained unchanged.ConclusionsOur study confirmed that basal-bolus insulin therapy is feasible, effective, and safe in patients with long-standing T2DM, and does not impair their quality of life.