Nutritional and metabolic consequences of the early Maillard reaction of heat treated milk in the pig

Summary Background During the processing of foods, the Maillard reaction may occur contributing to altering the nutritional value of proteins. In dairy products the formation of lactuloselysine reduces the availability of lysine but the effects on the other nutrients are not very well known. Aim of the study Determination of the consequences of a high level of lactulose-lysine in milk on the bioavailability of skim milk nutrients and the kinetics of their appearance in the portal blood and of their urinary and faecal excretions and extrapolation to lower heat treatments and to man, using the pig model. Methods Sub-adult pigs were fitted, under anaesthesia, with permanent catheters in the portal vein, carotid artery and urethra, and with an electromagnetic flow probe around the portal vein. Each animal was successively fed with two experimental meals containing an equal amount of dried skim milk (SM), either lyophilised or heat treated to obtain an intense Maillard reaction, (M-SM) resulting in a 50 % lysine blockage. Portal and arterial concentrations and flux of individual amino acids (AA), glucose, galactose and fructoselysine were measured for a period of 12h after the meals. Lysine, fructoselysine and AA excreted in the urine and faeces within 72h were also determined. Results In M-SM containing 50 % blocked lysine, no other AA was chemically modified. Fructoselysine appeared in the portal blood very late compared to amino acids resulting from a very slow release and corresponded to 8.2 and 18.6 % of the ingested amount after 12 and 72h, respectively. Significant changes of the appearance in the portal blood were observed only for lysine (−60 %), alanine (−17 %) and cystine (+37 %). A small decrease in the digestibility of most AA during the same period was observed, which was significant after 48h for lysine, phenylalanine, cystine, aspartic acid, glycine and total AA (−6 %). Conclusion It was confirmed that lactuloselysine was not bioavailable. The loss in protein nutritive value was mainly due and proportional to the deterioration of lysine and, to a lesser extent, to the decrease in the digestibility of some essential AA. Taking into account the very high level of lactuloselysine in the M-SM sample studied, it may be concluded that in common foods such as milk, infant formulas, biscuits, bread, pasta, containing lower levels of blocked lysine, the nutritional loss is primarily due to the loss of lysine and to a less extent to the decrease in the digestibility of other essential AA. Received: 24 July 2001, Accepted: 12 November 2001     

Peripheral multineuritis pointing at systemic sarcoidosis

We report a patient with a peripheral neuropathy as the first symptom of sarcoidosis. The systemic illness was proved by the presence of typic granulomes in the bone marrow. The fact that sarcoidosis is the cause for the neuropathy is supported by the temporary relation and by the good response of all clinical picture to the corticosteroid therapy.Sarcoid neuropathy can rarely be the presenting feature of sarcoidosis.     

Does the evidence about health risks associated with nitrate ingestion warrant an increase of the nitrate standard for drinking water?

Several authors have suggested that it is safe to raise the health standard for nitrate in drinking water, and save money on measures associated with nitrate pollution of drinking water resources. The major argument has been that the epidemiologic evidence for acute and chronic health effects related to drinking water nitrate at concentrations near the health standard is inconclusive. With respect to the chronic effects, the argument was motivated by the absence of evidence for adverse health effects related to ingestion of nitrate from dietary sources. An interdisciplinary discussion of these arguments led to three important observations. First, there have been only a few well-designed epidemiologic studies that evaluated ingestion of nitrate in drinking water and risk of specific cancers or adverse reproductive outcomes among potentially susceptible subgroups likely to have elevated endogenous nitrosation. Positive associations have been observed for some but not all health outcomes evaluated. Second, the epidemiologic studies of cancer do not support an association between ingestion of dietary nitrate (vegetables) and an increased risk of cancer, because intake of dietary nitrate is associated with intake of antioxidants and other beneficial phytochemicals. Third, 2–3 % of the population in Western Europe and the US could be exposed to nitrate levels in drinking water exceeding the WHO standard of 50 mg/l nitrate, particularly those living in rural areas. The health losses due to this exposure cannot be estimated. Therefore, we conclude that it is not possible to weigh the costs and benefits from changing the nitrate standard for drinking water and groundwater resources by considering the potential consequences for human health and by considering the potential savings due to reduced costs for nitrate removal and prevention of nitrate pollution.     

Motor performance and functional ability in preschool- and early school-aged children with Juvenile Idiopathic Arthritis: a cross-sectional study

Objective  

To describe the level of motor performance and functional skills in young children with JIA.     

Why did soft drink consumption decrease but screen time not? Mediating mechanisms in a school-based obesity prevention program

Objectives  

This paper aims to identify the mediating mechanisms of a school-based obesity prevention program (DOiT).     

An evaluation of alcohol attendances to an inner city emergency department before and after the introduction of the UK Licensing Act 2003

Background  

The Licensing Act 2003 (The Act) was implemented on the 24th November 2005 across England and Wales. The Act allowed more flexible and longer opening hours for licensed premises. We investigated the effect of The Act on alcohol related attendances to an inner city emergency department in Birmingham, UK.     

Transepithelial paracellular leakiness induced by chronic phorbol ester exposure correlates with polyp-like foci and redistribution of protein kinase C-alpha

Although exposure of LLC-PK1 epithelial cell sheets to phorbol esters (TPA) causes a near immediate and total decrease of transepithelial electrical resistance (TER), continuation of exposure for 3 to 4 days results in a tachyphylactic response as TER begins to return to control levels. Recovery of TER is maximal by 5 to 6 days, but reaches only 70 to 80% of control level. A reciprocal change in the transepithelial flux of D-mannitol indicates that the TER decrease is indicative of an increase in tight junction permeability. Exposure of cell sheets to TPA for several days also results in the appearance of multilayered polyp- like foci (PLFs) across the otherwise one cell layer thick cell sheets. The pattern of penetration of the electron dense dye, ruthenium red, from the apical surface, across the tight junction and into the lateral intercellular space indicates that the tight junctions of the cell sheet become uniformly leaky after acute exposure to TPA. However, when exposure is continued for several days, only the junctions of cells in the PLFs manifest leakiness. The decrease in TER following acute TPA exposure correlates with the translocation of protein kinase C-alpha (PKC alpha) into a membrane-associated compartment. With exposure of several days, only a trace of PKC alpha is visible by Western immunoblot, and this is in the membrane-associated compartment. Immunofluorescent microscopy indicates that the trace of PKC alpha seen in the Western immunoblots is ascribable distinctly to cells of the PLFs. Monolayer areas between PLFs show no discernible immunofluorescent signal. The data therefore indicate that tight junction barrier function may be restored in certain areas by the down regulation of PKC alpha from the membrane-associated compartment. Failure to down regulate may result in the paracellular leakiness and abnormal cell architecture of the PLFs. Possible implications of this model for in vivo epithelial tumor promotion are discussed.      

Chemoprevention of spontaneous tumorigenesis in nullizygous p53- deficient mice by dehydroepiandrosterone and its analog 16alpha-fluoro- 5-androsten-17-one

Transgenic mice with both alleles of the p53 tumor suppressor gene product 'knocked out' by gene targeting are susceptible to early development of tumors, chiefly lymphomas and sarcomas. Compared with the control group, administration of dehydroepiandrosterone (DHEA) at 0.3% of the diet to male p53-deficient mice extended their lifespan by delaying death due to neoplasms (from 105 to 166 days on study, P = 0.002), primarily by suppressing lymphoblastic lymphoma (from 45 to 6% of neoplastic deaths, P = 0.010). Treatment with a synthetic DHEA analog, 16alpha-fluoro-5-androsten-17-one (compound 8354), at 0.15% of the diet also increased lifespan, to 140 days for mice that developed tumors (P = 0.037). The effects of these steroids on lifespan and tumor development did not appear to be strongly related to inhibition of food consumption and weight gain, in that a group pair-fed with control diet to the reduced food consumption of the DHEA-treated group developed and died of the same types of neoplasms at the same rate as the controls fed ad libitum. The chemopreventive effect of these steroids has been proposed to be due to suppression of DNA synthesis by inhibition of glucose 6-phosphate dehydrogenase, the rate-limiting enzyme of the pentose phosphate pathway. Although DHEA and its analog are strong non- competitive inhibitors of this enzyme in vitro, treatment with DHEA did not deplete cellular nucleotide pools in the liver, as would have been predicted. The chemopreventive effect of DHEA in this model may be due to steroid-induced thymic atrophy and suppression of T cell lymphoma, permitting these mice to survive long enough to develop tumors with longer latency.