In this study, diethylnitrosamine-treated male mice were assigned to 3 groups: a 35% high fat ethanol liquid diet (EtOH) with casein as the protein source, the same EtOH liquid diet with soy protein isolate as the sole protein source (EtOH/SPI) and a chow group. EtOH feeding continued for 16 wks. As expected, EtOH increased the incidence and multiplicity of basophilic lesions and adenomas compared to the chow group, p<0.05. Soy protein replacement of casein in the EtOH diet significantly reduced adenoma progression when compared to the EtOH and EtOH/SPI group, p<0.05. Tumor reduction in the EtOH/SPI group corresponded to reduced liver injury associated with decreased hepatic tumor necrosis factor α (Tnfα) and Cd14 antigen (Cd14) expression and decreased nuclear accumulation of NFκB1 protein compared to the EtOH group (p<0.05). Detection of sphingolipids using high resolution MALDI-FTICR Imaging mass spectrometry revealed increased accumulation of long acyl chain ceramide species, and sphingosine-1-phosphate (S1P) in the EtOH group that were significantly reduced in the EtOH/SPI group. Chronic EtOH feeding also increased mRNA expression of β-catenin transcriptional targets, including cyclin D1 (Ccnd1), matrix metallopeptidase 7 (Mmp7) and glutamine synthetase (Glns), which were reduced in the EtOH/SPI group, p<0.05. We conclude that soy prevents tumorigenesis by reducing pro-inflammatory and oxidative environment resulting from EtOH-induced hepatic injury, and by reducing hepatocyte proliferation through inhibition of β-catenin signaling. These mechanisms may involve changes in sphingolipid signaling.
In 1948, we had occasion to undertake a series of nitrogen-balance experiments on African patients in Mulago hospital, with a view to assessing their state of nutrition with respect to protein. Some had been admitted to hospital suffering from severe hookworm anaemia, others with enlargement of the liver and spleen sufficient to bring them into hospital. Others bore the diagnosis simply of 'malnutrition'. They all gave a history, extending over years, of a diet grossly deficient in protein, and from which animal protein was almost absent. Malnutrition of the type encountered here differs from that seen in Europe and America in that very serious protein deficiency may accompany a diet of reasonable calorie value. Bayliss's dictum 'Take care of the calories, and the protein will take care of itself' is emphatically not true in this part of Africa. This is because the common carbohydrate staples, sweet potato, cassava, and plantain contain z % or less of protein.Accurate figures for food consumption among the general population are lacking, but the following data are of interest. They were calculated from figures in a report of a cost-of-living survey carried out by the East African Statistical Department (1952). The number of individuals (all adult male labourers) observed was I 10, and the period of observation 30 consecutive days, The daily food consumption was: protein 53 g, carbohydrate 525 g, fat 42 g. This provided 2647 Cal. Only 9 g of the protein were of animal origin. Neither milk, eggs, butter nor cheese were consumed.Our subjects all gave a history of a diet consisting mainly of sweet potato, cassava, or plantain. Groundnuts or beans or both were eaten about once weekly, meat or fish not more often than once monthly, and eggs, milk, or cheese were never consumed. Although, in the absence of diet surveys, we cannot say what proportion of the population live on a diet of this kind, it is quite certain that the type of case with which we have been dealing is extremely common, and examples can be obtained from the general wards of the hospital whenever required. We were not surprised to find that these subjects retained nitrogen when placed on a diet high in animal protein and calories. But as the period of observation extended, and the nitrogen retention continued, we began to realize that some mechanism or mechanisms, not hitherto clearly recognized, must be playing an important part. We have made a long series of observations on the haematology and serum protein of these subjects. We shall, however, confine ourselves in this paper to the question of nitrogen and phosphorus balances.https://www.cambridge.org/core/terms. https://doi
Abstract. We describe the inhibitory effect of prostaglandins (PGs) on in vivo rat renal ammonia synthesis. The influence of systemic pH upon urinary PG excretion and ammoniagenesis was also investigated. Finally, PG production by incubated rat renal cortical slices was suppressed to investigate the PG-ammonia interplay in the absence of changes in renal blood flow, glomerular filtration rate, ambient electrolyte concentrations or extrarenal hormonal factors.In vivo ammonia synthesis doubled and PG excretion fell by 44% in normal rats, after intravenous administration of 1 mg/kg of meclofenamate. Higher doses of meclofenamate further augmented ammonia production and further reduced PG excretion. PG depletion was also associated with an increase in fractional excretion of ammonia (FENH3) that was independent of changes in urine flow rate or pH.Acute metabolic acidosis (AMA) increased total ammonia synthesis but also stimulated PG production. Administration of meclofenamate to rats with mild AMA markedly reduced urinary PG excretion, further augmented ammonia synthesis, and significantly increased the FENH3. Inhibition of stimulated PG synthesis during severe AMA did not increase ammoniagenesis or FENH3. Acute metabolic alkalosis did not alter production of PGs or ammonia, but reduced the FENH3 by A preliminary abstract was presented at
I n the course of a long-term study of the nitrogen balance of African subjects who had previously consumed for a long time a diet very low in protein, we observed no correspondence between the gain in weight during rehabilitation on a high-protein, highcalorie diet and the gain to be expected from the observed retention of nitrogen (Holmes, Jones & Stanier, 1954).Our calculations of tissue gain were based on the assumption that the nitrogen retained was converted into protein, and that the building of this protein into tissue would involve the deposition of two parts of water to one part of protein. On the more probable assumption that the retention of I g nitrogen would involve the deposition of 3 0 g tissue (Edelman, Olney, James, Brooks & Moore, 1952), the discrepancy between the observed and expected weight changes would be considerably greater.If nitrogen is retained by the body without corresponding gain in weight, some other body constituents must have been lost. Such loss might be of water, fat, or minerals; of these the most probable is water. Indeed it is well known that undernourished persons frequently show an increase in extracellular fluid, to the point of displaying gross oedema, and that during rehabilitation the excess of fluid disappears, often with demonstrable loss of body-weight, in spite of a high calorie and protein intake. We determined extracellular fluid by the thiocyanate method, and demonstrated that it was initially high, and that it later decreased. But we have found that the changes, though very considerable, were in fact quite insufficient to account for the discrepancies between expected and observed changes in body-weight. We have tried to solve the problem by three separate lines of approach.( I ) We have followed changes in body composition by determining total body water and extracellular water by dilution methods.(2) We have determined balances of nitrogen, sulphur, phosphorus, calcium, potassium and calories with the threefold object of making sure that sulphur and phosphorus as well as nitrogen were retained in the body, that there was no defect in absorption, and to discover whether potassium was being excreted or retained.(3) We have studied the water and protein content of muscle tissue obtained at autopsy or operation.
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