Unbalanced Protein Research Articles

Functional alterations in the rat kidney induced either by diabetes or high protein diet.

The aim of this study was to compare the effect of long-term diabetes with that of a long-term high protein diet in vivo on the kidney function and in vitro on cellular parameters of isolated glomeruli of BB rats. Four groups of rats were investigated: Group 1 = normoglycaemic (N) rats > 250 days old; group 2 = age-matched diabetic (D) rats with a diabetes duration of more than 150 days; group 3 = BB rats which were fed a protein diet of 8% (low protein = LP) and group 4 = rats which received a high protein (HP) diet (32%) for more than 80 weeks. From 24-h-urine samples albumin, urea, creatinine and electrolyte excretion were estimated. At the end of the study the total kidney weight was determined and glomeruli were isolated for in vitro experiments. Hyperglycaemic and HP fed rats were characterised by a significantly increased excretion of albumin, urea and different electrolytes compared to normoglycaemic or LP fed animals. Creatinine excretion was neither affected by hyperglycaemia nor HP diet. HP and D caused a significant increase in total kidney weight when compared to the LP and N group, respectively (N: 1.79 +/- 0.08; D: 2.33 +/- 0.09; LP: 2.26 +/- 0.18; HP: 3.28 +/- 0.46 g; p < 0.05). The increased kidney weight of diabetic and HP rats correlated well with a significant enhanced DNA content of isolated glomeruli (N: 3.41 +/- 0.15; D: 4.45 +/- 0.19; LP: 4.18 +/- 0.35; HP: 6.40 +/- 0.62 micrograms/1000 glomeruli; p < 0.02). In addition, glomeruli obtained from either D or HP fed BB rats incorporated significantly more 3H-thymidine into their DNA indicating an elevated rate of DNA synthesis. The results demonstrate that HP diet caused markedly altered kidney function and induced cellular changes of glomeruli which are interpreted as enhanced proliferative processes. These alterations are comparable to those associated with diabetes mellitus. An unbalanced high protein diet represents a considerable risk factor for the development of functional and structural impairments of the kidney and should absolutely be avoided in patients suffering from diseases which are known to be associated with kidney alterations.

Adipokine genetics: Unbalanced protein secretion by human adipose tissue as a cause of the metabolic syndrome

Subcutaneous and visceral adipose compartments act, not only as fatty acid depots, but also as active endocrine organs that undergo hyperplastic changes and significantly enhance their function in obesity. Akipokines and other proteins secreted by both adipocytes and stromal cells play a central role in peripheral insulin resistance and the metabolic syndrome (MS). Minor alleles of the adipokine genes substantially contribute to MS. The most important consequence of MS is low-level systemic inflammation supported by adipose-specific synthesis of proinflammatory soluble molecules. Proinflammatory signals are secreted into the bloodstream and spread to peripheral tissues that contain their receptors. The signals provided by adipose tissue stimulate the development of secondary complications of MS, including cardiovascular disorders (CVDs) and nonalcoholic fatty liver disease. The review describes the physiological effects of adiponectin, leptin, resistin, visfatin, and apelin and the influence of the minor alleles of the adipokine genes on the development of the secondary complications of MS.

Unbalanced protein S deficiency due to warfarin treatment as a possible cause for thrombosis

The prothrombin time/International Normalized Ratio is an accurate parameter for following most warfarin-treated patients. However, it reflects mostly factor VII levels, and significant disproportionate alterations in other vitamin K-dependent factors may not be reflected properly. We report a rare case of a woman who developed arterial thrombosis whilst receiving therapeutic doses of warfarin, and was found to have a significant and unbalanced protein S deficiency. Discontinuation of warfarin resulted in complete normalization of coagulation factors, and no further thrombotic events under treatment with enoxaparin, with a follow-up of 2.5 years.

Influence of pollen quality on ovarian development in honeybee workers ( Apis mellifera scutellata)

Protein-rich diets are known to promote ovarian and egg development in workers of the honeybee, Apis mellifera, even in the presence of a queen. Since the main source of protein for honeybees is pollen, its quality and digestibility might be important dietary factors determining reproductive capacity. We have compared the effect of two types of pollen—sunflower, Helianthus annuus, and aloe, Aloe greatheadii var davyana—on ovarian development in A. mellifera scutellata workers. Under queenright conditions in the field, worker bees exhibited greater ovarian development when feeding on aloe pollen than on sunflower pollen. In their midgut, we observed higher extraction efficiency for aloe (80%) than for sunflower (69%) pollen. This may be attributed to the morphology and size of the two kinds of pollen grains and explains, together with the high protein content of aloe pollen (32% dry mass in bee-collected pollen) compared to sunflower pollen (15%), why aloe pollen promoted higher ovarian development. However, in the laboratory workers sustained on aloe pollen had significantly less-developed ovaries and higher mortality than those fed sunflower pollen. These detrimental effects may be due to an unbalanced protein:carbohydrate ratio. We discuss the effects of unbalanced diets on the physiology and ecology of honeybee reproduction.

Amino Acid Adequacy in Pathophysiological States

Amino acid utilization and, therefore, demand differ between the healthy state and various disease states. In the healthy state most circulating amino acids are derived from dietary proteins that are stored and broken down in the gut and released gradually into the portal circulation, and from continuous turnover of body protein. In disease states, the amino acid composition of amino acids derived from periferal protein breakdown and released in the circulation, is different, for example because a substantial part of the branched-chain amino acids is broken down to yield glutamine and alanine, which are released in the circulation. It appears to be advantageous to mimic this continuous autoinfusion in patients, dependent of parenteral of enteral tube feeding. In disease, different endpoints should be used to assess the adequacy of the administered amino acid mix. Maintenance of a positive nitrogen balance and growth is less important than support of wound healing and immune function. Several amino acids such as glutamine, cysteine, and taurine are shown or suggested to be conditionally essential in disease, and to form substrate in the stressed patient for anabolic processes in liver, immune system, and injured sites. Amino acid toxicity is rare, and protein restriction for patients with renal or liver failure is obsolete because this only aggravated malnutrition. A true example of protein toxicity consists of gastrointestinal hemorrhage that precipitates hepatic encephalopathy in liver insufficiency, most likely because hemoglobin is an unbalanced protein because it lacks the essential amino acid isoleucine.

Nitrogen supplementation of corn silages. 1. Effects on feed intake and milk production of dairy cows.

Feed intake and milk production responses to N supplementation of corn silage-based diets were measured in three 3 x 3 Latin square experiments. In each experiment, 9 Holstein cows received total mixed rations (TMR), based on corn silage. In Exp. 1, midlactation cows were used to study effects of diets with different ratios of effective rumen-degradable protein (ERDP; g) to fermentable metabolizable energy (FME; MJ), providing a large deficiency (RL), a slight deficiency (RM), and a slight excess (RH) in relation to the target level of 11 g of ERDP/MJ of FME, respectively, for lactating cows. Diets were formulated to be isoenergetic, and to satisfy the metabolizable protein requirements. In Exp. 2, early-lactation cows were used to evaluate effects of different proportions of quickly and slowly rumen-degradable protein (RDP), achieved by replacing soybean meal with urea in the concentrates (0, 0.5, and 1% urea). Experiment 3 investigated effects of synchronizing the availability of FME and ERDP in the rumen. Midlactation cows received a diet containing, on a dry matter (DM) basis, 45% corn silage, 5% ryegrass hay, 35% energy-rich concentrate, and 15% protein-rich concentrate (crude protein: 38% of DM; urea: 2% of DM). The protein-rich concentrate was fed either once (D1) or twice (D2) per day before the meal, or included in the TMR (DU). Treatment RL led to lower DM intake and milk yield, but higher milk production efficiency; there were no significant differences between treatments RM and RH. There were no significant treatment effects on DM intake, milk yield, or milk composition in Exp. 2. Manipulating rumen synchrony by altering the timing of feeding affected milk yields, with D1 cows producing significantly less than D2 and DU cows, which were similar. The amount of ERDP in the diet should be matched to the amount of fermentable energy available to maximize intake, milk yields, and the conversion of feed N into milk protein. However, this study showed only small benefits to altering the diurnal pattern of supply of RDP and FME, and only with extreme feeding strategies that would not be used in practice. Urine volume increased in response to increased or unbalanced protein supply. Analysis of the allantoin:creatinine ratio in spot samples of urine was not useful in identifying predicted differences in microbial protein yield from the rumen.

The effects of quantity and quality of diet nitrogen on the growth, efficiency of food utilization, nitrogen budget, and metabolic rate of fifth-instar Spodoptera eridania larvae (Lepidoptera: Noctuidae)

Relative growth rate and relative nitrogen accumulation rate for fifth-instar Spodoptera eridania larvae vary less than 20% on artificial diets in which protein content varies more than 250%, due to compensatory adjustments in consumption rate and changes in efficiencies of food and nitrogen utilization. The substitution of zein for two-thirds of the casein in a diet containing 26.0% protein results in a 25% decrease in both relative growth and nitrogen accumulation rates, due to reduced values of relative consumption rate, relative nitrogen consumption rate, approximate digestibility, approximate digestibility of nitrogen and efficiency of conversion of digested nitrogen. Although larval growth rate is relatively independent of diet nitrogen, larval composition is highly dependent upon both nitrogen quantity and quality. As diet nitrogen increases, larval nitrogen content increases and fat content decreases. Larvae on diets containing a mixture of casein and zein produce 3.5–3.9 times as much uric acid and respire at rates significantly higher than larvae on diets containing the same total amount of protein but lacking zein. Thus, there is a measurable metabolic cost associated with processing low quality protein. We conclude, however, that elevated metabolic rates of larvae on diets containing nutritionally unbalanced protein are not the cause of reduced growth rates. On these diets, growth is limited byan amino acid present in limiting quantities, and the elevated metabolic rate is due, at least in part, to increased synthesis of uric acid. Finally, we discuss the possibility that variation in amino acid profiles across host plant species might be a factor favouring specialization in insect herbivores.

Unbalanced growth and latent killing of Escherichia coli following exposure to sulfur mustard

A study has been made of the effects of unbalanced metabolism on the survival of sulfur-mustard-treated Escherichia coli, strains 15T-A-U- (thymine, arginine and uracil requiring) and 15T-PA- (thymine and phenylalanine requiring). The following results were obtained. 1. 1. Pre- and post-treatment growth conditions significantly affected the sensitivity of bacteria to sulfur mustard. The largest resistance was observed when bacteria were cultured before treatment in media containing thymidine, but lacking the required amino acid and uracil. Such bacteria were also immune to thymineless death and more resistant, to other bifunctional alkylating agents, mitomycin C and the decay of incorporated [ 3H]thymidine than were exponentially growing bacteria. 2. 2. The development of the resistant state could not be attributed to the completion of DNA replication, the attainment of the stationary growth phase, or the inhibition of protein synthesis but appeared to be largely due to the low levels of unbalanced metabolism to which the mustard-treated cells were subsequently subjected. Thus, resistant cells, on post-treatment incubation in nutritionally deficient media, were considerably more refractory to latent killing effects and to thymineless death than were exponentially growing bacteria. 3. 3. The latent killing of mustard-treated cells and thymineless death were strikingly similar phenomena. Both processes were often similarly affected by nutritionally induced changes, had the same maximal rates, and were accompanied by a stimulated incorporation of [ 32P]P 1 into a RNA-like product, while unbalanced protein synthesis played only a minor, or indirect role in killing. The most notable difference between latent and thymineless killing was a dose-dependent decrease in the lag before onset of killing. 4. 4. Unbalanced metabolism affected the stability of both DNA and RNA. DNA became increasingly more difficult to isolate in highly polymerized form and some of the DNA was actually degraded to acid-soluble products. Mustard-treated bacteria, during latent killing, rapidly depolymerized 35 % of their DNA, a process which preceded the degradation of RNA, while untreated bacteria, during thymineless death, degraded their DNA much later, following the breakdown of RNA. The depolymerization of DNA did not occur spontaneously but depended on the presence of glucose in the incubation medium, suggesting that the breakdown of bacterial DNA is either the cause or effect of unbalanced metabolism. 5. 5. In contrast to the bifunctional sulfur mustard, the monofunctional analog, β-chloroethyl-β-hydroxyethyl sulfide, was considerably less lethal to bacteria, failed to inhibit bacterial DNA synthesis and did not promote the breakdown of DNA during post-treatment incubation. These results suggest that some cross-alkylating reactions are particularly effective for initiating unbalanced metabolism. 6. 6. The mechanism of death by unbalanced metabolism is discussed with special emphasis on the involvement of nucleases.

Relationship between thymineless death and ultraviolet inactivation in Escherichia coli.

Gallant, J. (Johns Hopkins University, Baltimore, Md.), and S. R. Suskind. Relationship between thymineless death and ultraviolet inactivation in Escherichia coli. J. Bacteriol. 82:187-194. 1961.-At 37 C, cultures of Escherichia coli strain B3 growing in the absence of thymine undergo unbalanced growth and thymineless death. Thymineless death also occurs at 37 C in 2 mug of chloramphenicol per ml despite virtually complete inhibition of cell growth and net protein synthesis. Thymineless cultures growing at 25 C exhibit unbalanced synthesis of ribonucleic acid and of protein without lethality. Examination of the kinetics of ultraviolet inactivation of cells grown under these three conditions indicates that the mean lethal dose of ultraviolet irradiation decreases with unbalanced protein synthesis whether or not thymineless death occurs, whereas the latter is specifically correlated with a transition from multihit to single hit inactivation kinetics. The time course of this transition correlates well with that of thymineless death, and preirradiated cells show a shorter lag period before the onset of thymineless death. These results, therefore, suggest that thymineless death is due to an inactivation of those cellular units which are sensitive to ultraviolet irradiation, presumably nuclei or some nuclear function.