scholarly journals THE MAINTENANCE OF BLOOD COLLOID: PASSAGE OF STORED GUM ACACIA FROM THE CELLS TO THE CIRCULATION AFTER PLASMAPHERESIS

1950 ◽  
Vol 92 (1) ◽  
pp. 77-83 ◽  
Author(s):  
R. E. Knutti ◽  
R. A. Warrick ◽  
J. B. Goetsch

Removal of blood plasma by plasmapheresis from dogs made hypoproteinemic by injections of gum acacia over long periods of time, has resulted in the removal of more gum acacia than was originally present in the plasma. Gum acacia injections had been discontinued previous to the start of the experiments, and hence it must be concluded that the excess amounts of acacia were derived from deposits in the various organs. These observations verify the previous suggestion that the increase in blood acacia in the hypoproteinemic dog on a low protein diet is due to the transfer of acacia to the blood from its sites of deposit in the body. The experiments further suggest that the colloid content of the blood stream is maintained at the expense of tissue colloids, and support the idea that colloidal substances may pass in and out of cells.

1938 ◽  
Vol 67 (5) ◽  
pp. 675-690 ◽  
Author(s):  
S. C. Madden ◽  
W. E. George ◽  
G. S. Waraich ◽  
H. Whipple

When blood plasma proteins are depleted by bleeding, with return of the washed red cells (plasmapheresis) it is possible to bring dogs to a steady state of hypoproteinemia and a uniform plasma protein production on a basal low protein diet. These dogs are clinically normal with normal appetite, no anemia and normal nitrogen metabolism. These dogs become test subjects by which various factors relating to plasma protein production may be tested. The normal dog (10 to 13 kg.) has a substantial reserve store of plasma protein building material (10 to 60+ gm.) which requires 2 to 6 weeks plasmapheresis for its complete removal. After this period the dog will produce uniform amounts of plasma protein each week on a fixed basal diet. Dogs previously depleted by plasmapheresis and then permitted to return to normal during a long rest period of many weeks, may show much higher reserve stores of protein building material in subsequent periods of plasma depletion (see Table 1). Under uniform conditions of low protein diet intake when plasmapheresis is discontinued for 2 weeks the plasma protein building material is stored quantitatively in the body and can subsequently be recovered (Table 4) in the next 2 to 3 weeks of plasmapheresis. Given complete depletion of plasma protein building reserve stores the dog can produce very little (2± gm. per week) plasma protein on a protein-free diet. This may be related to the wear and tear of body protein and conservation of these split products. Abscesses produced in a depleted dog during a fast may cause some excess production of plasma protein which is probably related to products of tissue destruction conserved for protein anabolism. Gelatin alone added to the basal diet causes very little plasma protein production but when supplemented by tryptophane gives a large protein output, while tryptophane alone is inert.


1950 ◽  
Vol 91 (4) ◽  
pp. 425-431 ◽  
Author(s):  
R. E. Knutti ◽  
J. B. Goetsch ◽  
R. A. Warrick

Dogs were made hypoproteinemic by repeated injections of gum acacia, and the acacia injections were discontinued. Diets of varying protein content were then given. When a high protein diet is provided the plasma protein concentration increases; with a low protein diet, or under conditions of fasting, the plasma protein concentration diminishes. Similarly, plasma acacia concentration shows increases and decreases which are reciprocal to the protein variations. Total circulating plasma protein and total circulating plasma acacia show similar changes. In all instances total circulating colloid (acacia plus protein) concentration adds up to an amount within normal limits for protein alone. The results indicate that under these conditions, acacia stored in the body (principally in the liver) can be removed from its site of deposit and returned to the blood. The data also show that dogs in which acacia is deposited in large quantities, require a larger amount of protein in the diet to maintain a constant plasma protein content than do normal dogs. It appears that the mechanism for maintenance of peripheral colloidal material may be dependent on differences in intracellular and extracellular colloidal osmotic pressure. The experiments also support the idea that plasma protein molecules, as well as gum acacia, may pass in and out of cells through the cell membranes.


1972 ◽  
Vol 27 (3) ◽  
pp. 527-536 ◽  
Author(s):  
J. W. T. Dickerson ◽  
P. C. R. Hughes ◽  
P. A. McAnulty

1. Weanling (24-d-old) rats of a black and white hooded strain were allowed free access for 28 d to a diet containing 5% casein supplemented with methionine, and sucrose as the carbohydrate. Controls were fed on a 25% casein diet with a corresponding reduction in sucrose. Animals given the deficient diet were killed either at 52 d of age or after subsequent rehabilitation on the 25% casein diet when aged 140 d. These animals were compared with controls killed at these two ages and at the start of the experiment.2. The skeletons were X-rayed, skeletal maturity was determined according to a scoring system, and various bones were measured. The forebrain and cerebellum were analysed for cholesterol and DNA and the brain stem for cholesterol only. The DNA content of the paired quadriceps muscles and the livers was also determined.3. On the low-protein diet the body-weight rose by 7 g compared with the control value of 115 g. On rehabilitation, the body-weight of the previously malnourished group showed the expected growth spurt, but failed to attain that of the controls at 140 d.4. With the exception of the pelvis width, all the bones grew a little during the period on the low-protein diet. After rehabilitation, the hind limb, pelvis, iliac and spine lengths and the bi-iliac width remained smaller than these measurements in the corresponding controls, whereas there was no difference in the length of the fore limb, width of the pelvis or in the bone maturity score.5. The forebrains and cerebellums of the malnourished rats did not increase in weight, whereas some increase occurred in the brain stem. The concentration of cholesterol in the forebrains of the deficient animals was the same as that in controls of the same age, but on rehabilitation the concentration did not rise to the control value. The concentration of cholesterol in the cerebellum and brain stem of the deficient rats was lower than in controls of the same age but, whereas that in the cerebellum attained an almost normal level on rehabilitation, that in the brain stem remained significantly lower. The low-protein diet prevented the normal increase in cerebellum DNA and the amount remained low in the rehabilitated animals.6. The experimental diet caused a complete cessation of growth of the quadriceps muscles, and even after rehabilitation they weighed less than their controls. The DNA content, however, was not significantly lower.7. The low-protein diet did not permanently affect either the weight or DNA content of the liver.


2020 ◽  
Vol 26 (1) ◽  
pp. 53-64
Author(s):  
Peter Kelechi Ajuogu ◽  
Mohammed AK Al-Aqbi ◽  
Robert A Hart ◽  
Mitchell Wolden ◽  
Neil A Smart ◽  
...  

Background: Studies have shown that the amount of protein in the diet affects the hypothalamic-pituitary-testis axis and sub-optimal quantity reduces male fertility potential in both animals and humans. However, individual research reports on the factors associated with male infertility are collectively uncharacterized. Aim: We systematically reviewed, and meta-analysed animal (rats) studies on the effect of low protein diet on factors associated with male infertility. Methods: PubMed Central, EMBASE and Scopus databases were searched from inception to 30 March 2019 for the study concepts and related keywords in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol. Data on the outcome measures were extracted and pooled across trials using random-effects model and expressed as mean differences (MD) at a 95% confidence interval (CI). Results: Twelve trials identified from 3327 studies, met our inclusion criteria in the comparison of a low protein diet (2–10% protein) vs control protein diet (17–23% protein). The results showed that a low protein diet caused a significant reduction in the body weight ( P = 0.0001) testis weight ( P = 0.0001), seminal vesicle weight ( P = 0.0003), epididymis weight P = 0.02), serum testosterone ( P = 0.001) and follicle-stimulating hormone (FSH) concentrations ( P = 0.04) compared with the control treatments. No effect on luteinizing hormone (LH) plasma concentration ( P = 0.13) was observed. Conclusion: This study revealed that low protein diet caused significant reductions in body weight, testis, epididymis and seminal vesicle weights, serum testosterone and FSH concentration in rats. We infer that sub-optimal protein consumption reduces the gonadal and endocrine function, and consequently male infertility.


1992 ◽  
Vol 82 (2) ◽  
pp. 191-198 ◽  
Author(s):  
M. Langran ◽  
B. J. Moran ◽  
J. L. Murphy ◽  
A. A. Jackson

1. Urea kinetics were measured by using prime/intermittent oral doses of [15N15N]urea in five healthy men taking formula diets adequate in energy and containing either 70 or 35 g of protein/day. In some studies the low-protein diet was supplemented with non-starch polysaccharides in the form of ispaghula husk or ripe bananas. 2. On the 70 g of protein/day diet urea production was 132% of intake. Only 54% of the urea produced was excreted in the urine with 46% being salvaged in the colon; 90% of the salvaged nitrogen was retained in the metabolic nitrogen pool. 3. On the 35 g of protein/day diet the small decrease in urea production rate compared with that on the 70 g of protein/day diet was not significant, but only 36% of the urea produced was excreted in urine, with the majority, 64%, being salvaged. 4. The extent of urea-nitrogen salvaging on the 35 g of protein/day diet was similar in magnitude to the decrease in nitrogen intake, with the effect that the sum of intake and salvaged nitrogen did not differ between the 35 and the 70 g of protein/day diets. This implies that quantitative control is exerted over the rate at which urea nitrogen is salvaged. 5. The addition of non-starch polysaccharides to the 35 g of protein/day diet had a demonstrable effect upon faecal weight and composition, but did not exert any significant influence upon urea kinetics. 6. It is concluded that large changes in the rate of urea production are not necessary for adaptation to a low-protein diet, rather the salvaging of urea nitrogen in the lower bowel appears to be an important mechanism through which the body adapts to a low-protein diet. The salvaging of urea nitrogen by the colon makes an important contribution to the conservation of body nitrogen.


1970 ◽  
Vol 75 (2) ◽  
pp. 279-285 ◽  
Author(s):  
K. T. Jagusch ◽  
B. W. Norton ◽  
D. M. Walker

SUMMARYEighteen male cross-bred lambs (aged 2–5 days) in two equal groups were given artificial milk diets of either low- or high-protein content; subgroups of three lambs were slaughtered after 2, 4 and 6 weeks on experiment. The composition of the change in empty body weight (E.B.W.), and the chemical composition of the change in weight of the separate compartments and organs, were determined by the comparative slaughter method.Lambs given the high-protein diet made significant gains in weight and in all chemical components in all periods. The composition of their E.B.W. was closely related to E.B.W. regardless of age. Lambs given the low-protein diet made only small gains in weight in 6 weeks, of which 76% was fat. The chemical composition of their E.B.W. was closely related to E.B.W. within each age group. The net gain of protein of these lambs in 6 weeks represented only 1% of the total weight gain, and over 50% of the protein gain was in wool. The skin and blood lost protein during the first 2 weeks, and failed to recover this loss during the remaining 4 weeks. Other organs lost protein initially but recovered this loss between 2 and 6 weeks.It was concluded that the initial loss of protein represented the labile protein reserves of the lamb, and the subsequent recovery was an adaptation to the low-protein diet. Furthermore, the results with both diets indicated that the skin and blood were the most inefficient of the organs in the body in utilizing the available N during a period of protein deficiency, or during a period of abundance in the dietary supply of N.


2005 ◽  
Vol 289 (6) ◽  
pp. E1115-E1118 ◽  
Author(s):  
K. Morten ◽  
P. Field ◽  
N. Ashley ◽  
K. A. Williams ◽  
D. Harris ◽  
...  

Zidovudine (AZT) lowers the perinatal transmission of HIV but can impair mitochondrial function by depleting mitochondrial DNA (mtDNA). AZT therapy and perinatal nutritional deprivation affect the body fat distribution, which influences glucose tolerance. We sought to model intrauterine exposure to AZT in humans to determine whether it interacts with low-protein diet (LPD) to impact on birth weight and glucose homeostasis in the offspring. Pregnant dams and their offspring were given AZT, an LPD, or AZT and an LPD (LPD + AZT). AZT reduced mtDNA copy number in liver and birth weight in the offspring and increased their fasting glucose and insulin ( P = 0.021, 0.03, 0.001, and 0.011 respectively) at 6–8 wk of age. LPD decreased litter size and birth weight ( P = 0.01 and 0.012). In the LPD + AZT group, birth weight and litter size were reduced compared with untreated controls, and fasting blood glucose and insulin were raised. There was a significant interaction between LPD and AZT on fasting insulin levels ( P = 0.025). Islet size was not significantly affected, but the mean β-cell area/islet was reduced in the LPD + AZT group compared with controls ( P < 0.05). Early exposure to AZT interacts with LPD to impair fetal development in this model. This combination appeared to impair the supply of insulin and, hence, glucose homeostasis, perhaps as a result of impaired mitochondrial function. Although it is not certain that this can be extrapolated to humans, maternal nutritional deprivation combined with AIDS therapy could influence both birth weight and onset of diabetes.


2005 ◽  
Vol 93 (1) ◽  
pp. 47-52 ◽  
Author(s):  
A. C. B. Paula ◽  
J. S. Gracioso ◽  
W. Toma ◽  
R. Bezerra ◽  
M. A. J. Saad ◽  
...  

Protein malnutrition can adversely affect all tissues. The aim of the present study was to test the hypothesis that protein deprivation influences gastric ulcer formation, as well as metabolism and organ growth, in rats. In the present study, there was a significant reduction in the body and organ weight of rats fed a low-protein diet (P<0·001). Malnourished rats were less susceptible to ulceration of the gastric mucosa in ethanol and indomethacin models of acute gastric ulcers when compared with rats fed a normoproteic diet (17 % protein). Mucus production and prostaglandin E2 formation increased in malnourished rats, possibly explaining the lower number of acute ulcers in these animals. Pylorus ligature altered gastric juice composition (increased pH and gastric volume, and decreased total acid concentration) in the animal group fed a low-protein diet compared with the group fed a diet containing 17 % protein (P<0·05). The gastric mucosa was more damaged in malnourished rats than in normal rats evaluated for 14 d after acetic acid injection (P<0·001). Malnourished rats exhibited resistance to acute gastric lesions, owing to an increase in prostaglandin GE2 release and mucus secretion, which protected their gastric mucosa. This phenomenon was not seen in subchronic gastric ulceration.


1996 ◽  
Vol 90 (3) ◽  
pp. 215-225 ◽  
Author(s):  
Tracey S. Meakins ◽  
Alan A. Jackson

1. Urea kinetics were measured in six healthy men using prime/intermittent oral doses of [15N15N] urea, after five days consuming one of four diets which varied in their nitrogen content: a reference diet (REF, 70 g of protein and 11.2 g of N); a low-protein diet (LP, 30 g of protein and 4.8 g of N); a low-protein diet with 6.9 g of urea added (LP-U1, 30 g of protein and 8 g of N); a low-protein diet with 13.7 g of urea added (LP-U2, 30 g of protein and 11.2 g of N). 2. Apparent nitrogen balance on the REF diet was significantly better than on the LP or the LP-U1 diets. The addition of the higher level of urea in the LP-U2 diet enhanced apparent nitrogen balance compared with the LP or LP-U1 diets, and was not different to apparent nitrogen balance on the REF diet. 3. On the LP, LP-U1 and LP-U2 diets, the rate of endogenous urea production was not different, and was about 60% of that on the REF diet, a statistically significant difference. The addition of a dietary supplement of urea increased the rate of urea appearance in the urea pool in direct relation to the dose of urea taken. There was no difference in the rate of appearance between the REF and LP-U2 diets, for both of which the rate of appearance was significantly greater than on the LP diet. 4. The excretion of urea in urine on the LP diet was 62% of that on the REF diet, a significant difference. There was no significant difference in the rate of urea excretion between the REF, LP-U1 and LP-U2 diets. 5. The rate of urea hydrolysis by the colonic microflora on the REF diet was more than twice that on the LP or LP-U1 diets. Supplementation with urea at the higher level, LP-U2, significantly increased hydrolysis to the same level as on the REF diet. Most of the nitrogen derived from urea hydrolysis was retained in the metabolic pool (>80%), with no difference in the rate of retention between the REF and LP-U2 diets, both greater than the LP or LP-U1 diets. 6. The dietary supplements of urea increased the size of the body urea pool significantly. Renal clearance of urea was highest on the REF diet and decreased 13–29% on the low-protein diets. Bowel clearance was highest on the REF diet and decreased 46–55% on the low-protein diets. Neither urinary excretion of urea nor urea hydrolysis in the bowel were related simply to the concentration of urea in blood. Urea hydrolysis related most closely to the rate of appearance of urea in the urea pool. 7. The salvage of urea nitrogen was increased on the highest level of supplementation, but the overall sensitivity of the system was low, suggesting that other factors might be limiting for effective urea hydrolysis and the salvage of urea nitrogen.


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