scholarly journals Pathogenesis of oedema in protein-energy malnutrition: the significance of plasma colloid osmotic pressure

1979 ◽  
Vol 42 (1) ◽  
pp. 21-31 ◽  
Author(s):  
Marta Fiorotto ◽  
W. A. Coward
Keyword(s):  
Interstitial Fluid ◽  
Control Diet ◽  
Protein Energy Malnutrition ◽  
Colloid Osmotic Pressure ◽  
Protein Diet ◽  
Water Filtration ◽  
Low Protein Diet ◽  
Oedema Formation ◽  
Low Protein ◽  
Protein Energy

1. Rats were made oedematous by feeding them low-protein diets (protein: energy (P:E) 0.005) ad lib., and measurements were made of plasma and interstitial fluid colloid osmotic pressures (πp and πi respectively) and interstitial fluid hydrostatic pressure (Pi) before, and at the onset of, oedema formation. Taken together as (πp − πi + Pi) these forces oppose capillary pressure (Pc) and thus determine rates of transcapillary water filtration. Interstitial fluid was sampled, in non-oedematous and oedematous animals, from perforated capsules implanted subcutaneously for the measurement of Pi. Blood, plasma and interstitial fluid volumes were also determined.2. In Expt I comparisons were made between animals fed on a control diet (P:E 0.210) and the lowprotein diet. In normal animals the ratio πp:πi was approximately 2, but in protein deficiency it was increased since reductions in the absolute value of πi matched those in πp. These changes were observed 2 weeks after the start of the experiment and became more exaggerated when oedema appeared (weeks 18–22).3. Pi was normally negative with respect to atmospheric pressure but increased to values close to zero when oedema formation occurred.4. Despite the reductions in πp that were seen in the protein-deficient animals the sum of the forces opposing filtration (πp − πi + Pi) did not change significantly during the experiment.5. Plasma and interstitial fluid volumes expressed per kg body-weight (measured using 125I-albumin and 35SO42−) were unchanged as πp initially decreased in the protein-deficient animals but increased markedly with the onset of oedema.6. In Expt 2 comparisons were made between animals fed the low-protein diet ad lib. and others fed on the control diet in restricted amounts so that weight loss was the same in the two groups of animals.7. The wasting induced by restriction of the control diet did not produce reductions in πp or πi and values for Pi were normal. Changes in the animals fed on the low-protein diet were similar to those observed in Expt I. By using 51Cr-labelled erythrocytes it was shown that the expansion in plasma volume that occurred when oedema appeared in the protein-deficient animals was mainly due to a reduction in total erythrocyte volume. Blood volume did not increase significantly.8. It was concluded that in the hypoproteinaemia induced in the experimental animals reductions in the value of πp, which might otherwise result in an imbalance of forces that would produce excessive rates of transcapillary water filtration, were compensated for by reductions in πi. Increases in Pi also compensated but were quantitatively less important.9. The significance of the results is discussed in terms of the pathogenesis of oedema in kwashiorkor and the concept of an oncotic threshold for oedema formation in hypoproteinaemia.

Protein-energy malnutrition induces an aberrant acute-phase response and modifies the circadian rhythm of core temperature

2013 ◽  
Vol 38 (8) ◽  
pp. 844-853 ◽  
Author(s):  
Shari E. Smith ◽  
Rafaela Andrade Ramos ◽  
Roberto Refinetti ◽  
Jonathan P. Farthing ◽  
Phyllis G. Paterson
Keyword(s):  
Core Temperature ◽  
Acute Phase ◽  
Acute Phase Response ◽  
Protein Energy Malnutrition ◽  
Phase Response ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Low Protein ◽  
Mean Temperature ◽  
Protein Energy

Protein-energy malnutrition (PEM), present in 12%–19% of stroke patients upon hospital admission, appears to be a detrimental comorbidity factor that impairs functional outcome, but the mechanisms are not fully elucidated. Because ischemic brain injury is highly temperature-sensitive, the objectives of this study were to investigate whether PEM causes sustained changes in temperature that are associated with an inflammatory response. Activity levels were recorded as a possible explanation for the immediate elevation in temperature upon introduction to a low protein diet. Male, Sprague-Dawley rats (7 weeks old) were fed a control diet (18% protein) or a low protein diet (PEM, 2% protein) for either 7 or 28 days. Continuous core temperature recordings from bioelectrical sensor transmitters demonstrated a rapid increase in temperature amplitude, sustained over 28 days, in response to a low protein diet. Daily mean temperature rose transiently by day 2 (p = 0.01), falling to normal by day 4 (p = 0.08), after which mean temperature continually declined as malnutrition progressed. There were no alterations in activity mean (p = 0.3) or amplitude (p = 0.2) that were associated with the early rise in mean temperature. Increased serum alpha-2-macroglobulin (p < 0.001) and decreased serum albumin (p ≤ 0.005) combined with a decrease in serum alpha-1-acid glycoprotein (p < 0.001) suggest an atypical acute-phase response. In contrast, a low protein diet had no effect on the signaling pathway of the pro-inflammatory transcription factor, NFκB, in the hippocampus. In conclusion, PEM induces an aberrant and sustained acute-phase response coupled with long-lasting effects on body temperature.

scholarly journals Reasons why hypoalbuminaemia may or may not appear in protein-energy malnutrition

1977 ◽  
Vol 38 (1) ◽  
pp. 115-126 ◽  
Author(s):  
W. A. Coward ◽  
R. G. Whitehead ◽  
P. G. Lunn
Keyword(s):  
Amino Acid ◽  
Dietary Restriction ◽  
Protein Energy Malnutrition ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Albumin Concentration ◽  
Plasma Albumin ◽  
Low Protein ◽  
Protein Energy ◽  
Plasma Albumin Concentration

1.Investigations have been carried out in experimentally-malnourished rats in an attempt to explain the reasons for the development of the two main forms of protein-energy malnutrition in children, kwashiorkor and marasmus.2.Isoenergetic diets with values for protein: energy (P:E) of 0.21 (control diet; C) 0.032 (low-protein diet; LP) and 0.005 (very-low-protein diet; VLP) were fed to groups of twenty-six rats either ad lib. or in restricted amounts from 5 weeks of age. Rats were killed at the start of the experiment and 1, 2 and 3 or 4 weeks later. Estimations were made of plasma albumin, insulin, corticosterone and amino acid concentrations and of the total protein content of the gastrocnemius muscles and liver.3.Rats given diet LP ad lib. gained weight slowly and by week 1 plasma albumin concentration was slightly reduced. Rats given diet VLP ad lib. gradually lost weight and plasma albumin concentrations decreased continuously.4.In contrast the major effect of dietary restriction during the first 2 weeks of the experiment was to maintain plasma albumin concentrations at normal values, irrespective of the diet given.5.At later stages, however, when the ‘restricted’ animals had become very severely wasted, albumin concentrations decreased rapidly to values approaching those found in rats given diet VLP ad lib.6.When diets LP and VLP were given ad lib. body protein was proportionally distributed in favour of muscle rather than liver. For ‘restricted’ rats the reverse was true, at least up to the time when plasma albumin concentration began to decrease.7.Plasma corticosterone concentrations increased and insulin concentrations decreased when diets LP and VLP were fed in both an ad lib. and a ‘restricted’ regimen but the effects were significantly greater in the latter situation.8.Ad lib. feeding of diets LP and VLP produced a distorted plasma amino acid pattern resembling that of kwashiorkor, but although dietary restriction resulted in a decrease in total amino acid concentration, the plasma concentration ratio, non-essential amino acids:essential amino acids was virtually unaffected.9.It was concluded that whilst the lower the protein concentration in the diet the greater is the extent of hypoalbuminaemia which develops, dietary restriction with an increase in plasma glucocorticoid concentration and body-wasting can initially delay the development of the hypoalbuminaemia. However, in the final stages of wasting which ensue, low plasma albumin concentrations can appear because of a failure of the mechanisms which had earlier been able to preserve them at normal levels. It is possible that these two separate and distinct routes to hypoalbuminaemia observed in this study may have parallels in human situations in developing countries.

scholarly journals Pancreatic islet insulin secretion and metabolism in adult rats malnourished during neonatal life

2002 ◽  
Vol 87 (2) ◽  
pp. 147-155 ◽  
Author(s):  
Francisco B. Barbosa ◽  
Kirsten Capito ◽  
Hans Kofod ◽  
Peter Thams
Keyword(s):  
Insulin Secretion ◽  
Control Diet ◽  
Phospholipase A ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Lactation Period ◽  
Adult Rats ◽  
Glycerophosphate Dehydrogenase ◽  
Low Protein ◽  
Protein Group

Pancreatic islets were isolated from rats that had been nursed by dams fed with a control or an 8·7 % protein diet during the first 12 d of the lactation period. Glucose-induced insulin secretion from islets in the 8·7 % protein group was reduced 50 %. The islet insulin and DNA content were similar, whereas the pancreatic insulin content was reduced by 30 % in the rats fed 8·7 % protein. In order to elucidate the mechanism responsible for the attenuation of insulin secretion, measurements were performed of the activity of several islet enzymes that had previously been supposed to be involved in the coupling of glucose stimulation to insulin secretion. Islet glucose oxidation was unaffected, but glucose-stimulated hydrolysis of phosphatidylinositol was reduced by one-third in the islets of rats fed 8·7 % protein. The activity of mitochondrial glycerophosphate dehydrogenase was similar in islets of rats fed the 8·7 % protein diet and those fed the control diet. The activity of Ca-independent phospholipase A2was increased fourfold in the islets of rats fed 8·7 % protein. It is concluded that impairment of glucose-induced insulin secretion in rats fed a low-protein diet may be caused by attenuation of islet phosphatidylinositol hydrolysis, and it is tentatively suggested that the increased activity of Ca-independent phospholipase A2in islets of rats fed a low-protein diet may participate in the stimulation of apoptosis.

Green tea extract intake during lactation modified cardiac macrophage infiltration and AMP-activated protein kinase phosphorylation in weanling rats from undernourished mother during gestation and lactation

2016 ◽  
Vol 8 (2) ◽  
pp. 178-187 ◽  
Author(s):  
E. Matsumoto ◽  
S. Kataoka ◽  
Y. Mukai ◽  
M. Sato ◽  
S. Sato
Keyword(s):  
Protein Kinase ◽  
Green Tea ◽  
Control Diet ◽  
Protein Restriction ◽  
Protein Diet ◽  
Macrophage Infiltration ◽  
Low Protein Diet ◽  
Low Protein ◽  
Tea Extract ◽  
Amp Activated Protein Kinase

Maternal dietary restriction is often associated with cardiovascular disease in offspring. The aim of this study was to investigate the effect of green tea extract (GTE) intake during lactation on macrophage infiltration, and activation of adenosine monophosphate (AMP)-activated protein kinase (AMPK) and serine-threonine kinase Akt (Akt) in the hearts of weanlings exposed to maternal dietary protein restriction. Pregnant Wistar rats were fed control (C) or low-protein diets (LP) throughout gestation. Following delivery, the dams received a control or a GTE-containing control diet during lactation: control diet during gestation and lactation (CC), low-protein diet during gestation and lactation (LPC), low-protein diet during gestation and 0.12% GTE-containing low-protein diet during lactation (LPL), and low-protein diet during gestation and 0.24% GTE-containing low-protein diet during lactation (LPH). The female offspring were sacrificed at day 22. Biochemical parameters in the plasma, macrophage infiltration, degree of fibrosis and expression levels of AMPK and Akt were examined. The plasma insulin level increased in LPH compared with LPC. Percentage of the fibrotic areas and the number of macrophages in LPC were higher than those in CC. Conversely, the fibrotic areas and the macrophage number in LPH were smaller (21 and 56%, respectively) than those in LPC. The levels of phosphorylated AMPK in LPL and LPH, and Akt in LPH were greater than those in LPC. In conclusion, maternal protein restriction may induce macrophage infiltration and the decrease of insulin levels. However, GTE intake during lactation may suppress macrophage infiltration and restore insulin secretion function via upregulation of AMPK and insulin signaling in weanlings.

Hypoproteinemia and recovery from edema in dogs

1988 ◽  
Vol 254 (6) ◽  
pp. F887-F894
Author(s):  
J. A. Joles ◽  
H. A. Koomans ◽  
W. Kortlandt ◽  
P. Boer ◽  
E. J. Dorhout Mees
Keyword(s):  
Plasma Protein ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Recovery Period ◽  
Plasma Renin ◽  
Colloid Osmotic Pressure ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Sodium Balance ◽  
Low Protein

We studied the effects of hypoproteinemia following 12 days of repeated plasmapheresis and low-protein diet on sodium balance, fluid volumes, and renal hemodynamics in six conscious dogs on 50 mmol sodium intake. Measurements during hypoproteinemia were obtained during a 5-day recovery period starting 20 h after the final plasmapheresis session, with continued low-protein diet. During the plasmapheresis period sodium was retained. Sodium balance became negative on the first recovery day when plasma protein was 29 +/- 1 g/l (control 60 +/- 2 g/l, P less than 0.01), and plasma colloid osmotic pressure (COP) was 9 +/- 1 mmHg (control 22 +/- 1 mmHg, P less than 0.01). Subcutaneous fluid COP was lowered from 14 +/- 1 to 4 +/- 1 mmHg (P less than 0.01). Blood volume, plasma renin activity, and aldosterone were unchanged. Glomerular filtration rate and effective renal plasma flow were slightly reduced (NS), and filtration fraction was unchanged. After a second plasmapheresis period in three of the dogs, plasma protein fell to 26 +/- 1 g/l and COP to 7 +/- 1 mmHg. Now sodium was retained on the first day after stopping plasmapheresis, and renin and aldosterone were high. The next day, when plasma protein was again 29 +/- 1 g/l and COP 8 +/- 1 mmHg, these three dogs were able to completely excrete an infusion of 130 mmol sodium. These data suggest that the level of plasma COP below which dogs on a medium-sodium intake would retain sodium averages 8 mmHg, which is considerably lower than generally thought.

Increased NaCl preference of rats fed low-protein diet

1996 ◽  
Vol 270 (6) ◽  
pp. R1189-R1196 ◽  
Author(s):  
A. Okiyama ◽  
K. Torii ◽  
M. G. Tordoff
Keyword(s):  
Control Diet ◽  
Physiological Mechanism ◽  
Plasma Renin ◽  
Calcium Deficiency ◽  
Protein Deficiency ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Sodium Balance ◽  
Deficient Diet ◽  
Low Protein

Four studies were conducted to assess the effect of a low-protein diet on NaCl intake. Young rats fed either control (20% casein) or low-protein (5% casein) high-carbohydrate (CHO) diet were allowed to drink either water alone or water and 300 mM NaCl. Relative to rats fed control diet, rats fed the low-protein diet progressively increased NaCl intake so that, despite lower food and water intakes, they drank 180% more NaCl during the last 3 days of the 21-day test. Additional studies found that rats fed low-protein diet always maintained positive sodium balance, were neither sodium depleted nor hypovolemic, and had normal plasma renin activity and aldosterone concentrations. The elevated NaCl intake was not secondary to calcium deficiency and was unaffected by mineral supplementation of the protein-deficient diet. Increases in the diet's CH and/or fat content incidental to decreases in its protein content influenced, but could not completely account for, the effect of protein deficiency on NaCl intake. We conclude that protein deficiency is the primary cause of the elevated NaCl preference produced by being fed a low-protein diet and that a novel physiological mechanism underlies this behavior.

Development of β-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy

2002 ◽  
Vol 283 (3) ◽  
pp. R623-R630 ◽  
Author(s):  
Eric Bertin ◽  
Marie-Noëlle Gangnerau ◽  
Georges Bellon ◽  
Danièle Bailbé ◽  
Annick Arbelot De Vacqueur ◽  
...  
Keyword(s):  
Control Diet ◽  
Cell Mass ◽  
Energy Restriction ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Restricted Diet ◽  
Β Cell ◽  
Fetal Plasma ◽  
Low Protein

Fetal malnutrition is now proposed as a risk factor of later obesity and type II diabetes. We previously analyzed the long-term impact of reduced protein and/or energy intake strictly limited to the last week of pregnancy in Wistar rats. Three protocols of gestational malnutrition were used: 1) low-protein isocaloric diet (5 instead of 15%) with pair feeding to the mothers receiving the control diet, 2) restricted diet (50% of control diet), and 3) low protein-restricted diet (50% of low-protein diet). Only isolated protein restriction induced a long-term β-cell mass decrease. In the present study, we used the same protocols of food restriction to analyze their short-term impact (on day 21.5 of pregnancy) on β-cell mass development. A 50% β-cell mass decrease was present in the three restricted groups, but low-protein diet, either associated or not to energy restriction, increased fetal β-cell insulin content. Among all the parameters analyzed to further explain our results, we found that the fetal plasma level of taurine was lowered by low-protein diet and was the main predictor of the fetal plasma insulin level ( r = 0.63, P < 0.01). In conclusion, rat fetuses exposed to protein and/or energy restriction during the third part of pregnancy have a similar dramatic decrease in β-cell mass, and their ability to recover β-cell mass development retardation depends on the type of malnutrition used. Moreover, our results support the hypothesis that taurine might play an important role in fetal β-cell mass function.

THE EFFECT OF PARATHION ON THE LIVER AND KIDNEY CARBOXYLESTERASES AND THE PLASMA ACETYLCHOLINESTERASES OF RATS FED NUTRITIONALLY DEFICIENT DIETS

1966 ◽  
Vol 44 (6) ◽  
pp. 809-817 ◽  
Author(s):  
Sheila I. Read ◽  
E. J. Middleton ◽  
W. P. Mckinley
Keyword(s):  
Control Diet ◽  
Acetylcholinesterase Activity ◽  
Protein Diet ◽  
Female Rats ◽  
Male Rats ◽  
Low Protein Diet ◽  
Male And Female ◽  
Low Protein ◽  
Male And Female Rats ◽  
Liver And Kidney

Female rats were fed diets low in minerals, vitamins, or protein, or a control diet, both alone and supplemented with 10 parts per million (p.p.m.) parathion for 3 weeks. Male and female rats were fed control and tow-vitamin diets both with and without parathion supplementation (0–10 p.p.m.) for 3 weeks. The liver and kidney carboxylesterases (EC 3.1.1.1.), and the plasma acetylcholinesterases (EC 3.1.1.7.) of the male rats, were measured.In the female rats, a low-mineral diet resulted in an increase of carboxylesterases in the liver and kidney; a low-vitamin diet caused a marked increase in liver carboxylesterases but had no effect on the carboxylesterases of the kidney. Parathion at 10 p.p.m. in all diets greatly reduced the liver carboxylesterases but had less effect on kidney carboxylesterases, except in the case of the low-protein diet, for which the reduction was similar to that in the liver. Varying amounts of parathion added to the low-vitamin diet reduced the liver and kidney carboxylesterases, but to a less extent than when added to the control diet.The liver carboxylesterases of male rats were inhibited approximately 50% by 2 p.p.m. parathion in the control diet and by 4 p.p.m. parathion in the low-vitamin diet. However, inhibition of plasma acetylcholinesterase and kidney carboxylesterases was not marked until the 10 p.p.m. parathion level was fed. The acetylcholinesterase activity of the plasma of male rats did not decrease until the level of liver carboxylesterases was very low.

Weanling Rats Exposed to Maternal Low-Protein Diets during Discrete Periods of Gestation Exhibit Differing Severity of Hypertension

1996 ◽  
Vol 91 (5) ◽  
pp. 607-615 ◽  
Author(s):  
Simon C. Langley-Evans ◽  
Simon J. M. Welham ◽  
Rachel C. Sherman ◽  
Alan A. Jackson
Keyword(s):  
Blood Pressure ◽  
Control Diet ◽  
Plasma Renin ◽  
Late Gestation ◽  
Protein Diet ◽  
Male Rats ◽  
Low Protein Diet ◽  
Fetal Exposure ◽  
Low Protein ◽  
Protein Diets

1. In the rat, hypertension is induced by fetal exposure to maternal low-protein diets. The effect on blood pressure of undernutrition before conception and during discrete periods in early, mid or late pregnancy was assessed using an 18% casein (control) diet and a 9% casein diet to apply mild protein restriction. 2. The offspring of rats fed 9% casein developed raised blood pressure by weaning age. Feeding a low-protein diet before conception was not a prerequisite for programming of hypertension. 3. Hypertension was observed in rats exposed to low protein during the following gestational periods: days 0–7, days 8–14 and days 15–22. Blood pressure increases elicited by these discrete periods of undernutrition were lower than those induced by feeding a low-protein diet throughout pregnancy. The effect in early gestation was significant only in male animals. Post-natal growth of male rats exposed to low-protein diets was accelerated, but kidneys were small in relation to body weight. 4. Biochemical indices of glucocorticoid action in liver, hippocampus, hypothalamus and lung were elevated in rats exposed to low-protein diets in utero. The apparent hypersensitivity to glucocorticoids was primarily associated with undernutrition in mid to late gestation. 5. Plasma renin activity was elevated in rats exposed to 9% casein over days 15–22 of gestation. Animals undernourished over days 0–7 and 8–14 produced pups with lower plasma angiotensin II concentrations at weaning. 6. Fetal exposure to maternal low-protein diets for any period in gestation may programme hypertension in the rat. Alterations to renal structure, renal hormone action or the hypothalamic—pituitary-adrenal axis may all play a role in the programming phenomenon, either independently or in concert.

A Maternal Low-protein Diet during Gestation Induces Hepatic Autophagy-related Gene Expression in a Sex-specific Manner in Sprague-Dawley Rats

2021 ◽  
pp. 1-29
Author(s):  
Mingzhu Cai ◽  
Jie Zhang ◽  
Hong Chen ◽  
Yuan-Xiang Pan
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Control Diet ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Related Gene ◽  
Sprague Dawley ◽  
Protein Levels ◽  
Low Protein ◽  
Sprague Dawley Rats

Abstract This study investigates the mechanism by which maternal protein restriction induces hepatic autophagy-related gene expression in the offspring of rats. Pregnant Sprague-Dawley rats were fed either a control diet (C, 18% energy from protein) or a low-protein diet (LP, 8.5% energy from protein) during gestation, followed by the control diet during lactation and post-weaning. Liver tissue was collected from the offspring at postnatal day 38 and divided into four groups according to sex and maternal diet (F-C, F-LP, M-C, and M-LP) for further analysis. Autophagy-related mRNA and protein levels were determined by real-time PCR and Western blotting, respectively. In addition, chromatin immunoprecipitation (ChIP) was performed to investigate the interactions between transcription factors and autophagy-related genes. Protein levels of p-eIF2a and ATF4 were increased only in the female offspring born to dams fed the LP diet. Correlatively, the mRNA expression of hepatic autophagy-related genes including Map1lc3b, P62/Sqstm1, Becn1, Atg3, Atg7, and Atg10 was significantly greater in the F-LP group than in the F-C group. Furthermore, ChIP results showed greater ATF4 and C/EBP homology protein (CHOP) binding at the regions of a set of autophagy-related genes in the F-LP group than in the F-C group. Our data demonstrated that a maternal LP diet transcriptionally programmed hepatic autophagy-related gene expression only in female rat offspring. This transcriptional program involved the activation of the eIF2α/ATF4 pathway and intricate regulation by transcription factors ATF4 and CHOP.

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