EFFECTS OF N-METHYLAMINOETHANOL, AND N,N-DIMETHYL-AMINOETHANOL IN THE DIET OF PREGNANT RATS ON NEONATAL RAT BRAIN CHOLINERGIC AND PHOSPHOLIPID PROFILE

Abstract— Pregnant rats were fed for 15 days predelivery until 15 days postpartum a choline (Ch)-deficient diet (CD diet) or a CD diet supplemented with 0.8% Ch-CI (CS), 1% N -methylaminoethanol (MME) or 1% N,N -dimethylaminoethanol (DME). Gestation and parturition of the pregnant rats proceeded normally. However, all the pups born of dams fed the MME diet, and most of those born of dams fed the DME diet, died within 36 h of birth. No histological or cytological alterations were detected in the brain of the pups. Levels of Ch and acetylcholine (ACh) were elevated in the brain of pups born of dams fed the MME and DME diets, but not the CS diet. The content of total phospholipids in the brain of the pups was not altered by the diet fed to the dams. However, the phosphatidyl-Ch and phosphatidylaminoethanol (PAE) contents in the brain of the MME- and DME-exposed pups were markedly reduced. At the same time, significant amounts of DME, phosphatidyl-N-monomethylaminoethanol (PMME) and of phosphatidyl- N,N -dimethylaminoethanol (PDME) were present in the same brain areas. These results are evaluated and discussed in terms of providing a cause for the death of the MME- and DME-exposed neonatal rats.     

EFFECTS OF LYSINE AND THREONINE FORTIFICATION OF BREAD DURING GESTATION AND LACTATION ON OFFSPRING BRAIN LIPID DEVELOPMENT

Abstract– Offspring brain lipid development has been studied following the amino acid fortification of wheat diet fed to pregnant and lactating rats. Comparisons are made with a 13% casein diet which contains a similar quantity of protein of known high quality, with a 26% casein diet, and with a standard laboratory diet. Increased maternal energy intake was found, particularly during lactation, with protein quality improvement. Offspring of mothers receiving the unsupplemented bread diet had lower total brain cholesterol, phospholipid, cerebroside-sulfatide, and (for 4 of the 5 other diets) ganglioside-NANA levels in comparison to offspring whose mothers received the other diets. Brain cerebroside-sulfatide and cholesterol concentrations were also lower in the offspring whose mothers received the unsupplemented bread, suggesting impaired myelin formation. Phospholipid and ganglioside-NANA concentrations were not lower. Fortification of the bread diet with lysine resulted in increases in both the total levels and concentrations of cerebroside-sulfatide and cholesterol. When both lysine and threonine were added, the cerebroside-sulfatide and cholesterol levels and concentrations were similar to or greater than values for the two casein diets and the standard laboratory diet. The 26% casein diet did not result in higher lipid values than obtained with the 13% casein diet. This study demonstrates the adequacy of amino acid supplementation of a maternal cereal protein diet in allowing normal offspring brain lipid development.     

L-histidine induced changes in adenosine 3':5'-monophosphate levels in rat brain and amounts of apo-, holo-a and holo-b fatty acid synthetases in rat liver.

When fasted rats were fed a chow or fat-free diet supplemented 5% with L-histidine for three days, the brain adenosine 3′:5′-monophosphate (cAMP) level increased. A 50% increase occurred in rats fed a chow diet and 20% increase in rats fed a fat-free diet. Purification of liver fatty acid synthetase and the isolation of liver apo-, holo-$\text{a}$ and holo-$\text{b}$ fatty acid synthetases demonstrated that L-histidine feeding caused changes in the relative amounts of these enzymes. Apo- and holo-$\text{b}$ fatty acid synthetases increased while the holo-$\text{a}$ form simultaneously decreased. This effect was observed in rats fed either chow or fat-free diets supplemented with L-histidine.     

Protein-energy malnutrition during pregnancy alters caffeine's effect on brain tissue of neonate rats

We studied whether protein-energy malnutrition changed brain susceptibility to a small dose of caffeine in newborn rats. Since we had demonstrated previously that caffeine intake during lactation increased the brain neuropeptide on newborns, we investigated further the effects of the prenatal administration of caffeine on TRH and cyclo (His-Pro). From day 13 of gestation to delivery day, pregnant rats in one group were fed either a 20% or a 6% protein diet ad libitum, and those in the other group were pair-fed with each protein diet supplemented with caffeine at an effective dose of 2 mg/100 g body weight. Upon delivery, brain weight, brain protein, RNA, DNA and the neuropeptides thyrotropin-releasing hormone (TRH) and cyclo (His-Pro) were measured in the newborn rats. A 6% protein without caffeine diet caused reductions in brain weights and brain protein, RNA and DNA contents, but did not alter brain TRH and cyclo (His-Pro) concentrations in the newborn animals. In the offspring from dams fed a 6% protein diet, caffeine administration significantly elevated brain weights and brain contents of protein, RNA and DNA. In contrast, these values were similar between noncaffeine and caffeine-supplemented animals in a 20% protein diet group. Brain TRH and cyclo (His-Pro) concentrations were not changed by caffeine administration. These data suggest that caffeine augments protein synthesis in the newborn rat brain when malnourished, but that the same dose of caffeine did not affect protein synthesis in brains of newborn rats from normally nourished dams. Therefore, the present findings indicate that the nutritional status of mothers during pregnancy has important implication in the impact of caffeine on their offspring's brains.     

EFFECTS OF DIFFERENT LEVELS OF DIETARY PROTEIN ON BRAIN GLUTAMATE DEHYDROGENASE AND DECARBOXYLASE IN YOUNG ALBINO RATS

Abstract— Studies were carried out to identify the minimum levels of protein (casein) needed in the diet in order to prevent or reverse the deficits in brain enzymes previously found with protein deficiency. Groups of weanling albino rats were fed diets containing variable amounts of protein (5, 8, 10, 15 or 20 per cent in experiment I, and 5, 6, 7, 8 or 20 per cent in experiment II) for 5 or 10 weeks. Deficits in brain wt and brain glutamate dehydrogenase and decarboxylase were found to be prevented by a diet containing 8 per cent or more of protein, although for optimum growth 15 per cent protein in the diet was found to be necessary. Groups of rats were fed a 5 or 20% protein diet for 10 weeks after which the 5% protein animals were either continued on the diet for another 10 weeks or changed to one containing 8, 10, 15 or 20% protein. The brain enzyme deficits found with the 5% protein diet were found to be fully reversed by feeding a 10% protein diet during rehabilitation.     

Studies on limiting essential amino acids in grieves as source of dietary protein for rainbow trout (oncorhynchus mykiss)

Diets were computed to contain equal concentrations of digestible crude protein either of wheat gluten (diet 1) or of grieves (diets 2–8). Per kg dry diet, 41 g crystalline amino acids were supplemented. All diets contained at least 1.2 g Lys per MJ digestible energy (DE). In diet 2, ratios of Met + Cys, Trp, Leu, Ile and Phe to Lys were about equal to those in diet 1. In each of diets 3–7, one of the respective amino acids, in diet 8 all five were replaced by Glu in the supplemented mixture of amino acids.

Each diet was fed to triplciate groups of 20 trout during a trial lasting 66 days. Trout fed the diet containing wheat gluten consumed more dry matter and showed higher growth rates as well as higher protein contents in their gained body mass than trout fed diets based on grieves. Supplementing Met plus Trp significantly improved dry matter intake, growth rate and protein content of gain, though not to the level of trout fed the wheat gluten diet, whereas Leu, Ile and Phe showed no such effect. When grieves were not supplemented with both Met and Trp, gain in body mass contained significantly more lipids. DE required per kg gain by trout fed wheat gluten, grieves + Met + Trp or grieves without supplementation of Met and Trp was 20.1, 21.2 and 29.9 MJ, respectively.     

Dietary iron and the integrity of the developing rat brain: a study with the artificially-reared rat pup.

Inadequate iron nutrition is thought to affect many aspects of brain development. Iron is a component of enzyme systems in DNA synthesis, the respiratory chain, neurotransmitter and lipid metabolism. The iron content of the striatum increases post-natally, with neuronal differentiation, myelin lipid and receptor formation: Seventy percent of the iron in the brain is associated with myelin. In an attempt to dissociate the global effects of under-and/or malnutrition and to produce exclusively an iron deficiency, we have used the gastrostomy-reared rat pup fed milk substitutes which vary only in their iron content. To ensure the pups did not have adequate iron reserves at birth, dams were fed a meal diet of low iron content (3 ppm) throughout gestation. The pups were then artificially reared on milk with (43 ppm), and without added iron (2.5 ppm) from 6 up to 21 days after birth. At 21 days of age, body weights of iron deficient pups were about 90% those of control animals. At 21 days of age, the pups were weaned, then fed standard laboratory rat chow. Brain was examined at 42 days of age (for young adults) and up to 6 months of age (180 days as mature adults). Morphometric analysis of sagittal sections of the cerebellum at 21 and 63 days of age revealed a deficit in white matter formation in pups fed low-iron at 21 days of age when compared to controls. This deficit was partially recouped by age 63 days. By contrast, animals fed milk supplemented with iron showed greater definition in white matter formation than controls at 21 days of age; indicative of precocious maturation of the white matter tracts. Our findings indicate that iron deficiency, without under/mal-nutrition and other variables, does not result in extensive growth deficits in body and brain weight. However, the iron status profoundly influences the development of myelination in that the process is delayed in iron deficiency.     

Body weight deficit in the absence of reduction in cerebrum weight and nucleic acid content in progeny of swine restricted in protein intake during pregnancy

Fifty-six castrated male progeny of crossbred (Chester White x Landrace x Large White x Yorkshire) dams fed an adequate diet (control, C), a control diet fed at one-third of C (restricted, R), or diets severely deficient in protein (PF) or restricted in nonprotein calories (RCal) were killed at age 25 weeks. Dams were fed their respective diets in the following regimens: C, 1.8 kg (6000 kcal daily) throughout pregnancy; R, 0.6 kg of C diet daily for 70 days, then 1.8 kg of C daily to parturition at about 114 days; PF, 1.8 kg of a "protein-free" diet (less than 0.2% protein) throughout pregnancy; RCal, 0.6 kg daily (2000 kcal) of a diet containing three times the concentration of protein, minerals, and vitamins provided by the C diet for 70 days, then 1.8 kg of C daily to parturition. All dams were fed an adequate diet ad libitum through a 28-day lactation. Castrated male progeny were assigned to one of two replicates based on birth date and fed a corn-soybean meal diet ad libitum from weaning to age 25 weeks, supplemented from age 10 to 12 weeks with 0, 110, or 220 mg/kg of thyroprotein (iodinated casein). Cerebrum weight was unaffected by maternal diet, despite a significant (P less than 0.001) reduction in body weight of progeny of PF dams compared with other groups, resulting in a higher relative cerebrum weight in progeny of PF dams than in progeny of C, R, and RCal dams. Absolute and relative weights of RNA, DNA, and total protein in cerebrum were unaffected by maternal diet. Thyroprotein supplementation to the diet of the progeny had no effect on cerebrum weight or its protein or nucleic acid content. It is concluded that maternal protein deprivation but not restriction of feed or nonprotein calorie intake to one-third of recommended allowance during gestation results in stunting of body weight in young adult progeny but does not affect cerebrum weight, cerebrum cell number (DNA), or protein synthetic activity (RNA), or RNA-to-protein ratio.     

EFFECTS OF DIETARY PROTEINS ON FETAL BRAIN PROTEIN AND GLUTAMIC ACID METABOLISM IN RAT

Abstract— The effects of feeding dietary wheat and Bengal gram proteins to pregnant rats on brain protein and glutamic acid metabolism in 15-, 17- and 19-day fetuses were investigated. Wheat and Bengal gram diets resulted in loss of brain weight with decreased DNA, RNA, protein, free x amino N and deficits in the activities of brain glutamine synthetase, glutaminase I. glutaminase II and glutamate decarboxylase at all the gestational ages studied without any change in glutamine transferase activity. The concentrations of the amino acids alanine, glutamic acid, glutamine and GABA were found to be significantly lower on wheat and Bengal gram diets than the control on a 10% casein diet. The wheat with lysine and Bengal gram with methionine, cystine and tryptophan resulted in similar mean values of all the characteristics studied to the mean values observed in rats on the control diet. However, glutaminase I activity remained significantly low on lysine fortified wheat diet, and aspartic acid content was found to increase on both fortified and unfortified wheat and Bengal gram diets. A 20% casein diet showed increased brain weight, DNA. RNA. protein and free x amino N concentrations as compared with the 10% casein diet, while the other parameters remained unchanged.     

High-unsaturated-fat, high-protein, and low-carbohydrate diet during pregnancy and lactation modulates hepatic lipid metabolism in female adult offspring

Whether a high-unsaturated-fat, high-protein (HFP), and low-carbohydrate (CHO) diet during gestation has long-lasting beneficial effects on lipid metabolism in the offspring was investigated using a mouse model. Female mice were fed either a standard (CHO rich) chow diet or a CHO HFP diet, before and during gestation and lactation. All offspring were weaned onto the same chow until adulthood. Although liver cholesterol concentration and fasting plasma triglyceride (TG), cholesterol, and free fatty acid concentrations were not affected in either male or female HFP offspring, hepatic TG concentration was reduced by approximately 51% (P < 0.05) in the female adult offspring from dams on the HFP diet, compared with females from dams on the chow diet (a trend toward reduced TG concentration was also observed in the male). Furthermore, hepatic protein levels for CD36, carnitine palmitoyltransferase-1 (CPT-1), and peroxisomal proliferator activated receptor-alpha (PPAR-alpha) were increased by approximately 46% (P < 0.001), approximately 52% (P < 0.001), and approximately 14% (P = 0.035), respectively, in the female HFP offspring. Liver TG levels were negatively correlated with protein levels of CD 36 (r = -0.69, P = 0.007), CPT-1 (r = -0.55, P = 0.033), and PPAR-alpha (r = -0.57, P = 0.025) in these offspring. In conclusion, a maternal HFP diet during gestation and lactation reduces hepatic TG concentration in female offspring, which is linked with increased protein levels in fatty acid oxidation.     

Effect of dietary caffeine and zinc on the activity of antioxidant enzymes,zinc, and copper concentration of the heart and liver in fast-growing rats

The purpose of this study was to determine the relationship between concentrations of Zn and Cu and the activities of superoxide dismutase and glutathione peroxidase in the heart and liver of young rat pups whose dams were fed a diet supplemented with caffeine and/or Zn. Four groups of dams with their newborn pups were fed one of the following diets for 22 d: 20% protein basal diet; the basal diet supplemented with caffeine (2 mg/100 body wt); the basal diet supplemented with Zn (300 mg/kg diet); or the basal diet supplemented with caffeine plus Zn. The Cu levels in the livers of the pups were decreased by maternal intake of the caffeine and Zn diet. The maternal intake of the caffeine diet increased Mn-superoxide dismutase (MnSOD) activity and Cu, Zn-superoxide dismutase (CUZnSOD) in the heart of the pups. On the other hand, the activity of Cu,ZnSOD was significantly reduced in the liver of pups whose dams consumed a caffeine, Zn, or caffeine plus Zn diet. Cu, ZnSOD activity in the liver of the pups seems to be correlated with Cu levels in the tissue. Selenium-dependent glutathione peroxidase (GSH-Px) activities in the heart and liver showed no difference among the groups. The effect of dietary caffeine and/or Zn on the activity of antioxidant enzymes in the heart and liver were different in young rats. The activities of these enzymes in the heart were lower than in the liver of 22-d-old rats. Our experiments indicate that the heart has limited defenses against the toxic effects of peroxides when compared to the liver.     

Influences of maternal caffeine on the neonatal rat brains vary with the nutritional states

The potential effect of maternal caffeine ingestion upon total brain protein and the concentration of two prototype neuropeptides, thyrotropin-releasing hormone (TRH) and its derivative, cyclo (His-Pro) in neonates was examined during the nursing period in the context of variable maternal protein intake. Maternal caffeine intake (2 mg/100 g body weight) significantly increased the total brain protein of neonates derived from dams fed a 6% casein diet, but not from dams fed a 12%- or 20%-casein diet. Maternal caffeine consumption significantly increased the amount of cyclo (His-Pro) in the neonatal brains in all groups. The percent increments in pups from dams fed 6%, 12%, and 20% casein diets were respectively 137%, 131%, and 120%. By contrast, no significant alterations were observed in TRH concentrations between caffeine and control groups. It is concluded that maternal caffeine can influence neonatal brain protein and cyclo (His-Pro) during nursing under conditions of protein-energy malnutrition.     

Effects of postnatal protein undernutrition on myelination in rat brain

Pups were subjected, from birth, to protein undernutrition by feeding the lactating dams 8% casein (CS) or 8% soy protein (SP) diet up to weaning; the weanlings were fed the same diets until 6 weeks of age. At 3 and 6 weeks of age, myelin was isolated from the brains and characterized. The quantities of myelin and its content of cholesterol, galactolipids and phospholipids, were significantly depressed in the 8% CS and 8% SP groups but not when soy protein was fed at the same level as casein (25%) in the control. Furthermore, the severity of the deficits in myelination showed a differential pattern depending on the type of dietary protein fed. At weaning, the deficits with the 8% SP diet were 1.5-2.0-times greater than with the corresponding casein diet. A more pronounced retardation in the initiation, progression and capacity of myelination in postnatal soy protein undernutrition was indicated.     

Phospholipid supplementation reverses behavioral and biochemical alterations induced by n-3 polyunsaturated fatty acid deficiency in mice

This study investigated the effects of a diet deficient in alpha-linolenic acid followed or not by supplementation with phospholipids rich in n-3 polyunsaturated fatty acids (PUFA) on behavior and phospholipid fatty acid composition in selected brain regions. Three weeks before mating, two groups of mice were fed a semisynthetic diet containing both linoleic and alpha-linolenic acid or a diet deficient in alpha-linolenic acid. Pups were fed the same diet as their dams. At the age of 7 weeks, a part of the deficient group was supplemented with n-3 PUFA from either egg yolk or pig brain phospholipids for 2 months. In the open field, rearing activity was significantly reduced in the deficient group. In the elevated plus maze (anxiety protocol), the time spent on open arms was significantly smaller in deficient mice than in controls. Using the learning protocol with the same task, the alpha-linolenic acid deficiency induced a learning deficit. Rearing activity and learning deficits were completely restored by supplementation with egg yolk or cerebral phospholipids, though the level of anxiety remained significantly higher than that of controls. There were no differences among the 4 diet groups for either the Morris water maze or passive avoidance. In control mice, the level of 22:6 n-3 was significantly higher in the frontal cortex compared to all other regions analysed. The frontal cortex and the striatum were the most markedly affected by the deficiency. Supplementation with phospholipids restored normal fatty acid composition in brain regions except for frontal cortex. Egg yolk or cerebral phospholipids are an effective source of n-3 PUFA for reversing behavioral changes and altered fatty acid composition induced by a diet deficient in n-3 PUFA.     

Supplementation of orotic acid to the casein, but not to egg protein, soy protein, or wheat gluten diets, increases serum ornithine carbamoyltransferase activity

Effects of dietary supplementation of orotic acid to a diet containing the casein protein were compared with diets containing egg protein, soy protein, or wheat gluten on lipid levels in the liver and serum and activities of ornithine carbamoyltransferase (OCT) and alanine aminotransferase in the serum of rats. We found that supplementation of orotic acid to each diet increased the contents of the liver total lipids, triacylglycerol, and phospholipids compared with those not supplemented. The contents of liver total lipids, triacylglycerol, cholesterol, and phospholipids in rats fed the casein diet were significantly higher than those of rats fed the other three diets when orotic acid was supplemented. The levels of triacylglycerol, cholesterol, and phospholipids in the serum of rats fed the casein diet were markedly decreased by addition of orotic acid. The supplementation of orotic acid significantly increased the activities of both serum OCT and alanine aminotransferase in rats fed the casein diet, but not in rats fed the other diets. In conclusion, liver lipid accumulation induced by dietary orotic acid depends on the type of dietary protein. The enhancement of serum OCT activity may result from liver lipid accumulation in rats fed the casein diet supplemented with orotic acid, demonstrating hepatic damage.     

A high cholesterol diet ameliorates renal tubular lesions in diabetic rats

These studies examine the effect of cholesterol feeding in normal rats and in rats with streptozotocin-induced diabetes mellitus. Four groups were studied: normal rats fed either a standard rat chow or a standard rat chow supplemented with cholesterol and diabetic rats fed standard chow or standard chow plus cholesterol. Diabetic rats fed a standard diet excreted more creatinine and urea in the urine, had higher levels of blood urea nitrogen, and lower serum albumin levels than rats fed standard diet plus cholesterol. Blood glucose levels were similar in the two groups; however, diabetic rats given cholesterol had a greater body weight at the end of the study than diabetic rats eating standard chow. Urine volumes and sodium and potassium excretion in the urine were greater in diabetic rats fed a standard diet than in those fed a high cholesterol diet. Diabetic rats fed a standard diet had distinctive renal lesions characterized by swelling of tubular epithelial cells with clearing of cytoplasm. The nephron segments involved by this striking vacuolar change were the distal convoluted tubule and the thick limbs of Henle's loop. These lesions were identical to those described by Armanni-Ebstein in severely glycosuric patients. These lesions were not observed in any of the animals of the other three groups (including diabetic rats fed a high cholesterol diet). Glomeruli were normal in animals of all groups. Thus, cholesterol administration prevents the development of the Armanni-Ebstein lesions in diabetic rats despite persistent hyperglycemia. The mechanism by which cholesterol administration prevents the accumulation of glycogen in distal tubule cells has not been elucidated. It is suggested that glycogen accumulation in distal tubular segments may explain the greater urine volumes, natriuresis, kaliuresis, and proteinuria observed in diabetic animals fed a standard diet when compared with rats fed the same diet plus cholesterol.     

L-histidine-induced suppression of lipogenic enzymes.

Diets supplemented 5% with L-histidine produce hypercholesterolemia and increase cholesterol biosynthesis in rat liver. We now report an $\text{inhibitory}$ effect of L-histidine on lipogenic enzymes in the liver. In this study, L-histidine was added to chow and fat-free diets and fed to rats for 18 days. After two days of fasting, the rats were refed the same diet for three days prior to sacrifice. L-histidine decreased fatty acid synthetase activity by 51% when it was added to the chow diet and by 26% when it was added to the fat-free diet. Isocitrate dehydrogenase activity was not altered significantly in rats fed diets supplemented with L-histidine.     

The effects of elk velvet antler consumption on the rat: development, behavior, toxicity and the activity of liver gamma-glutamyltranspeptidase

The effect of exposure to, followed by consumption of, a diet containing 10% powdered elk velvet antler (EVA) from the 18th day of gestation to the 88th day after birth was examined in male and female Fischer 344 rats. There were no teratogenic effects of EVA exposure in utero or differences in birth outcomes between pups born to regular chow fed and EVA chow fed dams. Growth curves of the EVA fed rats were identical to those of regular chow fed rats, as were developmental milestones of pinna development and eye-opening. Acoustical startle and righting reflexes, developmental and behavioral indices, were identical. Blood glucose levels were comparable in EVA chow fed and regular chow fed rats, indicating that EVA is without effect on glucose balance. There were no signs of toxicity in the EVA chow fed compared to regular chow fed rats as judged from plasma enzyme markers of liver damage: plasma levels of alanine aminotransferase were 50% lower in EVA chow fed rats compared to regular chow fed rats; and plasma levels of gamma-glutamyltranspeptidase (gammaGT) were the same. The activity of gammaGT displayed a decrease in the livers of EVA chow fed rats, more so in the male (22%) than in the female (14%), suggestive of an androgenic effect. A possible hepatobeneficial effect of the EVA induced decrease in liver gammaGT is discussed. In summary, dietary10% EVA chow is without long term effect on growth, development and behavior is non-toxic and may be hepatobeneficial.     

Maternal zinc deficiency reduces NMDA receptor expression in neonatal rat brain, which persists into early adulthood

Prenatal and early postnatal zinc deficiency impairs learning and memory and these deficits persist into adulthood. A key modulator in this process may be the NMDA receptor; however, effects of zinc deficiency on the regulation of NMDA receptor activity are not well understood. Female Sprague-Dawley rats were fed diets containing 7 (zinc deficient, ZD), 10 (marginally zinc deficient, MZD) or 25 (control) mg Zn/g diet preconception through postnatal day (PN) 20, at which time pups were weaned onto their maternal or control diet. Regulation of NMDA receptor expression was examined at PN2, PN11, and PN65. At PN2, expression of whole brain NMDA receptor subunits NR1, NR2A, and NR2B was lower in pups from dams fed ZD and MZD compared to controls, as analyzed using relative RT-PCR and immunoblotting. At PN11, whole brain and hippocampi NR1, NR2A, NR2B and PSA-NCAM (polysialic acid-neural cell adhesion molecule) expression and the number of PSA-NCAM immunoreactive cells were lower in pups from dams fed ZD compared to controls. Whole brain brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) concentrations were lower in pups from dams fed ZD or both low zinc diets, respectively. Whole brain NR1 expression remained lower in previously zinc-deficient rats at PN65. These data indicate potential mechanisms through which developmental zinc deficiency can impair learning and memory later in life.     

A comparative study of serum lipoproteins in rabbits fed a natural ingredient diet or low-fat, cholesterol-free, semipurified diets containing casein or isolated soy protein

In rabbits fed a cholesterol-free, semipurified diet containing isolated soy protein, the average total serum cholesterol level was similar to that of rabbits fed a natural ingredient (chow) diet. However, the cholesterol and protein levels in very low density (VLDL) and low density lipoproteins (LDL) tended to increase, while the levels in high density lipoproteins (HDL) were reduced to about half of those on the chow diet, with little change in the cholesterol to protein ratio. Substitution of casein for soy protein in the semipurified diet caused a four- to five-fold increase in total serum cholesterol and a doubling of lipoprotein protein, with an increase of 1.4- to 3.0-fold in the cholesterol to protein ratio of the different lipoprotein fractions. Analysis of the apoproteins (apo) of the plasma lipoproteins indicated that apo B, E, and C all tended to increase in the VLDL and LDL of rabbits fed the soy protein diet compared with those fed chow diet. The levels of each of the apoproteins were increased further by substituting casein for soy protein in the semipurified diet. In this case, apo E showed the greatest relative increase (2.7-fold) in VLDL, while apo B and E were increased to a similar extent (about 4-fold) in LDL. Apo C was approximately doubled in each of these fractions. The apo A content in HDL of rabbits fed the semipurified diets was about half that of rabbits fed chow diet. No marked changes were noted in the apo E or C content of HDL. Separation of isoforms of the soluble apoproteins showed variations between individual animals, but these variations seemed largely unrelated to diet. The results of these studies indicate that semipurified diets produce changes in the serum lipoprotein patterns of rabbits that are only partly due to the protein component of these diets.