Showing papers in "Nutritional Neuroscience in 2001"
TL;DR: Selenium will influence compounds with hormonal activity (and neurotransmitters) in the brain, and this is postulated to be the reason selenium affects moods in humans and behavior in animals.
Abstract: Similar to other tissues selenium from selenomethionine is deposited in the brain at higher concentrations than selenium in other forms Vitamin E has a greater effect than selenium in reducing lipid peroxidation in various brain regions Selenium does not have as great effect on glutathione peroxidase (GPX) activity in the brain as in most other organs Prolonged selenium and iodine deficiencies will compromise thyroid hormone homeostatus in the brain and this is due to changes in deiodinases activities and lipid peroxidation Even though selenium deficiency results in reduced GPX activity and selenium content in the brain, there is no reduction in thioredoxin reductase activity or selenoprotein W levels Selenoprotein P is taken up in greater amounts by the brain but not by other organs in selenium deficient animals, suggesting a critical function of this selenoprotein in this organ Selenium will influence compounds with hormonal activity (and neurotransmitters) in the brain, and this is postulated to be the reason selenium affects moods in humans and behavior in animals Even though selenium counteracts the neurotoxicity of mercury, cadmium, lead and vanadium, it causes them to accumulate in the brain, presumably in a nontoxic complex
150 citations
TL;DR: There was a significant improvement in “Quality of Memory” and the associated “Secondary memory” factor at all time points following 400 mg of Ginseng, and this represents the first demonstration of a modulation of mood and cognitive performance by acute administration of Ginsang.
Abstract: Recent evidence suggests that chronic administration of Ginseng can improve cognitive performance in animals and in humans. No previous study has examined the possibility of cognitive effects following single doses of Ginseng in healthy adults. The present study investigated whether acute administration of Ginseng (G115, Pharmaton SA) had any consistent effect on mood and four aspects of cognitive performance ("Quality of Memory", "Speed of Memory", "Quality of Attention" and "Speed of Attention") that can be derived by factor analysis of the Cognitive Drug Research computerised assessment battery. The study followed a placebo-controlled, double-blind, balanced, crossover design. Twenty healthy young adult volunteers received 200, 400, and 600 mg of G115, and a matching placebo, in counterbalanced order, with a 7 day wash-out period between treatments. Following a baseline cognitive assessment, further test sessions took place 1, 2.5, 4 and 6 h after the day's treatment. The most striking result was a significant improvement in "Quality of Memory" and the associated "Secondary Memory" factor at all time points following 400 mg of Ginseng. Both the 200 and 600 mg doses were associated with a significant decrement of the "Speed of Attention" factor at later testing times only. Subjective ratings of alertness were also reduced 6 h following the two lowest doses. To the best of our knowledge this represents the first demonstration of a modulation of mood and cognitive performance by acute administration of Ginseng.
127 citations
TL;DR: The most striking result was a dose-dependent improvement in performance on the “quality of memory” factor for the highest dose, and further analysis revealed that this effect was differentially targeted at the secondary memory rather than the working memory component.
Abstract: We have previously shown differential cognitive improvements following single doses of Ginkgo biloba and of Ginseng. There is also evidence that chronic administration of a combination of standardised extracts of Ginkgo biloba and Panax ginseng may improve aspects of cognitive performance both in pathological populations and the healthy middle aged. No investigation has thus far looked either at the cognitive effects of single doses of such a combination, nor the effects of the combination on healthy young volunteers. The present study investigated whether acute administration of a combination of standardised extracts of Ginkgo biloba (GK501, Pharmaton SA) and Ginseng (G115, Pharmaton SA) had any consistent effect on mood and aspects of cognitive performance ("quality of memory", "secondary memory", "working memory", "speed of memory", "quality of attention" and "speed of attention") that can be derived by factor analysis of the cognitive drug research computerised assessment battery. The study followed a placebo-controlled, double blind, balanced, crossover design. Twenty healthy young adult volunteers received 320, 640, and 960 mg of the combination, and a matching placebo, in an order dictated by random allocation to a Latin square, and with a seven-day wash-out period between treatments. Following a baseline cognitive assessment, further test sessions took place 1, 2.5,4 and 6 h after the day's treatment. The most striking result was a dose-dependent improvement in performance on the "quality of memory" factor for the highest dose. Further analysis revealed that this effect was differentially targeted at the secondary memory rather than the working memory component. There was also a dose dependent decrement in performance of the "speed of attention" factor for both the 320 and 640 mg doses. These results are discussed in the context of previous findings within this series of studies.
104 citations
TL;DR: A daily supplement of S-PS does not affect memory or other cognitive functions in older individuals with memory complaints, and there were no significant interactions between treatment and ‘severity of memory complaints’.
Abstract: Phosphatidylserine (PS) is a phospholipid widely sold as a nutritional supplement. PS has been claimed to enhance neuronal membrane function and hence cognitive function, especially in the elderly. We report the results of a clinical trial of soybean-derived PS (S-PS) in aging subjects with memory complaints. Subjects were 120 elderly (> 57 years) of both sexes who fulfilled the more stringent criteria for age-associated memory impairment (AAMI); some also fulfilled the criteria for age-associated cognitive decline. Subjects were allocated at random to one of the three treatment groups: placebo, 300mg S-PS daily, or 600mg S-PS daily. Assessments were carried out at baseline, after 6 and 12 weeks of treatment, and after a wash-out period of 3 weeks. Tests of learning and memory, choice reaction time, planning and attentional functions were administered at each assessment. Delayed recall and recognition of a previously learned word list comprised the primary outcome measures. No significant differences were found in any of the outcome variables between the treatment groups. There were also no significant interactions between treatment and 'severity of memory complaints'. In conclusion, a daily supplement of S-PS does not affect memory or other cognitive functions in older individuals with memory complaints.
64 citations
TL;DR: Overall THC produced short-term increases in palatable food intake following both peripheral and central administration, and resulted in an “inverted U” dose-response curve at all time points.
Abstract: To further study effects of delta9-tetrahydrocannabinol (THC) on food intake, male Lewis rats were maintained on rat chow and, on testing days, presented with chocolate cake batter (CCB) for 4h in addition to chow. Chow intake was not affected by THC administration in either experiment. In experiment 1 (n = 13) THC was administered intraperitoneally, and low doses produced increases in CCB intake for up to 1 h while the highest dose significantly decreased CCB intake over this same time period. In experiment 2 (n = 10) THC was injected intracerebroventricularly. Doses of 2.5, 10 and 25 microg significantly increased CCB intake for up to 1 h while stimulatory effects following 5 microg lasted up to 2h. Overall THC produced short-term increases in palatable food intake following both peripheral and central administration. Intraperitoneal administration resulted in an "inverted U" dose-response curve at all time points, while all central doses resulted in increased intake early in the time course and the hyperphagic effects were of greater duration than those following peripheral administration.
56 citations
TL;DR: Taurine can be considered as one of the determinant nutritional molecules during development and regeneration of the central nervous system.
Abstract: Taurine is an amino acid known to possess trophic properties in the central nervous system. The relevance of its presence in maternal milk is related to its role as an essential nutrient. Taurine deficiency around birth produces anatomical and functional modifications in the brain and in the retina. In addition, taurine favors neuron proliferation and survival, as well as neurite extension. The mechanisms by which taurine exerts its trophic role in the regenerating retina are related to increases in calcium fluxes, to modifications of protein phosphorylation, and to influence of the target organ. Moreover, taurine-zinc interaction might be crucial in the development of structures such as the hippocampal formation. Thus, taurine can be considered as one of the determinant nutritional molecules during development and regeneration of the central nervous system.
54 citations
TL;DR: The reported results are more or less identical; reduction of autistic behaviour, increased social and communicative skills, and reappearance of autistic traits after the diet has been broken.
Abstract: Autism is a developmental disorder for which no cure currently exists. Gluten and/or casein free diet has been implemented to reduce autistic behaviour, in addition to special education, since early in the eighties. Over the last twelve years various studies on this dietary intervention have been published in addition to anecdotal, parental reports. The scientific studies include both groups of participants as well as single cases, and beneficial results are reported in all, but one study. While some studies are based on urinary peptide abnormalities, others are not. The reported results are, however, more or less identical; reduction of autistic behaviour, increased social and communicative skills, and reappearance of autistic traits after the diet has been broken.
54 citations
TL;DR: In young adults, with neuroticism scores above rather than below the median, the taking of 300 mg PS each day for a month was associated with feeling less stressed and having a better mood.
Abstract: There have been previous reports that supplements of phosphatidylserine (PS) blunted the release of cortisol in response to exercise stress and that it improved mood. The present study extended these observations by considering whether PS supplementation influenced subjective feelings of stress and the change in heart rate when a stressful mental arithmetic task was performed. In young adults, with neuroticism scores above rather than below the median, the taking of 300mg PS each day for a month was associated with feeling less stressed and having a better mood. The study for the first time reports an improvement in mood following PS supplementation in a sub-group of young healthy adults.
48 citations
TL;DR: In the past decade or so, a convincing link between oxidative stress and degenerative conditions has been made and with the knowledge that oxidative changes may actually trigger deterioration in cell function, a great deal of energy has focussed on identifying agents which may have possible therapeutic value in combating oxidative changes.
Abstract: In the past decade or so, a convincing link between oxidative stress and degenerative conditions has been made and with the knowledge that oxidatiye changes may actually trigger deterioration in cell function, a great deal of energy has focussed on identifying agents which may have possible therapeutic value in combating oxidative changes One agent which has received attention, because of its powerful antioxidative effects, particularly in neuronal tissue, is lipoic acid
42 citations
TL;DR: It is concluded that the rats with a spontaneous and marked dietary preference have a characteristic peptidergic profile and this model integrates information provided by the energy stores and translated by peripheral messengers such as leptin which could act in a counterregulatory manner to limit the overweight induced by the ingestion of unbalanced diets.
Abstract: Neuropeptides present in the hypothalamus and new messengers in the periphery such as leptin modulate food intake in mammals. Neuropeptide Y (NPY) and galanin in microdissected brain areas and plasma leptin levels were measured by specific radioimmunoassays during the resting period in rats selected for their strong preference either for carbohydrate or fat, but with identical energy intake. NPY concentrations were 23% lower (p <.02) in carbohydrate-preferring (CP) than in fat-preferring (FP) rats in the parvocellular part of the paraventricular nucleus (PVN), which is one of the main areas involved in the regulation of feeding behavior. On the other hand, galanin was significantly (+25%, p = .03) higher in CP rats than in FP rats in the magnocellular part of the PVN. Plasma leptin was more than 50% higher in FP rats than in CP rats (p < .01) and highly correlated with the fat preference (r = 0.57; p = .003) and body weight gain. We conclude that the rats with a spontaneous and marked dietary preference have a characteristic peptidergic profile. Due to their anatomical relationships, neuropeptide Y could act in conjunction with galanin in a peptidergic balance located in the paraventricular nucleus. This model integrates information provided by the energy stores and translated by peripheral messengers such as leptin which could act in a counterregulatory manner in order to limit the overweight induced by the ingestion of unbalanced diets.
23 citations
TL;DR: Whether PLP and PL can, in vivo, protect monkey CA1 neurons from ischemic insult is studied and suggested that PL (perhaps PLP intracellularly) is useful as a novel neuroprotectant in primates.
Abstract: Previously, in monkeys undergoing 20 min whole brain ischemia we demonstrated that the activated calpain-induced lysosomal disruption with the resultant leakage of cathepsins B and L, causes neuronal death in the cornu Ammonis (CA) 1 sector on day 5. Selective cathepsin inhibitors significantly protected ischemic CA1 neurons from delayed necrosis. Recently, pyridoxal phosphate (PLP) and pyridoxal (hydrochloride) (PL) were demonstrated to inhibit cathepsins B and L in vitro, because the active aldehyde at position 4 of the pyridine ring has an affinity for the active site -SH of cysteine residues of cathepsins. Here, we studied whether PLP and PL can, in vivo, protect monkey CA1 neurons from ischemic insult. In monkeys undergoing 20 min whole brain ischemia, 15 mg/kg body weight/day of drugs were intravenously injected for 10 days before and after the ischemic insult. Histological analysis of the surviving CA1 neurons was done using the hippocampus resected on day 5 after ischemia. For PLP or PL, approximately 17% (P = 0.0639) or 54% (P < 0.0001) of the total population (100%) of control CA1 neurons were, respectively, saved from the ischemia-induced neuronal death, showing a remarkable contrast to the surviving neurons (approximately 3.9%) in non-treated monkeys. These data suggested that PL (perhaps PLP intracellularly) is useful as a novel neuroprotectant in primates.
TL;DR: Results indicate that there are few neurobehavioral alterations resulting from developmental SJW treatment in rats, and whole and regional brain weights of offspring at adulthood indicated no significant effects of SJW.
Abstract: Increasing widespread use of St. John's Wort (SJW, Hypericum perforatum) has led to concerns about its use in pregnant women. Behavioral and physiological alterations resulting from developmental treatment were investigated in Sprague-Dawley rats exposed to diets containing 0, 180, 900, 1800 or 4500ppm SJW beginning on gestational day 3 and ending at offspring weaning on postnatal day (PND) 21. These dietary doses span 1-25 times the recommended human dose. Post-weaning behavioral assessments of male and female offspring included: open field activity, acoustic startle, performance of complex and Morris water mazes, and activity in an elevated plus-maze. There were no SJW effects on maternal weight gain or duration of gestation; offspring body weights were similar to controls from PND 2 through PND 56 after which, some treated groups weighed significantly less than the controls. There were no SJW-related behavioral alterations on any measure. Whole and regional brain weights of offspring at adulthood indicated no significant effects of SJW. These results indicate that there are few neurobehavioral alterations resulting from developmental SJW treatment in rats.
TL;DR: LP rats present an increased responsiveness of BAR and BJR, which could contribute to their normal levels of cardiovascular parameters, in spite of the possible increase in the sympathetic vasomotor tonus observed with the prazosin protocol.
Abstract: The present study evaluated the effects of a low-protein diet (LP, 6% protein) on cardiovascular reflexes of Male Fisher rats. Three experimental groups, and their respective controls (15% protein), were used: (1) Baroreceptor reflex (BAR); (2) Bezold-Jarisch reflex (BJR); and (3) Prazosin treated. Dietary restriction began after weaning (three weeks) and lasted for a period of five weeks, after which animals were subjected to the experimental protocols. The BAR group was evaluated through injections of phenylephrine (0.5-5.0 microgram/Kg, i.v.) and sodium nitroprusside (0.7-7.0 microgram/Kg, i.v.) while the BJR was evaluated through injections of serotonin (2.5-10 microgram/Kg, i.v.). Our results showed an increased baroreflex gain bradycardia for the LP group (-0.96+/-0.34 vs. -2.12+/-1.06 bpm/mmHg) and a larger bradycardia for the BJR the LP group (160+/-18% greater than controls). Basal cardiovascular parameters were not different between LP and control rats, however LP animals treated with prazosin resulted in a larger fall of blood pressure (-19+/-3 vs. -28+/-5 mmHg). In conclusion, LP rats present an increased responsiveness of BAR and BJR, which could contribute to their normal levels of cardiovascular parameters, in spite of the possible increase in the sympathetic vasomotor tonus observed with the prazosin protocol.
TL;DR: This review will discuss how the gustatory system is used by the rat to aid in the recovery from deficiencies of sodium, vitamin B, and individual essential amino acids.
Abstract: Humans and animals have an impressive ability to use behavioral means to recover from nutritional deficits. Under some conditions, recovery ray be manifest in the form of a specific appetite for the missing nutrient. This review will discuss how the gustatory system is used by the rat to aid in the recovery from deficiencies of sodium, vitamin B, and individual essential amino acids. While it is likely that a deficient rat will use all available cues to guide intake of a limited nutrient, the role of taste can be partitioned out using techniques that measure immediate behavioral responses to brief exposures of taste stimuli and/or by measuring responsiveness before and after nerve transection. Taste can be used to identify stimuli in the environment as well as serve to motivate intake in terms of producing a particular affective reaction. Compensatory alterations in these aspects of the gustatory system are considered for three types of deficiencies. For learned appetites the utility of conditioning paradigms is presented as a potential means to gain a further understanding of behavioral recovery from specific micronutrient deficiencies.
TL;DR: It is suggested that a balanced diet containing a natural Trp rich-protein increases the plasma Trp/LNAA ratio over a long period, leading to a probable increase in brain serotonin activity.
Abstract: Brain serotonin synthesis depends on the uptake of its precursor, tryptophan (Trp), and is correlated to the plasma ratio of Trp to large neutral amino acids (LNAA) which compete for the same trans...
TL;DR: In this paper, the brain glutathione (GSH), a key component of antioxidant defense important for minimizing ischemic injury, was also responsive to short-term sulfur amino acid deficiency.
Abstract: Dietary sulfur amino acid content is a major determinant of glutathione concentration in some tissues. We examined whether brain glutathione (GSH), a key component of antioxidant defense important for minimizing ischemic injury, was also responsive to short-term sulfur amino acid deficiency. Female Long-Evans adult rats were fed a sulfur-deficient L-amino acid defined diet for five days; the control diet was supplemented with L-cystine and L-methionine (n = 6). Sulfur amino acid deficiency was confirmed by a reduction in liver cysteine and GSH concentrations, marked decreases in food intake, and weight loss. GSH concentration analyzed by reverse-phase high performance liquid chromatography was significantly depressed in the neocortex and thalamus of deficient rats. Brain cysteine was not decreased in a parallel manner. Classical glutathione peroxidase activity was increased in the liver and brain of sulfur amino acid deficient rats. This suggests an upregulation of antioxidant defense but these findings may be complicated by alterations in tissue composition. The depletion of brain GSH by a reduced supply of dietary precursors may be important during brain ischemia when the rate of GSH utilization and the need for synthesis are increased.
TL;DR: The results showed that malnutrition caused a delay in the latency of all BAEPs waves in rats of all ages, however, environmental stimulation reduced these latencies, reversing some damage caused by malnutrition.
Abstract: It has been shown that environmental stimulation may reduce the damage caused by malnutrition to morphological and behavioural parameters; however, there are no data on the effects of stimulation on the Brainstem Auditory Evoked Potentials (BAEPs). The aim of this study was to evaluate the effects of protein malnutrition, nutritional recovery and environmental stimulation on the BAEPs of the rat. On the first day of life, the animals were divided into Well-nourished (W) and Malnourished (M) groups. At weaning, half the M rats were submitted to nutritional recovery (R) until the test day. All groups were subdivided into Stimulated (S) and Non-Stimulated (N) rats. BAEPs was tested in animals exposed to clicks of 90, 80 and 70 dB of intensity. The BAEPs latencies of waves I, II, III and IV in the left ear were analysed in independent groups of rats on the 14th, 18th, 22nd, 32nd, and 42nd days of age. Statistical analysis showed diet and environmental stimulation interaction on the latencies of waves I, II, III and IV at all tested ages. WN rats showed longer latencies of waves I, II, III and IV than WS rats, and MN rats also showed longer latencies of these waves compared to WN, MS and RN at all tested ages. The results showed that malnutrition caused a delay in the latency of all BAEPs waves in rats of all ages. However, environmental stimulation reduced these latencies, reversing some damage caused by malnutrition. These data suggest that the auditory brainstem pathway is vulnerable to nutritional insults, and its structures show plasticity with environmental stimulation.
TL;DR: The results may suggest that a relative large number of myelinated group A afferent fibers in the sural nerve of undernourished and malnourishing animals suffer severe alterations on their electrophysiological properties of generation and propagation of the action potential during the postnatal development of the rat.
Abstract: The aim of this study was to analyze the possible alterations produced by inadequate perinatal food intake, in quantity (undernutrition) or quality (malnutrition), on the generation and propagation of the compound action potential (CAP) evoked in sensory sural nerves, during the postnatal development of the rat. Low intensity stimulation (2-3 times the threshold of the most excitable nerve fibers; xT) of the sural nerve evoked an early potential (CAP-A component) which is due to activation of low-threshold, fast-conducting myelinated group A afferent fibers. Meanwhile, at higher stimulus intensity (20-30T) it produced a second, long-lasting potential (CAP-C component) probably due to activation of high-threshold, slow-conducting group Adelta or C afferent fibers. Compared to control nerves, the CAP-A component, but not the CAP-C component of undernourished and malnourished nerves showed significant changes in amplitude, area, electrical threshold and conduction velocity (except absolute refractory period) at several postnatal ages. Our results may suggest that a relative large number of myelinated group A afferent fibers in the sural nerve of undernourished and malnourished animals suffer severe alterations on their electrophysiological properties of generation and propagation of the action potential during the postnatal development of the rat.
TL;DR: CHP levels are increased in obese women and inversely related to their C-peptide/insulin molar ratio, which is interesting as the greater insulin response seen in normal persons after oral glucose compared to intravenous glucose has been postulated to be due to a decrease in HIC by some gut factor.
Abstract: Cyclo (His-Pro) (CHP) is a gut-brain peptide whose plasma levels in humans are increased after glucose ingestion and preferentially altered by oral glucose ingestion compared to intravenous administration in rats, suggesting a role in the enteroinsular response to nutrient ingestion. We were interested in examining levels of CHP in women of differing weights and comparing these levels to various parameters of insulin secretion. Plasma from 26 fasting, nondiabetic women ranging from 21 to 70 years of age and weighing 43 to 114 kg was assayed for CHP. Insulin and C-peptide levels were measured in 17 of the 26. Fasting CHP levels were elevated in obese compared to nonobese women (2075+/-144 vs. 905+/-187 pg/ml; p < 0.001) and were related by regression analysis to weight (r = 0.668, p < 0.001) and body mass index (r = 0.636, p = 0.001). The fasting C peptide/insulin molar ratio, which may be used as an estimate of hepatic insulin clearance (HIC), was inversely related to CHP levels (r = -0.568, p = 0.017). We conclude CHP levels are increased in obese women and inversely related to their C-peptide/insulin molar ratio. The elevation of CHP in those with a decrease in this estimate of HIC (obese) is interesting as the greater insulin response seen in normal persons after oral glucose compared to intravenous glucose has been postulated to be due to a decrease in HIC by some gut factor. The presence of such a factor in excess in the obese might explain part of their hyperinsulinemia.
TL;DR: The effect of diet restriction and tyrosine appeared to be both pre- and post-synaptic, indicating modulation of cholinergic activity by adrenergic tone, and may have implications for the treatment of mood changes associated with weight loss and semi-starvation.
Abstract: We have studied the effects of diet restriction (DR) to 60% and 40% of daily requirements, and tyrosine administration on cognitive function in mice, to define the nutritional-neurochemical interactions on autonomic tone involved in behavior and energy regulation. Cognitive function in the Morris Water maze was significantly impaired after 40% DR compared to both control and 60% DR. It was restored after tyrosine in association with increased M1 cholinergic and β-adrenergic receptor function, and decreased α-adrenergic function. DR to 40% significantly decreased choline uptake (p <.05) and M1 receptor number (Bmax) (p <.05), without changes in affinity (Kd), choline acetyl transferase (ChAT) or acetyl cholinesterase (AChE) activity. Tyrosine administration significantly increased choline uptake (Bmax) (p <.05) and M1 density in the 40% DR (p <.01) without changes in affinity. ChAT activity was decreased after tyrosine significantly after 40% DR (p <.05) while AChE was not affected. Both M1 mRNA and protei...
TL;DR: Plasma galanin levels were decreased in both intermittent and 72h continuous HA exposed rats, suggesting that changes in levels of these peptides may be responsible for anorexia at HA.
Abstract: Anorexia causing weight loss at high altitude (HA) is a major problem. Neuropeptide Y (NPY) and galanin are considered to have appetite regulatory function. The present study was therefore undertaken to investigate the changes in these two peptides at simulated HA and its possible role in anorexia. Male Sprague-Dawley rats (n = 8 in each group) were exposed to simulated HA (7620 m) for 1, 7, 14 and 21 days for 6 h a day and to an altitude of 6,096 m for 72 h to study the effect of intermittent and continuous exposure, respectively. NPY and galanin levels were estimated in different brain parts and plasma of exposed and unexposed control animals. Significant reduction in food intake was observed in rats during both intermittent as well as continuous exposure. In case of 72 h continuous exposure severe reduction in food intake was observed (73.2%) with reduction in body mass (approximately 29.7g/rat in 48h). Hypothalamic NPY levels were decreased by 54.7, 35.0 and 15.4% in 1, 7, and 14 days, respectively, in case of intermittent exposure to HA. However in case of 72 h HA exposure no significant change in hypothalamic and circulating NPY levels were observed. Plasma galanin levels were decreased in both intermittent and 72 h continuous HA exposed rats. Hypothalamic galanin levels were also decreased in 72h exposed rats. The changes in levels of these peptides may be responsible for anorexia at HA.
TL;DR: The pleasures of the palate deal with us like the Egyptians thieves, who strangle those whom they embrace.
Abstract: Tell me what you eat, and I will tell you what you are (Anthelme Brillat-Savarin). When I behold a fashionable table set out in all its magnificence, I fancy that I see gouts and dropsies, fever and lethargies, with other innumerable distempers, lying in ambuscade among the dishes. Nature delights in the most plain and simple diet. Every animal, but man, keeps to one dish. Herbs are the food of this species, fish of that, and flesh of a third. Man falls upon everything that comes in his way; not the smallest fruit or excrescence of the earth, scarce a berry or a mushroom can escape him (Joseph Addison). The pleasures of the palate deal with us like the Egyptians thieves, who strangle those whom they embrace (Seneca). Let food be your medicine and medicine be your food (Hippocrates).
TL;DR: The present results indicate that glucose deprivation does not contribute to feeding elicited by MA-induced inhibition of fatty acid oxidation in rats fed a carbohydrate-free, high-fat diet.
Abstract: In the present study we investigated whether glucose deprivation contributes to feeding induced by mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in Sprague-Dawley rats fed a carbohydrate-free, high-fat diet (HF-rats). The results show that inhibition of fatty acid oxidation by MA, reflected by a decrease in plasma beta-hydroxybutyrate, elicited eating in the HF-rats and that the eating response was not associated with a decrease in circulating glucose. The effect of MA on food intake was tested in two different substrains (Zur:SD and Ico:OFA SD) of Sprague-Dawley rats. The threshold dose of MA for eliciting eating was much higher in Zur:SD (between 800 and 1,600 micromol/kg) in comparison to Ico:OFA SD rats (between 200 and 400 micromol/kg). At a high dose of MA (1,200 micromol/kg), but not at a low dose (400 micromol/kg) the feeding response in the Ico:OFA SD rats was associated with hyperglycemia due to an increase in glycogenolysis. Unlike in Zur:SD, in Ico:OFA SD rats the higher doses of MA (800 and 1,200 micromol/kg but not 400 micromol/kg) produced a long-term suppression of feeding, which partly might be causally related to the observed inhibitory effect of MA on gastric emptying. The present results indicate that glucose deprivation does not contribute to feeding elicited by MA-induced inhibition of fatty acid oxidation in rats fed a carbohydrate-free, high-fat diet.
TL;DR: Wistar rats grown up during the early postnatal life in artificially built normal, small or large litters developed a significantly different body weight and this difference persisted also during adulthood when they had free access to food and water.
Abstract: Wistar rats grown up during the early postnatal life (3-21 days after birth) in artificially built normal, small or large lifters developed a significantly different body weight This difference persisted also during adulthood when they had free access to food and water The influence of iontophoretically administered cholecystokinin (CCK8S), serotonin (5-HT) or co-ejection of both on firing of lateral hypothalamic neurons was investigated in adult, urethane anesthetized rats of the three groups The responsiveness to CCK8S was significantly higher in large- and small-litter rats than in the normal control group The differences were greater in males than in females They resulted in the male large-litter group from an increase of excitatory responses, whereas in the male small-litter group the proportion of inhibitory responses was augmented Co-administration of 5-HT generally reduced the neuronal responsiveness Especially in the large-litter group excitatory responses were significantly reduced It may be speculated that the availability of food in the early postnatal life influences the development of the hypothalamic regulatory network in such a way that it stabilizes the high or low food ingestion all the life At least in males, a changed responsiveness and type of response to cholecystokinin of lateral hypothalamic neurons might be involved in this altered regulation
TL;DR: The higher but constitutive expression of transferrin mRNA at later ages, when the blood-brain barrier segregates the brain from other body parts, may indicate that molecules released from the brain interior are responsible for regulating transcription of the transferrin gene.
Abstract: As transferrin in the brain may originate principally from synthesis by three different cell types, i.e. hepatocytes, oligodendrocytes and choroid plexus, this study employed a morphological analysis to specifically address oligodendrocytic expression of transferrin mRNA in young (P17) and adult (P50) rats. In spite of a lowering of the concentration of brain iron by approximately 22% in the young iron deficient rats transferrin mRNA expression in oligodendrocytes was not affected when measured by quantitative densitometry. In adult rats, the baseline transferrin mRNA expression in oligodendrocytes was higher than in the young animals, but did not change in spite of a reduction in brain iron by approximately 19%. Brain iron and transferrin mRNA expression in oligodendrocytes were unaltered in iron overloaded rats when compared to age-matched controls. As transferrin expression was lower in the young rat, when constituents from the blood have a relatively higher concentration in the brain than during adulthood, it seems unlikely that blood-borne factors such as transition metals act as inducers of transferrin gene expression in oligodendrocytes. Instead, the higher but constitutive expression of transferrin mRNA at later ages, when the blood-brain barrier segregates the brain from other body parts, may indicate that molecules released from the brain interior are responsible for regulating transcription of the transferrin gene.
TL;DR: Malnutrition resulted in a delay of normal development of the brainstem auditory pathway indicated by the increases in the interpeak intervals of BAEPs waves, and environmental stimulation reduced these intervals, promoting faster nervous impulse transmission.
Abstract: The aim of this study was to investigate the effects of malnutrition, nutritional recovery, environmental stimulation and click intensity on the interpeak intervals of the waves of the Brainstem Auditory Evoked Potentials (BAEPs). The animals were divided into Well-nourished (W) and Malnourished (M) groups. At weaning, half of the M rats were submitted to nutritional recovery (R) until the test day. These groups were further subdivided into Stimulated (S) and Non-stimulated (N) rats. The BAEPs interpeak intervals I-III, I-IV and III-IV were analysed in independent groups of rats on the 18th, 22nd, 32nd and 42nd days of age. During the lactation period, stimulated rats presented shorter I-III, I-IV and III-IV interpeak intervals than Non-stimulated animals. This analysis also indicated a diet x stimulation x age interaction during the lactation period. The WN and MN groups showed a longer I-IV interval than the WS and MS groups, respectively, on the 18th and 22nd day of age, and the MN group also presented a longer I-IV interpeak interval than the WN group on the 22nd day of age. During the post-lactation period, stimulated animals showed shorter I-III and I-IV intervals than non-stimulated rats. Post hoc analysis indicated longer I-III and I-IV interpeak intervals in the MN than in the WN, RN and MS groups. Additionally, malnourished animals showed longer I-III and I-IV intervals than well-nourished and recovered rats when exposed to clicks of 90, 80 or 70 dB intensity. Malnutrition resulted in a delay of normal development of the brainstem auditory pathway indicated by the increases in the interpeak intervals of BAEPs waves, and environmental stimulation reduced these intervals, promoting faster nervous impulse transmission.
TL;DR: This review and commentary is the first effort to comprehensively discuss the issue of FBP induced neurotoxicity and suggests that much of this information supports the role of a theoretical model, the neuro-immune-endocrine system, in organizing and helping to explain the complex pathogenesis ofFBP neurotoxicity.
Abstract: The American diet is among the safest in the world; however, diseases transmitted by foodborne pathogens (FBPs) still pose a public health hazard. FBPs are the second most frequent cause of all infectious illnesses in the United States. Numerous anecdotal and clinical reports have demonstrated that central nervous system inflammation, infection, and adverse neurological effects occur as complications of foodborne gastroenteritis. Only a few well-controlled clinical or experimental studies, however, have investigated the neuropathogenesis. The full nature and extent of neurological involvement in foodborne illness is therefore unclear. To our knowledge, this review and commentary is the first effort to comprehensively discuss the issue of FBP induced neurotoxicity. We suggest that much of this information supports the role of a theoretical model, the neuro-immune-endocrine system, in organizing and helping to explain the complex pathogenesis of FBP neurotoxicity.
TL;DR: Data suggest differential vulnerability to neonatal food and sensory deprivation of the neural mechanisms underlying maternal performance and complete recovery of maternal responsiveness alterations was obtained when sensory stimulation was associated to the maternal experience.
Abstract: The study examines the effects of two paradigms of neonatal food deprivation (daily mother-litter separation, Experiment 1 or nipple-ligation of mothers, Experiment 2) associated or not to early sensory stimulation (daily handling or the exposure to an enriched sensory environment) during the preweaning period of Wistar strain female rats. The effects of experimental manipulations were evaluated by measuring the nest building, retrieving latencies and nursing time of adult dams along three successive parturitions. Undernourished dams of Experiment 1, showed significant alterations in maternal responsiveness in the first delivery, which were attenuated by the maternal experience of two additional parturitions. Moreover, maternal alterations were importantly compensated by the association to early sensory stimulation (except nest building). Underfed mothers of Experiment 2 exhibited less alterations of the maternal response during the first parturition, and these were ameliorated by the maternal experience ...
TL;DR: The results show that despite the extreme somatic and behavioral changes observed the neurotransmitter systems studied were at a certain extent shielded from the insult.
Abstract: Malnutrition by severe protein deprivation induces deleterious consequences in the nervous system particularly in the initial period of development. These deficits can alter several important events during development, such as the expression of neurotransmitters. The induction of nutritional deficiency by using low protein diet, similar to that consumed by low income populations in Brazil, was applied in rats to investigate the effect of malnutrition on cells containing γ-aminobutyric acid (GABA) and acetylcholine in the retina. GABA immunoreactivity was present in cells in the inner nuclear and ganglion cell layers and in processes in the inner and outer plexiform layers in retinas of control and malnourished animals. At postnatal day 8, there is a decrease (ca. 40%) of the GABAergic neurons in malnourished animals. At P13 and P21 the percentage of these neurons increased and was equivalent to control animals in the adult. Glutamic acid decarboxylase activity did not show significant changes between the ...
TL;DR: Cholesterol may enhance the effects of angiotensin III, at least, at the cortical level after cholesterol intake, according to the results of this study, which may indicate that the metabolism of ang Elliotensin II to angiotENSin III by aminopeptidase A is increased, but angiotsin III metabolism by isinopePTidases B and M is not modified after cholesterol Intake.
Abstract: Although hypercholesterolemia and hypertension have been extensively associated, the regulatory mechanism underlying this relationship is poorly understood. Systemic and local renin-angiotensin systems are involved in the control of blood-pressure. Angiotensin II has been considered as the main effector peptide of renin-angiotensin system. However, other peptides derived from the metabolism of angiotensin II, as angiotensins III and IV have been shown to play significant roles. The aim of this study is to analyse the effect of dietary cholesterol on the activity of the enzymes involved in the metabolism of angiotensins II and III. Soluble and membrane-bound aminopeptidase A (aspartyl- and glutamyl-aminopeptidases), B (arginyl-aminopeptidase) and M (alanyl-aminopeptidase) activities were measured in the frontal cortex of male and female mice fed a cholesterol enriched-diet (1% cholesterol; 0.5 cholic acid). Soluble and membrane-bound aminopeptidases B and M did not change in male or female cholesterol groups. Significant increases were observed in membrane-bound aspartyl- and glutamyl-aminopeptidase activities in both cholesterol groups. Soluble aspartyl- and glutamylaminopeptidases did not change in male cholesterol group, but significant decreases were detected in female cholesterol group. Our results may indicate that the metabolism of angiotensin II to angiotensin III by aminopeptidase A is increased, but angiotensin III metabolism by aminopeptidases B and M is not modified after cholesterol intake; so cholesterol may enhance the effects of angiotensin III, at least, at the cortical level.