The two basic questions in food intake study are what we eat, and how much do we eat. Most research is directed toward the control of how much is eaten. This is likely the result of the increased ...number of individuals with eating disorders in the Western world. Feeding behavior is highly complex, and is controlled by many psychological, physiological, biochemical, and immunological factors. The aim of this review is to clarify the involvement of fatty acids in eating disorders such as anorexia and binge eating disorder. The review will describe the modified fatty acid profile observed in individuals with anorexia or binge eating disorder, and discuss on what factors fatty acids can exert beneficial effects. In addition, the differences and similarities between anorexia and binge eating disorder will be discussed. We suggest that beneficial effects of essential fatty acids on both anorexia and binge eating disorder can be explained by the stabilizing effect of those fatty acids on the neuronal membrane fluidity index.
This study was conducted to examine the relation between iron status and neurobehavioral development in premature infants.
Infants born before 34 weeks postmenstrual age and who were medically stable ...were studied. Anemia was defined as hemoglobin < or =10 g/Dl and low iron stores as a serum ferritin concentration < or =75 microg/l. The infants were classified as anemic with low ferritin (Group 1; n=18), anemic with normal ferritin (Group 2; n=14), and nonanemic with normal ferritin (Group 3; n=21). A total of 18 reflexes were behaviorally evaluated at 37 weeks postmenstrual age and "reflex scores" were compared between the groups. Higher scores reflect a greater percentage of abnormal reflexes.
Infants in group 1 (anemia/low ferritin) had a significantly higher reflex score (51.45+/-18.32%) than infants in Group 3 (38.32+/-17.75%). Group 2 had an intermediate score (45.40+/-21.70%), but not different from the other two groups.
These data indicate that low iron status, both measured by anemia and ferritin levels, is related to poorer neurobehavioral status in premature infants.
Our previous study demonstrated that an olfactory bulbectomy in rats induced short-term, multifaceted, devastating Alzheimer’s-like effects, which included cognitive impairment, hyperactivity, ...hyperthermia, and increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. In addition, the rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of neurofibrillary tangles. Here, we examined the long-term effects of the surgery and found that olfactory bulbectomy also rendered the rats to become anemic with brain iron overload. Additionally, a significant reduction in the membrane fluidity index in frontal cortex synaptosomes was found. Treatment with a mixture of
n
− 3/
n
− 6 of fatty acids restored the unwanted effect. The beneficial effects of fatty acids are mediated via the effects of fatty acids on the neuronal membrane structure and fluidity. These findings are similar to Alzheimer’s symptoms, which suggest this model can be used as an animal model for Alzheimer’s disease. We recommend using this model to scan potential new anti-Alzheimer’s drugs.
Test anxiety is an incapacitating academic syndrome. This study shows that administration of a polyunsaturated fatty acid mixture of omega-3 and -6 can improve the behavioral variables associated ...with this type of anxiety, i.e. appetite, mood, mental concentration, fatigue, academic organization and poor sleep, as well as lowering elevated cortisol level, with a corresponding reduction of anxiety.
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•OBX rats mimic many symptoms of Alzheimer's disease.•OBX rats were hyperactive, hyperthermic, and anorectic.•OBX rats expressed increased homocysteine and pro-inflammatory cytokine ...levels.•Pretreatment with omega-3/omega-6 fatty acids protected the rat from the damaging effects of OBX.
While the removal of the rat's olfactory bulb is considered a valid animal model of depression, recently studies found that those rats exhibited an increase in the hyperphosphorylation of brain Tau proteins and in the number of tangles. The present study investigated the possibility of using rat's olfactory bulbectomy as a putative model for Alzheimer's disease. Olfactory bulbectomy indeed mimics a complex of Alzheimer's symptoms. We evaluated the effect of pretreatment with a specific mixture of omega-3/omega-6 fatty acids: After olfactory bulbectomy, the rats were cognitive impaired, hyperactive, anorectic, and hyperthermic and expressed increased levels of homocysteine and pro-inflammatory cytokines, including IL-17A. Pretreatment with a specific mixture of omega-3/omega-6 fatty acids blocked these adverse effects. We recommend using this model to scan potential new anti-Alzheimer's drugs and to investigate the role of fatty acids in Alzheimer's disease.
α‐Synuclein (α‐Syn) is a neuronal protein that accumulates progressively in Parkinson's disease (PD) and related synucleinopathies. Attempting to identify cellular factors that affect α‐Syn ...neuropathology, we previously reported that polyunsaturated fatty acids (PUFAs) promote α‐Syn oligomerization and aggregation in cultured cells. We now report that docosahexaenoic acid (DHA), a 22:6 PUFA, affects α‐Syn oligomerization by activating retinoic X receptor (RXR) and peroxisome proliferator‐activated receptor γ2 (PPARγ2). In addition, we show that dietary changes in brain DHA levels affect α‐Syn cytopathology in mice transgenic for the PD‐causing A53T mutation in human α‐Syn. A diet enriched in DHA, an activating ligand of RXR, increased the accumulation of soluble and insoluble neuronal α‐Syn, neuritic injury and astrocytosis. Conversely, abnormal accumulations of α‐Syn and its deleterious effects were significantly attenuated by low dietary DHA levels. Our results suggest a role for activated RXR/PPARγ 2, obtained by elevated brain PUFA levels, in α‐Syn neuropathology.
Sleep deprivation is a major health problem in modern society. Deprivation of rapid eye movement (REM) sleep is particularly damaging to cognition and to spatial memory; however, the mechanisms that ...mediate these deteriorations in function are not known. We explored the possibility that REM sleep deprivation may provoke major changes in the immune system by inducing inflammation. Rats were subjected to 72 h of REM sleep deprivation, and the plasma levels of proinflammatory cytokines (IL-1, IL-1beta, IL-6, IL-17A, and TNF-alpha), an anti-inflammatory cytokine (IL-10), the inflammatory markers homocysteine, corticosterone, and hyperthermia were measured immediately after the deprivation period, and 7 days later. The results indicate that REM sleep deprivation induced an inflammatory response. The levels of the proinflammatory cytokines and markers were significantly elevated in sleep-deprived rats as compared to control rats. After 7 days of recovery, the levels of some markers, including hyperthermia, remained higher in sleep-deprived rats versus the control animals. IL-17A appears to play a pivotal role in coordinating the inflammation. These data shed new light on the mechanism of sleep deprivation-induced inflammation.
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