A tryptophan‐deficient corn‐based diet induces plastic responses in cerebellar cortex cells of rat offspring

Angel-Meza, A.R. Del; Ramı́rez-Cortés, L; Olvera‐Cortés, María Esther; Vega, M.I. Pérez; González-Burgos, Ignacio

doi:10.1016/s0736-5748(01)00004-1

Cited by 22 publications

(23 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…2 mothers however, some wonder excited the finding of a significant increase of plasma concentrations of 5-HT and 5-HIAA at day 18, (in spite of the withdrawal of tryptophan from diet at day 14.5 of pregnancy), the following drop at day 20.5, and disappearance at day 3 after parturition. Similar findings in brain tissues, as well increased free tryptophan plasma levels have been observed in protein malnourished rats Orozco-Suárez et al 2003;Del Angel-Meza et al 2001;Koski et al 1995).…”

Section: Discussionsupporting

confidence: 72%

Embryonic and postnatal development in experimental tryptophan deprived rats. A preliminary study

Imbesi

Castrogiovanni

2008

J Mol Hist

View full text Add to dashboard Cite

An ontogenetic and endocrinological study has been designed on developing rats in uterus of mothers tryptophan deprived at day 1 (exp. 1) and day 14.5 (exp. 2) of conception to verify the supposed determining role of the serotoninergic system (SS) in sexual differentiation in mammals. Tryptophan-free feeding has been pursued uninterruptedly in the litter after birth, during lactation and postnatal development. Tryptophan-free pregnant rats were obtained by exclusion of tryptophan sources from chow. In both exp. 1 and exp. 2 the litter showed at birth a significant physical under evolution, that worsened, during post-natal development, to a much more marked dwarfism in exp. 1 pups. At 30 days postnatal age, whereas the female exp. 1 rats showed a right-timed onset of puberty, neither descensus of the testes nor spermatogenesis could be observed in the male rats of the same experiment. Endocrinologically the males showed a significant reduction of plasma FSH levels, but also a slight increase of those of LH. Moreover, a marked hypoandrogenism and a severe hypoprolactinemia characterized the males of this group. Hypoprolactinemia was the major endocrinological finding also in the female litter, which, however, at 30 days p.n. age showed the typical histological patterns of a cycling ovary, i.e. growing secondary follicles with scattered antral spaces, and thus a right-timed pubertal maturation, in spite of the significant lower plasma levels of pituitary gonadotropins and sex steroids. When mothers were tryptophan deprived at 14.5 of pregnancy (exp. 2), the litters showed a less marked dwarfism, persistent, severe hypoprolactinemia as in exp. 1 rats, but a normal right-timed onset of puberty in both male and female rats. Taken together these findings confirm on the one hand the close relationship between SS and PRL. On the other hand, they suggest a major, crucial role of PRL played in the male rat before day 14.5 of intrauterine development, presumably intervening in the synthesis of LH receptors sites by the maturing Leydig cells in the male gonads. Growth hormone concentrations in both sexes dwarf rats were lower than in control rats.

show abstract

Section: Discussionsupporting

confidence: 72%

Embryonic and postnatal development in experimental tryptophan deprived rats. A preliminary study

Imbesi

Castrogiovanni

2008

J Mol Hist

View full text Add to dashboard Cite

show abstract

“…Maternal nutritional deficiency is capable of delaying pups cerebellar development, resulting in distinctive changes in the cerebellar cellular topography (Barnes and Altman 1973) and a decrease in cerebellar DNA and protein content along with a reduction in the molecular layer thickness (Shambaugh et al 1995). A reduction in the soma area of neurons in granule cell and Purkinje cell layers at P30, along with an enlargement of their dendrites, which persisted until P60 were also reported (del Angel-Meza et al 2001). Those results pointed to plastic changes evoked by malnutrition that persisted in adulthood.…”

Section: Discussionmentioning

confidence: 91%

Myelin basic protein accumulation is impaired in a model of protein deficiency during development

Montanha-Rojas

Ferreira

Tenório

et al. 2005

Nutritional Neuroscience

View full text Add to dashboard Cite

During the development of the central nervous system (CNS) there is a great possibility of permanent effects in consequence of environmental disturbances. Nutritional deficiency is one of the factors that impair the normal CNS formation. In general, the protein deficiency evokes, beyond the damages in the maturation of nervous system, several consequences in body growth, biochemical maturation, motor function and the major cognitive functions. These effects were observed in undernourished children all over the world. Even in a restricted period, the malnutrition status may evoke permanent impairments in feeding behavior and in metabolism. Rats submitted to malnutrition during development, showed a marked decrease in the number of myelinated fibers. This condition may reflect a failure in the beginning of the wrapping of axons by oligodendroglial processes and/or a delay in the myelin synthesis. Myelin basic protein (MBP) is an intracellular oligodendrocyte protein that is directly related to the formation of the myelin sheath. In this study we verified the temporal pattern of MBP expression, by immunohistochemical and immunoblotting analyses, in a model of protein malnutrition induced during the first half of the lactation period. We showed that MBP expression was impaired in our malnutrition model and that some of the effects were maintained in adulthood, with possible consequences in the maturation of myelin sheath.

show abstract

“…Our approach to treating MSUD is based on the idea that chronic mental health problems are rooted in cerebral amino acid deprivation early in life [4,15,64–71] and ongoing disturbances of brain protein and neurotransmitter metabolism caused by unbalanced amino acid and ketoacid delivery to the nervous system (Fig. 8) [1,3,7,13– 15,34].…”

Section: Discussionmentioning

confidence: 99%

Classical maple syrup urine disease and brain development: Principles of management and formula design

Strauss

Wardley

Robinson

et al. 2010

Molecular Genetics and Metabolism

169

150

View full text Add to dashboard Cite

Branched-chain ketoacid dehydrogenase deficiency results in complex and volatile metabolic derangements that threaten brain development. Treatment for classical maple syrup urine disease (MSUD) should address this underlying physiology while also protecting children from nutrient deficiencies. Based on a 20-year experience managing 79 patients, we designed a study formula to (1) optimize transport of seven amino acids (Tyr, Trp, His, Met, Thr, Gln, Phe) that compete with branched-chain amino acids (BCAAs) for entry into the brain via a common transporter (LAT1), (2) compensate for episodic depletions of glutamine, glutamate, and alanine caused by reverse transamination, and (3) correct deficiencies of omega-3 essential fatty acids, zinc, and selenium widespread among MSUD patients. The formula was enriched with LAT1 amino acid substrates, glutamine, alanine, zinc, selenium, and alphalinolenic acid (18:3n – 3). Fifteen Old Order Mennonite children were started on study formula between birth and 34 months of age and seen at least monthly in the office. Amino acid levels were checked once weekly and more often during illnesses. All children grew and developed normally over a period of 14– 33 months. Energy demand, leucine tolerance, and protein accretion were tightly linked during periods of normal growth. Rapid shifts to net protein degradation occurred during illnesses. At baseline, most LAT1 substrates varied inversely with plasma leucine, and their calculated rates of brain uptake were 20–68% below normal. Treatment with study formula increased plasma concentrations of LAT1 substrates and normalized their calculated uptakes into the nervous system. Red cell membrane omega-3 polyunsaturated fatty acids and serum zinc and selenium levels increased on study formula. However, selenium and docosahexaenoic acid (22:6n – 3) levels remained below normal. During the study period, hospitalizations decreased from 0.35 to 0.14 per patient per year. There were 28 hospitalizations managed with MSUD hyperalimentation solution; 86% were precipitated by common infections, especially vomiting and gastroenteritis. The large majority of catabolic illnesses were managed successfully at home using ‘sickday’ formula and frequent amino acid monitoring. We conclude that the study formula is safe and effective for the treatment of classical MSUD. In principle, dietary enrichment protects the brain against deficiency of amino acids used for protein accretion, neurotransmitter synthesis, and methyl group transfer. Although the pathophysiology of MSUD can be addressed through rational formula design, this does not replace the need for vigilant clinical monitoring, frequent measurement of the complete amino acid profile, and ongoing dietary adjustments that match nutritional intake to the metabolic demands of growth and illness.

show abstract

A tryptophan‐deficient corn‐based diet induces plastic responses in cerebellar cortex cells of rat offspring

Cited by 22 publications

References 29 publications

Embryonic and postnatal development in experimental tryptophan deprived rats. A preliminary study

Embryonic and postnatal development in experimental tryptophan deprived rats. A preliminary study

Myelin basic protein accumulation is impaired in a model of protein deficiency during development

Classical maple syrup urine disease and brain development: Principles of management and formula design

Contact Info

Product

Resources

About