J Nutrition June, 2006
Bone, Body Weight, and Weight Reduction: What Are the Concerns?
J. Nutr. 2006 136: 1453-1456 Of the U.S. population, 65% is either overweight or obese, and weight loss is recommended to reduce co-morbid conditions. However, bone mobilization and loss may also occur with weight loss. .. in women, this is due at least in part to a reduced dietary Ca intake and/or efficiency of absorption. …Combining energy restriction with exercise does not necessarily prevent bone loss, but may attenuate loss as was shown with additional Ca intake or osteoporosis medications. ..
Regulation of Protein Synthesis by Leucine Starvation Involves Distinct Mechanisms in Mouse C2C12 Myoblasts and Myotubes
J. Nutr. 2006 136: 1466-1471 Leucine modulates protein translation in higher eukaryotes by affecting phosphorylation and the function of proteins that regulate the initiation and/or elongation steps…A time course study showed that 1 h of leucine starvation decreased protein synthesis …
J. Nutr. 2006 136: 1570-1575 Docosahexaenoic acid [22:6(n-3)] is enriched in brain membrane phospholipids and essential for brain function. Neurogenesis during embryonic and fetal development requires synthesis of large amounts of membrane phospholipid. We determined whether dietary (n-3) fatty acid deficiency during gestation alters neurogenesis in the embryonic rat brain…These studies demonstrate that (n-3) fatty acid deficiency alters neurogenesis in the embryonic rat brain, which could be explained by delay or inhibition of normal development. [Vitamin C and E good for nervous system] A Combined Deficiency of Vitamins E and C Causes Severe Central Nervous System Damage in Guinea Pigs
J. Nutr. 2006 136: 1576-1581 A short period of combined deficiency of vitamins E and C causes profound central nervous system (CNS) dysfunction in guinea pigs. For this report, CNS histopathology was studied to define the nature and extent of injury caused by this double deficiency. Weanling guinea pigs were fed a vitamin E–deficient or –replete diet for 14 d. ..These results indicate that the paralysis and death caused by combined deficiency of vitamins E and C in guinea pigs is caused by severe damage in the brainstem and spinal cord. [All about amino acids] The Amino Acid Assessment Workshop Series – Part of Development of Year 2000 Dietary Guidelines
Introduction to the 1st Amino Acid Assessment Workshop – The 1st AAAW was held in Tokyo in June, 2001. The purpose of this AAAW was: i) to review the roles and metabolism of dietary amino acids in relation to cell and organ function and ii) to identify the possible consequences associated with abnormal or unusual, in particular, high, intakes in human subjects. The focus of the discussions was intended to be, as far as possible, on mechanisms and quantification. It was planned that a working framework for assessment of the consequences of abnormal amino acid intakes might be developed, together with a number of the details of a research program required to generate a sufficient knowledge base for purposes of making sound and effective recommendations and policies.
Introduction to the 2nd Amino Acid Assessment Workshop Metabolism and Function of Amino Acids J. Nutr. 133:2015S-2020S, June 2003 – The 2nd AAAW was held in Hawaii in October, 2002, and the major focus of this workshop was on how recent advances in biology made somewhat before and during this genome-sequencing era (and the associated technology) might help to better understand the mechanisms involved and improve the ability to predict the responses of individuals to altered intakes of amino acids and their safety. Some of the issues of interest in anticipation in this workshop were: i) to determine how to define and identify molecular signatures of a pathological response to amino acid intake; ii) to see if we can identify a distinct set of genes that differentiate adequacy from excess for specific amino acids; iii) to explore the power of a microarray approach to establish a molecular profile of amino acid adequacy/excess; and iv) to decide on which organs/tissues to focus a major effort with respect to assessing the pathophysiological consequences and mechanisms of excessive intakes. Should it be the brain, the liver and/or the gut, for example, and how might the effects in such organs be probed in a noninvasive way?
Introduction to the 3rd Amino Acid Assessment Workshop Required Intakes of Amino Acids J. Nutr. 2004 134: 1555S-1557S – The first two AAAWs, as noted above, focused attention largely on metabolism of amino acids, their mechanism(s) of action, and the function of amino acids. For this workshop we focus more attention on intakes to meet physiological needs, the host and dietary factors that affect these needs and the nature of the host response, variation in responses to and levels of intake of amino acids among individuals in populations. All of this is to be viewed with an eye as to how the upper level of the safe range may be determined/set. It is recognized that this will require an approach that differs from that established for nonnutrients, which is based on hazard identification, hazard characterization, exposure assessment, and risk characterization (14–18), involving a dose-response assessment to define levels of intake without appreciable adverse effects. However, it is clear from the recent initiative by the U.S. Food and Nutrition Board/Institute of Medicine (FNB/IOM), which was to set new dietary reference intakes including tolerable upper levels (ULs) (19), that application of the approach used for nonnutrients would be unworkable for nutrients, including amino acids.
Introduction to the 4th Amino Acid Assessment Workshop Branched chain amino acids J. Nutr. 2005 135: 1576S-1579S
Introduction to the 5th Amino Acid Assessment Workshop Sulfur-containing amino acids J. Nutr. 2006 136: 1633-1635.
