Showing papers in "Annual Review of Nutrition in 1987"
TL;DR: The pig as model: The PIG AS MODEL, a chronology of key events and stories from the build-up to the deadliest event in the history of the Great Fire of London, is described.
Abstract: ��:�����:�: ���f;��'::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::::: THE PIG AS MODEL . Maternal and Fetal Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Infant Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Carbohydrate and Lipid Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Amino Acid Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Vitamin and Mineral Nutrition . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CONCLUSION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
679 citations
TL;DR: A comparison of direct and indirect methods for Calorimetry with respect to the 2H2180 technology shows that direct methods are superior to indirect methods in terms of accuracy and efficiency.
Abstract: DIRECT AND INDIRECT CALORIMETRY .. . . . .... . . . . ... . . ..... . . . ..... . ..... . ..... . . ..... . 1 87 Introduction 1 87 Heat Balance Equation ...... 188 Direct Calorimetry . . . . ...... . ....... ...... . . . .. . . . . . . . . . . . . . . . ... . . . .. ..... .... 1 89 Indirect Calorimetry..... . . . . . . . . . . . . . . . . . .. . . . ..... . ... . . . . . . . . . . ... . . . . . . . . . . . . . . . . . ... . . . ...... 190 Indirect Calormietry with a Respiration Chamber 192 FUEL UTILIZATION IN MAN . . . ..... . . . . ..... . ....... .... . ....... ..... . ...... ... . . 193 Theoretical Limitations ..... . . . .. ..... ... . . . ..... . . . .... . . .... . . . . . .... . . .... . ..... .... 195 Physiological Considerations. .. . ........ . . . .... . ..... . . ..... . . .. . . . . .... . ..... . .... . . ...... .... 196 Stoichiometry .. . . ... . . . . . ... . . ........ . ... ...... ..... . . ..... ..... ......... . . ... . .... . . 200 NONCALORIMETRIC METHODS WITH REFERENCE TO THE 2H2180 TECHNIQUE . . . . . . . . . . .. . . . . ..... . . ..... . . ..... . . ... . . . ... . . . .... . .. . . . . ... . . ... . . . . ... . . 203
506 citations
TL;DR: The continuous turnover of intracellular protein and other macromolecules is a basic cellular process that serves, among other functions, to regulate cytoplasmic content and provide amino acids for ongoing oxidative and biosynthetic reactions during nutrient deprivation.
Abstract: The continuous turnover of intracellular protein and other macromolecules is a basic cellular process that serves, among other functions, to regulate cytoplasmic content and provide amino acids for ongoing oxidative and biosynthetic reactions during nutrient deprivation. The intensity of breakdown and pattern of regulation, though, vary widely among cells. Rat hepatocytes, for example, exhibit high absolute rates of proteolysis and regulatory effects that diminish during starvation, while corresponding responses in skeletal and cardiac muscle move in the opposite direction. It is also becoming apparent that effects of insulin and other acute regulatory agents on muscle breakdown are limited to nonmyofibrillar components. The latter may be sequestered and degraded within autophagic vacuoles, whereas myofibrillar proteins require an initial attack by calcium-dependent proteases in the cytosol. By contrast, most if not all of the breakdown of resident (long-lived) proteins as well as RNA in the hepatocyte can be explained by lysosomal mechanisms. The uptake of cytoplasmic components by lysosomes can be divided into two major categories, macroautophagy and micro- or basal autophagy. The first is induced by amino acid or insulin/serum deprivation. In the hepatocyte, amino acids alone can regulate this process almost instantaneously over two thirds of the full range of proteolysis, 4.5% to 1.5% per hour. Glucagon, cyclic AMP, and beta-agonists also stimulate macroautophagy in hepatocytes but have opposite effects in skeletal and cardiac myocytes. Basal autophagy differs from the macro type in that the cytoplasmic "bite" is smaller and sequestration is not acutely regulated. It is, however, adaptively decreased during starvation in parallel with absolute rates of basal turnover. Since endoplasmic reticulum comprises an appreciable fraction of the vacuolar content, volume sequestration would be compatible with the known heterogeneity of individual protein turnover if some proteins (or altered proteins) selectively bind to membranes. The amino acid control of macroautophagy in the hepatocyte is accomplished by a small group of direct inhibitors (Leu, Tyr/Phe, Gln, Pro, Met, Trp, and His) and the permissive effect of alanine whereas only leucine is involved in myocytes and adipocytes. Of unusual interest is the fact that the inhibitory amino acid group alone evokes responses in perfused livers that are identical to those of a complete plasma mixture at 0.5 and 4 times normal plasma levels but loses effectiveness almost completely at normal concentrations.(ABSTRACT TRUNCATED AT 400 WORDS)
407 citations
TL;DR: This chapter discusses the interactions of Tannins and Proteins in the context of determinants of infectious disease, as well as their roles in the food supply and animal welfare.
Abstract: INTRODUCTION 424 TANNINS 424 Chemistry 425 Condensed Tannins ....... . ..... ... ... 426 Hydrolyzable -Tannins ... 426 Assays 426 Biological Roles and Dietary Ef ects 428 Interactions of Tannins and Proteins 430 PROLINE-RICH PROTEINS 432 Background 432 Molecular Biology 433 Functional Aspects 433 SUMMARY AND FUTURE CONSIDERATIONS 435
393 citations
260 citations
248 citations
TL;DR: The hybrid gene approach, so successful for PEPCK and HMG-CoA reductase, also will be effective in defining cis-acting hormone- or metabolite-regulatory elements in other genes, and should be applicable to both transcriptional and post-transcriptional mechanisms.
Abstract: The mechanisms of the responses of an enzyme to different hormones and metabolites or several enzymes to a single hormone are surprisingly varied. There is neither an operon for lipogenic enzymes nor a common step at which hormones and metabolites coordinately regulate the expression of lipogenic genes. In bacteria, coordinated expression of several enzymes in a single metabolic pathway often is achieved by organizing the genes into operons. An operon is a group of genes linked together in a linear fashion and producing a polycistronic mRNA. Trans-acting factors regulate the transcription of these genes by interacting with promoter/regulatory sequences in the 5'-flanking region of the most 5'-ward of the genes. In vertebrate animals, however, coordinated control of gene transcription is not achieved by linking the individual genes, but by putting in the 5'-flanking regions of these genes a regulatory sequence that interacts with common trans-acting factors. Genes controlled by different hormones are expected to have regulatory elements for each hormone. The presence of glucocorticoid and cyclic AMP regulatory elements at the 5'-end of the PEPCK gene is consistent with this notion. Transcription is not the only step at which hormones and metabolites control the pathways for gene expression. The levels of the mRNAs for L-PK, ME, S11, and S14 are increased by T3 at post-transcriptional steps. Glucagon also regulates the accumulation of ME mRNA post-transcriptionally. Neither the mechanism nor the sequence organization of regulatory elements is known for post-transcriptional control of gene expression. In the case of PEPCK and HMG-CoA reductase, the next steps will be to determine more precisely the sequences in the 5'-region that mediate hormone sensitivity and feedback inhibition, respectively, and whether trans-acting factors are involved. For the other genes discussed, identification of the regulated step must precede identification of sequences that confer hormone or metabolite-sensitive regulation on a specific gene. In general, it is probable that the hybrid gene approach, so successful for PEPCK and HMG-CoA reductase, also will be effective in defining cis-acting hormone- or metabolite-regulatory elements in other genes. These techniques should be applicable to both transcriptional and post-transcriptional mechanisms. Our long-term objective is to understand the molecular basis of each event that intervenes between the binding of hormone or metabolite to its appropriate receptor and altered enzyme level.(ABSTRACT TRUNCATED AT 400 WORDS)
186 citations
158 citations
TL;DR: The Glucose-to-Lactate Conversion Take Place and the Fructose-2, 6-bisphosphate Paradox are studied to explore the role of fructose and its role in human and animal health.
Abstract: PERSPECTIVES AND SUMMARy 52 HISTORICAL BACKGROUND 53 Physiological Studies . . . . . ... . . . . . . . . ..... . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . ...... . . . . . . .. . . . . . 53 Biochemical Studies . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . .. . . . . . . . . . . . . . . . . .. . . . . . . . .. . . . . . . . . . . . . . . . . 54 EMERGENCE OF THE GLUCOSE PARADOX. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56 ATTEMPTS TO RESOLVE THE PARADOX . . . . . . . . . . . 56 Experiments in Animals. . . . . . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .... . . . . . . .. . . . . . . .... . . . . 57 Experiments in Humans . . . . . 61 A Noninvasive Approach . . . . . . . . . . . . . . . . . . . . .. ... . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . .... . . 62 UNRESOLVED PROBLEMS..... . 63 Why Is Glucose Not Used Efficiently by the Liver? ... . . . 63 1s Glucose-6-phosphatase Under Metabolic Control? 66 The Fructose-2, 6-bisphosphate Paradox . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 Where Does the Glucose-to-Lactate Conversion Take Place? ... .. . . . . . . . . .. . . . . . . ... . . . 67 Is There an Advantage to the Indirect Pathway? . ......... . . . . . . . . . . . . . . . . 68 CAN THE OLDER AND NEWER FlNDINGS BE RECONCILED? 68 IN RETROSPECT ..... . . .... . . . . . . . . . . . . . . . . . 69
137 citations
TL;DR: The anti-freezing properties of Vitamin B 12 have been studied through a variety of routes, including passive and active administration, as well as through a number of experimental procedures.
Abstract: INTRODUCTION 292 BACKGROUND INFORMATION 292 Chemistry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . 292 Diet ........ . . .. ........ ... . . . . . .. . ... .... . . . . . ......... . . . . . . . . . ... . .. 293 Absorption . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 293 Storage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 294 Plasma Binding of Vitamin BJ2 . . . . .... . . ........ . . ........ ....... ........ . . . . . . . .... 294 Entry of Cobalamin into the Cytoplasm of the Cell .... . . . . . . . . . .. .. . 296 RECOGNITION AND INVESTIGATION OF DEFICIENCY OF VITAMIN B12 ...... 297 DEFECTS IN THE ENTRY OF VITAMIN BI2 INTO THE BODy 298 Children Born of Mothers Deficient in Vitamin B 12 298 Defective Absorption of Vitamin B J2 299 TRANSCOBALAMINS .... 302 Transcobalamin II ... . . . . . . . . ...... . . ..... . . . . . . . . . ........ 302 Deficiency of R Binder . . . . . . . . . . . . . . . . . . . ..... . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . 305 Defective Retention or Mobilization of B J2 .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. 306 DISORDERS OF UTILIZATION 306 Cobalamin Mutant Classes A and B .. . . . . . . . . . . . ... .. 307 Cobalamin Mutant Classes C and D .. ... ..... .. . . .. . . .. .. . . . . ...... ..... . .. ....... 308 Cobalamin Mutant Classes E and G . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 313 Cobalamin F 314
TL;DR: A comparison of Amino Acid Transport Genes and BIOCHEMICAL and GENETIC APPROACHES to TRANSPORT shows how different approaches to transport have different effects on quality and efficiency.
Abstract: INTRODUCTION 75 CHARACTERIZATION OF AMINO ACID TRANSPORT SYSTEMS . .. . . . . ..... . . . . .. . 76 Neutral Amino Acid Systems: Na+ Dependent ......... .. ...... . . . ......... ...... ... ........ 76 Neutral Amino Acid Systems: Na+ Independent ... . . . ....... . . . ...... . . . . . . .. . . . . . ...... . . . 77 Cationic Amino Acid Systems ... . . . ...... . . . . . . . ..... . . . .. . . ..... . . . . . . . .. . . . . . . ... . . . . . . . .... . 78 Anionic Amino Acid Systems ..... . 79 REGULATION OF AMINO ACID TRANSPORT 79 System A. . . . . . . . . . . . . . . . . . . . . . . . . . . . ..... . . . . . . .. . . . . . . . ..... . . . . . . . . .. . . . .... 79 System L 82 System N. . . . . .... . . . . . . . . . . . . . . . . . . ......... . . .. ....... . . . . .... . . . . . . . ... . . . . . . . .. . . . . . . . . . . . . . . . . . . 83 BIOCHEMICAL APPROACHES TO TRANSPORT 83 GENETIC APPROACHES TO TRANSPORT 84 Cloning Human Amino Acid Transport Genes... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 86 CONCLUDING REMARKS 86
TL;DR: It is clear that many diseases are known to involve defects in vitamin B6 metabolism, but that even more await definitive studies, which have not yet been fully explored.
Abstract: It is clear that many diseases are known to involve defects in vitamin B6 metabolism, but that even more await definitive studies. Furthermore, some functions of vitamin B6, such as its role in glucocorticoid action (21), have been discovered so recently that the medical implications have not yet been fully explored.
TL;DR: The literature hsa been reviewed in an attempt to answer some of the questions related to the nutritional requirements of the elderly.
Abstract: The literature hsa been reviewed in an attempt to answer some of the questions related to the nutritional requirements of the elderly. Calories, protein, amino acids, carbohydrate, fat, vitamins A, B, C, D, calcium, iron, sodium, potassium, and fluid studies in the elderly are summarized. Nutritional recommendations are included.
TL;DR: This paper presents a probabilistic procedure for determining the intracellular structure of the cell wall of thelonol-BINDing protein and demonstrates its ability to reprogram the response of the immune system to accommodate these receptors.
Abstract: INTRODUCTION 321 CELLULAR RETINOL-BINDING PROTEIN 322 Detection and Quantitation 322 Physiochemical and Spectral Properties 323 Tissue and Cellular Distribution 324 Putative Functions 325 CELLULAR RETINOIC ACID-BINDING PROTEIN 328 Detection and Quantitation 328 Physiochemical and Spectral Properties 328 Tissue and Cellular Distribution 329 Putative Functions 329 CELLULAR RETINOL-BINDING PROTEIN TYPE II 330 Detection and Quantitation .... ........ . . . 330 Physiochemical and Spectral Properties 330 Tissue and Cellular Distribution 33 I Putative Functions 331 RELATEDNESS OF INTRACELLULAR VITAMIN A-BINDING PROTEINS ........ 332
TL;DR: The aim of this monograph is to provide a Discussion of the Foundations of Lipoprotein Metabolism and its Applications in Nutrition, as well as some of theMechanisms used in the Preparation and Administration of Lipofiltration.
Abstract: INTRODUCTION . ........ . . .. . . . . . . . . . .. . . . . . . . . . . . . . . . . . . ... . . . . . ....... . . . . ...... . . ....... . . . . ..... 273 OVERVIEW. . . . . ... .. . . . . ...... . . . . . . . . ... . . . . . . . . . . .. . . . . . . . ... . . . . . . ........ . .. . . . . 274 OBESITY AND CALORIC INTAKE.. . .. . . . . . . . . .... . . .. . . .... . . . .. ....... . . . ....... . . . ....... . . 275 Obesity and Cholesterol Metabolism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . 275 Obesity and Lipoprotein Metabolism.... . ... . . . . . . . . . . ......... 276 DIETARY CHOLESTEROL.... . . . . . ..... . . . . . . . ... . . . . . . .. . . . . . . . .... . . . . ..... . . . . . ..... . . . . . ..... 277 Dietary Cholesterol and Cholesterol Metabolism. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 Dietary Cholesterol and Lipoprotein Metabolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279 DIETARY FAT QUALITy.. . . . . . . . . .. . . . . . . . ... .. . . . . . . . ... . . . . . ..... . . . .... .. . . .. ...... . . . ....... 281 Dietary Fat and Cholesterol Metabolism . . . . .... . . . . .. . . . . . . . ..... .... . . . . ....... 281 Dietary Fat and Lipoprotein Metabolism . . . ..... . . .. .... . . . .... . . . ........ . . . ..... 282 DIETARY FAT AND CARBOHYDRATE QUANTITIES ... . . . ..... . . . . .. ... . . . . .... . . . . ... 283 Dietary Fat and Carbohydrate Quantity and Cholesterol Metabolism . ..... . . . . ..... . . 283 Dietary Fat and Carbohydrate Quantity and Lipoprotein Metabolism . . ..... . . . . . ..... 284 SUMMARY AND DiSCUSSION.. ... ....... . . . ........ . ...... . . ...... . . . . . ... .. . . . .... . . . . ....... 285
TL;DR: Despite the role of natural causes, the conclusion is inescapable that modern famines, like most of those in history, are man-made.
Abstract: Famines are sustained, extreme shortages of food among discrete populations sufficient to cause high rates of mortality. Signs and symptoms of prolonged food deprivation include loss of fat and subcutaneous tissue, depression, apathy, and weakness, which progress to immobility and death of the individual, often from superimposed respiratory or other infections. The social consequences of famines are disruption from mass migrations of people in search of food, breakdown of social behavior, abandonment of cooperative effort, loss of personal pride and sense of family ties, and finally a struggle for individual survival. Famines have been common ever since the development of agriculture made human settlements possible. Food shortages due to crop failures caused by natural disasters including poor weather, insect plagues, and plant diseases; crop destruction due to warfare; and enforced starvation as a political tool are by no means the only causative factors. Many of the worst famines have been due to poor distribution of existing food supplies, either because of inequities that result in a lack of purchasing power on the part of the poor or because of political interference with normal distribution or relief movements of food. Europe and Asia, which in the past experienced frequent severe famines, sometimes with deaths in the hundreds of thousands or millions, have now largely eliminated famines through social and technological change. However, in Africa, political and social factors have destroyed the capacity of many populations to survive drought-induced variations in local food supplies and prices. Thus, famines are due to varying combinations of inadequacy of food supplies for whatever reason and the inability of populations to acquire food because of poverty, civil disturbances, or political interference. Despite the role of natural causes, the conclusion is inescapable that modern famines, like most of those in history, are man-made.
TL;DR: This chapter discusses the evolution of Dietary Standards, Dietary recommendations 1835-1940, and Directions in RDA, which are Dietary Standards Based on Scientific Principles.
Abstract: Introduction ........ , , " 509 Evolution of Dietary Standards 510 Dietary recommendations 1835-1940 510 Recommended dietary allowances 515 Other dietary standards , , 516 RDA Are Dietary Standards Based on Scientific Principles 518 Primary use of RDA .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. .. . 518 Scientific bases for RDA 518 Purposes for Which RDA Have Been Used 522 Information and education 522 Food and nutrition regulations 524 Developm�nt of ,!�w and special foods 524 Therapeutic nutrltlOn ......... 525 Standards for food programs 525 Evaluating the Adequacy of Nutrient Intakes 526 The probability approach 527 Dietary Standards and Guidelines for Healthful Diets 529 Misunderstanding of RDA .. 529 Guidelines for healthful diets , 530 Directions in Dietary Standards and Guidelines 532 Directions in RDA , ........ , ....... ,. 532 Dietary guidelines ....... , 533 Diet and disease 534
TL;DR: The present study focuses on the development of a strategy for sustainable human nutrition in the developing world and its applications in the context of food and health.
Abstract: INTRODUCTION 466 HISTORICAL DEVELOPMENT 466 WEIGHT LOSS 467 NUTRITIONAL ADEQUACy 470 Protein Losses 471 Electrolyte and Mineral Losses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474 Vitamin Nutritional Status .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 477 CLINICAL PROBLEMS 477 APPROPRIATE TARGET POPULATION . 479 SUMMARY AND RECOMMENDATIONS 480
TL;DR: This study examines the relationship between diet, Nutrition, and Health Relationships, and Survey Characteristics in the context of national health and nutrition surveys and investigates the role of bias.
Abstract: BACKGROUND... . . . . . . . . . . ..... 442 National Health Examination Surveys 442 National Health and Nutrition Examination Surveys . . . ... . . . . . . . . . . . ......... 443 Hispanic HANES 445 Future NHANES 445 Survey Characteristics 445 FACTORS INFLUENCING USE AND INTERPRETATION 446 Nonresponse Bias 447 Measurement Bias 448 Weighting !" acto�s a�d Design Effects 449 Interpretative Criteria 450 ANALYSES AND RESULTS 451 Distributional Analyses 451 Diet, Nutrition, and Health Relationships ....... 457 CONCLUSIONS.... . . . . . . . . .. . . .. ..... . . . . . . ... . . . . . . . . . ........ . . . . . 458
TL;DR: The structure of DNA in the nucleus and its role in gene expression, as well as the role of phosphorous in this structure, are studied.
Abstract: INTRODUCTION 407 ORGANIZATION OF DNA IN THE NUCLEUS 408 CHROMATIN STRUCTURE AND GENE EXPRESSION...... ......... 410 NUTRIENT EFFECTS ON CHROMATIN STRUCTURE ...... 410 Higher·Order Structure . . . . . . . . . . . . . . 410 Chromatin Subunit Organization .... 414 Nutrient Effects on Nuclear Proteins..... 414 NUTRIENT EFFECTS ON DNA METHyLATION 415 CONCLUSIONS 417
TL;DR: Water Losses in the Very Immature, Vitamin D, Calcium, and Phosphorus Requirements, and Needs for Growth.
Abstract: IN TRODUC TION . . . . . . . . . . ... . . . . . . ... .. . . . . .. . . ..... . . . . . . . . . . . . . . ... . . . . . . . . ....... . . . . . . . . . . . . . . . . 92 Special Nutritional Problems of the Very Immature . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 92 WA TER REQUIREMEN TS . . . . . . . . . . . . . . . . . .. . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95 Water as a Major Nutrient . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . ...... . . . . . . . . . . . . . . . .. . . . . . . . . . . 95 Water Losses in the Very Immature. . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ... . . . . . . . . . . . 95 ENERGY RE QUIREMENTS . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ...... .. . . .... . . . . . . . . . . . . . . . . . . 96 Energy Needs for Growth . . . ........ . 96 Resting Metabolic Rate . . ...... . . . . ....... 97 Needs of Incidental Cold Stress......... . . . . ........ . . ....... . . . . .. 97 Losses of Unabsorbed Nutrients . ......... . 97 Provision of Dietary Energy . . . 98 PROTEIN REQUIREMENTS. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99 Needs for Growth . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . .... . . . ....... . . .... . . . . . . . . . . . . . . . . . . 99 Protein Requirement and Energy Intake ........ . . ....... 99 Protein Quality . . . . ....... . . . ........ . . . . . ...... . . . 100 Minimum and Maximum Intakes . . . . . .... . . . . . . . ... . . . . . . . . ..... . . .... . ... . ....... . . ...... . . . . . 1 00 CALCIUM AND PHOSPHORUS HOMEOS TASIS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 100 Metabolic Bone Disease of Prematurity . ........ 100 Vitamin D, Calcium, and Phosphorus Requirements .... . . . .... . . ....... . . . ....... ........ 1 0 1 E LEC TROLY TE N UTRITION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102 Sodium Requirements . . . . . . . . .. ..... . . . . . . .. . . . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . .. 102 Potassiu:.'" and Chloride Requirements .. . . . . . ...... . . . ...... . . . . . . . . . . . . .. .. . . . . . . .. . . . . .. .. . 103 TRACE NUTRIENT REQUIREMENTS . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103 Vitamins . . . ....... . ....... . . . . ...... . . . . . ...... . . . . . ..... . . . . ... . . . . . . . .. . . . 103 Iron and the Trace Elements . . . . 105 Carnitine and Essential Fatty Acids .. . ..... . ...... . . . ..... . . . .... . . . ....... . . .. 107 APPROACH TO FEEDING AND NUTRITION . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 Early Management. . ....... . . . . . . ......... 108 Later Management. . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . 108 CON CLUSION . . . . . . . . . .. . . . . ... . . . . . . . . . . . . . . . ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 10