J. Nutr. 1 May 2003; Vol. 133, No. 5 titles and available abstracts

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Hi All, See the below J. Nutr. 1 May 2003; Vol. 133, No. 5 and abstracts are

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J. Nutr. -- Table of Contents Alert

A new issue of Journal of Nutrition has been made available:

1 May 2003; Vol. 133, No. 5

Environmental Contamination and Chronic Inflammation Influence Human Growth

Potential

Noel W. s

J. Nutr. 2003;133 1237

Soy Isoflavones Exert Antidiabetic and Hypolipidemic Effects through the

PPAR Pathways in Obese Zucker Rats and Murine RAW 264.7 Cells

Orsolya Mezei, J. Banz, W. Steger, R. Peluso,

Todd A. Winters, and Neil Shay

J. Nutr. 2003;133 1238-1243

Dietary Soy Protein Maintains Some Indices of Bone Mineral Density and Bone

Formation in Aged Ovariectomized Rats

C. Blum, ne N. Heaton, Beth M. Bowman, Maren Hegsted,

and C.

J. Nutr. 2003;133 1244-1249

Soy Protein Isolate Enhances Hepatic Copper Accumulation and Cell Damage in

LEC Rats

Kayo Yonezawa, Sachiko Nunomiya, Mitsue Daigo, Yasumitsu Ogra, Kazuo

T. Suzuki, Katsuhiko Enomoto, Hitoshi Nakagama, Kunie Yoshikawa, and

Minako Nagao

J. Nutr. 2003;133 1250-1254

The Addition of Soybean Phosphatidylcholine to Triglyceride Increases

Suppressive Effects on Food Intake and Gastric Emptying in Rats

Megumi Nishimukai, Hiroshi Hara, and Yoritaka Aoyama

J. Nutr. 2003;133 1255-1258

New Leptin Receptor Mutations in Mice: Leprdb-rtnd, Leprdb-dmpg and

Leprdb-rlpy

Jung Han Kim, N. , Dawn Young, Son Yong Karst, Patsy M.

Nishina, and Jurgen K. Naggert

J. Nutr. 2003;133 1265-1271

Methylenetetrahydrofolate Reductase 677C->T Variant Modulates Folate Status

Response to Controlled Folate Intakes in Young Women

Cheryl L. Guinotte, G. Burns, A. Axume, Hiroko Hata,

Tania F. Urrutia, Alamilla, Dale McCabe, Anny Singgih, A.

Cogger, and Marie A. Caudill

J. Nutr. 2003;133 1272-1280

The Interaction between MTHFR 677 C->T Genotype and Folate Status Is a

Determinant of Coronary Atherosclerosis Risk

Domenico Girelli, Nicola elli, Francesca Pizzolo, Simonetta

Friso, Oliviero Olivieri, Chiara Stranieri, betta Trabetti,

Giovanni Faccini, Tinazzi, Pier Franco Pignatti, and o

Corrocher

J. Nutr. 2003;133 1281-1285

Several Culinary and Medicinal Herbs Are Important Sources of Dietary

Antioxidants

Steinar Dragland, Haruki Senoo, Kenjiro Wake, Kari Holte, and Rune

Blomhoff

J. Nutr. 2003;133 1286-1290

Betaine Supplementation Lowers Plasma Homocysteine in Healthy Men and Women

Gery R. Steenge, Petra Verhoef, and Martijn B. Katan

J. Nutr. 2003;133 1291-1295

Strawberry Anthocyanins Are Recovered in Urine as Glucuro- and

Sulfoconjugates in Humans

Felgines, Severine Talavera, Marie-e Gonthier, Odile

Texier, Augustin Scalbert, Jean-Louis Lamaison, and Christian Remesy

J. Nutr. 2003;133 1296-1301

Concentrations of Choline-Containing Compounds and Betaine in Common Foods

H. Zeisel, Mei-Heng Mar, tte C. Howe, and Joanne M. Holden

J. Nutr. 2003;133 1302-1307

Postprandial Kinetics of Dietary Amino Acids Are the Main Determinant of

Their Metabolism after Soy or Milk Protein Ingestion in Humans

Cecile Bos, Cornelia C. Metges, Gaudichon, Klaus J. Petzke,

E. Pueyo, Celine Morens, Everwand, Benamouzig, and

Tome

J. Nutr. 2003;133 1308-1315

Soy Isoflavones Do Not Modulate Circulating Insulin-Like Growth Factor

Concentrations in an Older Population in an Intervention Trial

F. , M. Newton, Chu Chen, S. Emerson,

D. Potter, White, and Johanna W. Lampe

J. Nutr. 2003;133 1316-1319

Folate Derived from Cecal Bacterial Fermentation Does Not Increase Liver

Folate Stores in 28-d Folate-Depleted Male Sprague-Dawley Rats

E. Sepehr, R. W. Peace, K. B. Storey, P. Jee, B. J. Lampi, and S. P.

J.

J. Nutr. 2003;133 1347-1354

Hydrolytic Activity toward Pyridoxine-5'-{beta}-D-Glucoside in Rat

Intestinal Mucosa Is Not Increased by Vitamin B-6 Deficiency: Effect of

Basal Diet Composition and Pyridoxine Intake

Amy D. Mackey, Siam O. Lieu, Carman, and F. ,

III

J. Nutr. 2003;133 1362-1367

Rye Bread in the Diet of Pigs Enhances the Formation of Enterolactone and

Increases Its Levels in Plasma, Urine and Feces

Knud Bach Knudsen, Anja Serena, Kirstin Bjornbak Kjaer, Inge

Tetens, Satu-Maarit Heinonen, Tarja Nurmi, and Herman Adlercreutz

J. Nutr. 2003;133 1368-1375

The Total Branched-Chain Amino Acid Requirement in Young Healthy Adult Men

Determined by Indicator Amino Acid Oxidation by Use of

L-[1-13C]Phenylalanine

Roya Riazi, J. Wykes, O. Ball, and B. Pencharz

J. Nutr. 2003;133 1383-1389

Cod Protein Lowers the Hepatic Triglyceride Secretion Rate in Rats

Isabelle Demonty, Yves Deshaies, Benoit Lamarche, and Helene Jacques

J. Nutr. 2003;133 1398-1402

Chronic Consumption of a Moderately Low Protein Diet Does Not Alter

Hematopoietic Processes in Young Adult Mice

Zhixin L. Huang and Pamela J. Fraker

J. Nutr. 2003;133 1403-1408

Dietary (n-3)/(n-6) Fatty Acid Ratio: Possible Relationship to

Premenopausal but Not Postmenopausal Breast Cancer Risk in U.S. Women

L. Goodstine, Tongzhang Zheng, Theodore R. Holford, Barbara A.

Ward, Darryl , H. Owens, and T. Mayne

J. Nutr. 2003;133 1409-1414

A Longitudinal Comparison of Body Composition by Total Body Water and

Bioelectrical Impedance in Adolescent Girls

M. , G. Bandini, Dung V. Compton, Elena N.

Naumova, and Aviva Must

J. Nutr. 2003;133 1419-1425

The Role of Passive Transport in Calcium Absorption

Felix Bronner, Boris Slepchenko, J. Wood, and le Pansu

J. Nutr. 2003;133 1426

Reply to Bonner et al.

C. McCormick

J. Nutr. 2003;133 1427

Supplement: 11th International Symposium on Trace Elements in Man and

Animals

Introduction

Janet C. King

J. Nutr. 2003;133 1429-1430

Trace Elements and Nitric Oxide Function

A. Marletta and M. Spiering

J. Nutr. 2003;133 1431-1433

Underwood Memorial Lecture: Human Zinc Homeostasis: Good but Not Perfect

Hambidge

J. Nutr. 2003;133 1438-1442

Trace Elements and Host Defense: Recent Advances and Continuing Challenges

Mark L. Failla

J. Nutr. 2003;133 1443-1447

Role of Copper, Zinc, Selenium and Tellurium in the Cellular Defense

against Oxidative and Nitrosative Stress

Lars-Oliver Klotz, Klaus-Dietrich Kroncke, Darius P. Buchczyk, and

Helmut Sies

J. Nutr. 2003;133 1448-1451

Zinc-Altered Immune Function

Klaus-Helge Ibs and Lothar Rink

J. Nutr. 2003;133 1452-1456

Selenium in the Immune System

R. Arthur, Roderick C. McKenzie, and Geoffrey J. Beckett

J. Nutr. 2003;133 1457-1459

Cellular Zinc and Redox States Converge in the Metallothionein/Thionein

Pair

Wolfgang Maret

J. Nutr. 2003;133 1460-1462

Selenium Deficiency and Viral Infection

Melinda A. Beck, Orville A. Levander, and Handy

J. Nutr. 2003;133 1463-1467

Iron Deficiency Alters Brain Development and Functioning

Beard

J. Nutr. 2003;133 1468-1472

Genetically Modified Plants for Improved Trace Element Nutrition

Bo Lonnerdal

J. Nutr. 2003;133 1490-1493

Novel Roles for Iron Regulatory Proteins in the Adaptive Response to Iron

Deficiency

S. Eisenstein and Kerry L. Ross

J. Nutr. 2003;133 1510-1516

Selenoprotein Metabolism and Function: Evidence for More than One Function

for Selenoprotein P

F. Burk, a E. Hill, and Amy K. Motley

J. Nutr. 2003;133 1517-1520

Regulation of Zinc Metabolism and Genomic Outcomes

J. Cousins, K. Blanchard, J. Bernadette , Li Cui,

Calvert L. Green, P. Liuzzi, Jay Cao, and A. Bobo

J. Nutr. 2003;133 1521-1526

http://www.nutrition.org/cgi/content

Genetic Defects in Copper Metabolism

Hoon Shim and Z. Leah

J. Nutr. 2003;133 1527-1531

Health Effects and Risk Assessment of Arsenic

O. Abernathy, J. , and L. Calderon

J. Nutr. 2003;133 1536-1538

Nutritional Factors May Modify the Toxic Action of Methyl Mercury in

Fish-Eating Populations

W. son and J. J. Strain

J. Nutr. 2003;133 1539-1543

The Metabolic Tune-Up: Metabolic Harmony and Disease Prevention

Bruce N. Ames

J. Nutr. 2003;133 1544-1548

Ferritin: At the Crossroads of Iron and Oxygen Metabolism

C. Theil

J. Nutr. 2003;133 1549-1553

Marginal Dietary Selenium Intakes in the UK: Are There Functional

Consequences?

Malcolm J. , Caroline S. Broome, and Francis MCArdle

J. Nutr. 2003;133 1557-1559

Approaches to Improve Iron Bioavailability from Complementary Foods

Lena sson

J. Nutr. 2003;133 1560-1562

Assessment of the Trace Element Status of Individuals and Populations: The

Example of Zinc and Copper

Hotz, Nicola M. Lowe, Magdalena Araya, and H. Brown

J. Nutr. 2003;133 1563-1568

Trace Element Biology: The Knowledge Base and its Application for the

Nutrition of Individuals and Populations

Vernon R. Young

J. Nutr. 2003;133 1581-1587

http://www.nutrition.org/cgi/content/abstract/133/5/1581S?etoc

Abstract Section: 11th International Symposium on Trace Elements in Man and

Animals Abstracts

J. Nutr. 2003;133 203-282

http://www.nutrition.org/cgi/content/full/133/5/203E?etoc

Postprandial Kinetics of Dietary Amino Acids Are the Main Determinant of

Their Metabolism after Soy or Milk Protein Ingestion in Humans

Cecile Bos, et al, and Tome

J. Nutr. 2003;133 1308-1315

Soy proteins have been shown to result in lower postprandial nitrogen retention

than milk proteins, but the mechanisms

underlying these differences have not been elucidated. To investigate this

question, we measured the postprandial kinetics of the

appearance of individual 15N-amino acids in the serum of healthy adults after

the ingestion of either 15N-soy (n = 8) or

15N-milk proteins (n = 8) in a mixed single meal (46 kJ/kg). The kinetics of

total and dietary amino acids (AA) in the peripheral

circulation were characterized by an earlier and higher peak after soy protein

ingestion. Dietary AA levels peaked at 2.5 h in the

soy group vs. 3.9 h in the milk group (P < 0.02). This time interval difference

between groups was associated with a faster

transfer of dietary N into urea in the soy group (peak at 3 vs. 4.75 h in the

milk group, P < 0.005) and a higher level of

incorporation into the serum protein pool from 3 to 8 h after the soy meal. The

dietary AA pattern in the peripheral blood

closely reflected the dietary protein AA pattern. Postprandial glucose, insulin,

and glucagon levels and profiles did not differ

between groups. Soy AA were digested more rapidly and were directed toward both

deamination pathways and liver protein

synthesis more than milk AA. We conclude that differences in the metabolic

postprandial fates of soy and milk proteins are due

mainly to differences in digestion kinetics; however, the AA composition of

dietary proteins may also play a role.

KEY WORDS: dietary protein • amino acids • postprandial metabolism • GC-C-IRMS •

humans

Bruce N. Ames

The Metabolic Tune-Up: Metabolic Harmony and Disease Prevention

J. Nutr. 2003 133: 1544S-1548S. [Abstract] [Full Text]

An optimum intake of micronutrients and metabolites, which varies with age and

genetic constitution, would tune up metabolism

and give a marked increase in health, particularly for the poor and elderly, at

little cost. 1) DNA damage. Inadequate intake of

folic acid causes millions of uracils to be incorporated into the DNA of each

cell with associated chromosome breaks,

essentially producing a radiation mimic. Deficiencies of the metabolically

connected vitamins B-6 and B-12, which are also

widespread, also cause uracil incorporation and chromosome breaks. Inadequate

iron intake (2 billion women in the world;

25% of U.S. menstruating women) causes oxidants to leak from mitochondria and

damages mitochondria and mitochondrial

DNA. Inadequate zinc intake (10% in the U.S.) causes oxidation and DNA damage in

human cells. 2) The Km concept.

Approximately 50 different human genetic diseases that are due to a poorer

binding affinity (Km) of the mutant enzyme for its

coenzyme can be remedied by feeding high-dose B vitamins, which raise levels of

the corresponding coenzyme. Many

polymorphisms also result in a lowered affinity of enzyme for coenzyme. 3)

Mitochondrial oxidative decay with age. This

decay, which is a major contributor to aging, can be ameliorated by feeding old

rats the normal mitochondrial metabolites acetyl

carnitine and lipoic acid at high levels. They restore the Km for acetyl

carnitine transferase and the velocity of the reaction as

well as mitochondrial function; reduce levels of oxidants, neuron RNA oxidation

and mutagenic aldehydes; and increase old-rat

ambulatory activity and cognition.

KEY WORDS: essential vitamins and minerals • DNA damage • aging • cancer

W. son and J. J. Strain

Nutritional Factors May Modify the Toxic Action of Methyl Mercury in

Fish-Eating Populations

J. Nutr. 2003 133: 1539S-1543S. [Abstract] [Full Text]

The historical record of clinical cases of methyl mercury poisoning dates back

to the 19th century when the first chemical

synthesis occurred. The potent fungicidal properties of both methyl and the

closely related ethyl mercury compound were

subsequently discovered, which led to widespread agricultural application for

prevention of fungal infection in seed grain.

Several catastrophic outbreaks of poisoning occurred in the mid-20th century

when the treated seed grain was mistakenly used

to prepare homemade bread. The largest outbreak took place in rural Iraq in the

early 1970s. Human poisonings also occurred

in Japan due to the release of methyl mercury into bodies of fresh and ocean

water. The most infamous outbreak occurred in

the area of Minamata Bay: methyl mercury, which was unwittingly discharged into

the ocean water, avidly accumulated in the

aquatic food chain to such an extent that people who consumed fish were severely

poisoned. Today, human exposure to methyl

mercury occurs from consumption of fish and sea mammals. Inorganic mercury that

is present in aquatic sediments is methylated

by microorganisms and accumulates in the aquatic food chain. Although no cases

of clinical poisoning have been reported, a

number of epidemiological studies have been carried out that raise the

possibility of prenatal damage. Previous studies

(especially the Iraq outbreak) indicate that the prenatal stage of the life

cycle is the most vulnerable. However, ongoing

epidemiological studies of heavy fish consumers of the Seychelles Islands in the

Indian Ocean do not reveal adverse effects. To

the contrary, the results of some developmental tests that were conducted on

prenatally exposed children indicate beneficial

outcomes that correlate with mercury levels during pregnancy. This article

discusses the potential role of micronutrients in fish as

a plausible explanation for these findings.

Lars-Oliver Klotz, Klaus-Dietrich Kröncke, Darius P. Buchczyk, and Helmut

Sies

Role of Copper, Zinc, Selenium and Tellurium in the Cellular Defense

against Oxidative and Nitrosative

Stress

J. Nutr. 2003 133: 1448S-1451S. [Abstract] [Full Text]

The trace elements copper, zinc and selenium are linked together in cytosolic

defense against reactive oxygen and nitrogen

species. Copper, zinc–superoxide dismutase catalyzes the dismutation of

superoxide to oxygen and hydrogen peroxide. The

latter and other hydroperoxides are subsequently reduced by the selenoenzyme

glutathione peroxidase (GPx). Cytosolic GPx

can also act as a peroxynitrite reductase. The antioxidative functions of these

trace elements are not confined to being

constituents of enzymes: 1) copper and zinc ions may stimulate protective

cellular stress-signaling pathways such as the

antiapoptotic phosphoinositide-3-kinase/Akt cascade and may stabilize proteins,

thereby rendering them less prone to

oxidation; and 2) selenium does not only exist in the cell as selenocysteine (as

in GPx) but also as selenomethionine, which is

regularly present in low amounts in proteins in place of methionine.

Selenomethionine catalyzes the reduction of peroxynitrite at

the expense of glutathione. Also, low-molecular-weight organoselenium and

organotellurium compounds of pharmacologic

interest catalyze the reduction of hydroperoxides or peroxynitrite with various

cellular reducing equivalents.