Zn & GI gene-expression; Sphingolipids; Thiols, GSH, Jejunum

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Several more citations with whole-text urls:

K. Blanchard and J. Cousins

Regulation of Intestinal Gene Expression by Dietary Zinc: Induction of

Uroguanylin mRNA by Zinc Deficiency [diarrhea signif]

J. Nutr. 2000 130: 1393S-1398S.

http://www.nutrition.org/cgi/reprint/130/5/1393S.pdf

The regulation of gene expression by nutrients plays an important role in the

overall manifestations of nutritional deficiencies. Insufficient intakes of

dietary

micronutrients, such as zinc, produce profound effects in multiple organs and

tissues. One of the major challenges, however, is to identify genes affected by

changes in nutritional status. Differential display of mRNA has proved to be a

valuable technique in meeting this challenge. In our ongoing search for genes

responsive to dietary zinc, we compared small intestinal mRNA from rats that

were fed zinc-deficient or -adequate diets using differential display to

generate 3' anchored expressed sequence tags (EST). EST for intestinal mRNAs

with altered expression due to zinc deficiency include two peptide hormones,

intestinal fatty acid binding protein, intestinal alkaline phosphatase II, a

proteasomal ATPase, cis-Golgi p28 and two subunits of the ubiquinone

oxidoreductase. The EST for one of the hormones yielded the sequence for the 3'

end of an mRNA encoding preprouroguanylin and was used to clone the remaining

portion of the rat cDNA via 5' rapid amplification of cDNA ends. Northern blot

analysis of RNA from rat intestine demonstrated that preprouroguanylin mRNA was

2.5-fold more abundant during zinc deficiency. Uroguanylin, a natriuretic

peptide hormone, is an endogenous ligand for the same guanylate cyclase C that

the Escherichia coli heat-stable enterotoxin (STa) binds when it causes

secretory diarrhea by activating the cystic fibrosis transmembrane conductance

regulator, thus altering fluid balance in the intestine. This suggests a

mechanism whereby zinc deficiency could induce uroguanylin levels in the

intestine and cause or potentiate diarrhea.

Lawrence J. Dahm and Dean P.

Rat Jejunum Controls Luminal Thiol-Disulfide Redox

J. Nutr. 2000 130: 2739-2745.

http://www.nutrition.org/cgi/reprint/130/11/2739.pdf

The control of luminal thiol-disulfide redox state may be important for several

intestinal functions, including absorption of iron or selenium and maintenance

of

mucus fluidity. Disulfides are present in the diet, and although luminal thiols

are supplied in bile, little is known about the ability of the small intestine

to reduce

disulfides to maintain the luminal thiol-disulfide redox state. The objective of

the current study was to determine whether the isolated, vascularly perfused

jejunum,

free from biliary thiols, could reduce intraluminal glutathione disulfide (GSSG)

to glutathione (GSH). GSSG was introduced in a deoxygenated solution to inhibit

the reoxidation of any GSH formed, and preparations were pretreated with

acivicin to inhibit the degradation of GSH by -glutamyltransferase. GSSG (250

µmol/L) was reduced to GSH, with the luminal redox potential (Eh) for GSSG/2GSH

changing from >0 to -111, -132 and -143 mV at 10, 20 and 30 min, respectively.

The Eh for luminal cystine/2cysteine was 20 mV more reducing than that for

GSSG/2GSH at each time point, suggesting that cysteine could function in the

reduction of GSSG in the lumen. Measurements in specific regions showed that

GSSG reduction was more rapid in the duodenum and proximal jejunum than in the

distal jejunum. Preparations without acivicin treatment showed that Eh values

were unaffected by inhibition of -glutamyltransferase despite differences in GSH

and cysteine pool sizes. Rat intestine has a mechanism to adjust the luminal

thiol-disulfide redox. In principle, dysfunction of this mechanism could

contribute to malabsorption or other nutritional disorders.

Hubert Vesper, Eva- Schmelz, na N. Nikolova-Karakashian, Dirck L.

Dillehay, V. Lynch, and Alfred H. Merrill, Jr.

Sphingolipids in Food and the Emerging Importance of Sphingolipids to

Nutrition

J. Nutr. 1999 129: 1239-1250.

http://www.nutrition.org/cgi/reprint/129/7/1239.pdf

Eukaryotic organisms as well as some prokaryotes and viruses contain

sphingolipids, which are defined by a common structural feature, i.e., a

" sphingoid base "

backbone such as D-erythro-1,3-dihydroxy, 2-aminooctadec-4-ene (sphingosine).

The sphingolipids of mammalian tissues, lipoproteins, and milk include

ceramides, sphingomyelins, cerebrosides, gangliosides and sulfatides; plants,

fungi and yeast have mainly cerebrosides and phosphoinositides. The total

amounts of sphingolipids in food vary considerably, from a few micromoles per

kilogram (fruits) to several millimoles per kilogram in rich sources such as

dairy products, eggs and soybeans. With the use of the limited data available,

per capita sphingolipid consumption in the United States can be estimated to be

on the order of 150–180 mmol (~115–140 g) per year, or 0.3–0.4 g/d. There is no

known nutritional requirement for sphingolipids; nonetheless, they are

hydrolyzed throughout the gastrointestinal tract to the same categories of

metabolites (ceramides and sphingoid bases) that are used by cells to regulate

growth, differentiation, apoptosis

and other cellular functions. Studies with experimental animals have shown that

feeding sphingolipids inhibits colon carcinogenesis, reduces serum LDL

cholesterol and elevates HDL, suggesting that sphingolipids represent a

" functional " constituent of food. Sphingolipid metabolism can also be modified

by constituents of the diet, such as cholesterol, fatty acids and mycotoxins

(fumonisins), with consequences for cell regulation and disease. Additional

associations among diet, sphingolipids and health are certain to emerge as more

is learned about these compounds.

Not yet available free online:

E. Lacy and Rosemore

Helicobacter pylori: Ulcers and More: The Beginning of an Era

J. Nutr. 2001 131: 2789S-2793S.

F. Krebs

Bioavailability of Dietary Supplements and Impact of Physiologic State:

Infants, Children and Adolescents

J. Nutr. 2001 131: 1351S-1354S.