Sodium <natrium; atomic weight 22.4X977) is an alkali metal with valence 1.


GLUT2 glucose transporter 2 (SLC2A2) MSG monosodium glutamate

NBC1 sodium/bicarbonate «»transporter 1 (SLC4A4) NHE1 sodium/hydrogen exc hanger-1 (SLCSLC9A1) SGLT1 sodium/glucose cotransporter 1 (SLC5A1)

Nutritional summary

Function: Sodium is the main cationic osmolyte in blood and extracellular fluid, and mediates active transport of numerous nutrients and metabolites in intestines, kidney, and many other tissues.

Food sources; Meats, pickled foods, and salty snacks are the major sodium sources. Requirements Intakes have to match sodium losses. Undermost situations a balance can be achieved with daily intakes ofa few hundred milligrams. Increased sweating (high with exertion, fever, heat, and high humidity) and diuresis can increase sodium needs to several grains per day. Very low sodium intake, for instance w ith fasting, can cause dizziness and weakness due to hypotension.

Excessive intake: I ligher than minimal sodium intakes may increase blood pressure, especially in genetically susceptible indiv ¡duals and when other hypertensive factors (obesity) are present.

Dietary sources

Most sodium in food comes from animal foods, added salt (NaC'l). and sodium salts, such as monosodium glutamatc (MSG), in commercial products. Sodium content of meats tends to correlate inversely with fat content, (,'hickcn (O.X6mg/g) and lish (0.78 mg/g) tend be higher in sodium than beef (0.57 mg^g) and pork (0.47 mg g), Kruits. vegetables, tubers, and grains by themselves have very low sodium content (typically less than 0.1 g-'kg).

Digestion and absorption

Sodium is absorbed nearly completely due to the great solubility of its salts in the aqueous environment of the digestive tract. Mechanisms of sodium uptake into ente-roeytes include cotransport with the sodium/glucose cotransporter (SGI.TI. SLC5AI) and other sodium «»transporters, There is net secretion of sodium into the duodenum, and net absorption in the jejunum. Most of the remaining sodium of the luminal contents are absorbed from the colon.

The driving torce for sodium absorption is the gradient between ihe near isotonic luminal contents and the low sodium concentration inside the intestinal cells. Sodium/ potassium-exchanging ATPase (EC3.6.3.9) pumps, concurrent to the sodium flow from the lumen into the cell, sodium across the basolateral side into the pericapillary space. Most sodium diffuses from there into capillary blood: smaller amounts leak across the tight junctions between the cntcrocytes back into the intestinal lumen. The main flux of sodium into small intestinal cntcrocytes is with bulk nutrients. About 26 g sodium are absorbed w ith lOQg glucose, for example. Since much of this sodium comes from secretions and paracellular back leakage, the few grams of ingested sodium have lit-ile influence on ov erall flux in health. The 2 liters of water absorbed along w ith 100 g glucose can become more important, particularly in diarrhea. The molecular coupling of sodium absorption with both nutrient and water absorption provides the molecular basis for the current practice of using mixed sodium glucose solutions tor rehydration in severe diarrhea.

Sodium also moves into enteroeyles via sodium/hydrogen exchangers 3 (Nlir.3. SLC9A3, oil luminal side) and 2 (Nillï.2. SI.C9A2. on basolateral side), which shuttle

t Small intestine: Enterocyte

HCOs -4

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