{"id":1070,"date":"2017-10-27T16:55:05","date_gmt":"2017-10-27T16:55:05","guid":{"rendered":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/?post_type=chapter&p=1070"},"modified":"2017-11-14T17:57:31","modified_gmt":"2017-11-14T17:57:31","slug":"13-2-sodium","status":"publish","type":"chapter","link":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/chapter\/13-2-sodium\/","title":{"raw":"13.2 Sodium","rendered":"13.2 Sodium"},"content":{"raw":"
\r\n\r\nSalt (NaCl) contributes almost all the sodium that we consume. 75-85% of the salt we consume is from processed foods, 10% is naturally in foods, and added salt contributes 10-15% of total salt intake1<\/sup>.\r\n\r\n95-100% of consumed sodium is absorbed2. Sodium is taken up into the enterocyte through multiple mechanisms before being pumped out of the enterocyte by sodium-potassium (Na+\/K+) ATPase. Sodium-potassium ATPase is an active carrier transporter that pumps 3 sodium ions out of the cell and 2 potassium ions into the cell, as shown below.\r\n
\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"635\"]\"\" Figure 13.21 Sodium-potassium ATPase (aka sodium-potassium pump), an active carrier transporter3<\/sup>[\/caption]\r\n\r\n<\/div>\r\nSodium is the major cation in extracellular fluid.\r\n\r\nSodium has 3 main functions1<\/sup>:\r\n\r\n1. Fluid balance\r\n\r\n2. Aids in monosaccharide and amino acid absorption\r\n\r\n3. Muscle contraction and nerve transmission (not discussed further below)\r\n\r\n

Fluid balance<\/h3>\r\n\r\nThe body regulates sodium and fluid levels through a series of processes as shown below. A decrease in plasma volume and blood pressure signals the kidney to release the enzyme renin. Renin activates angiotensin that is converted to angiotensin II. Angiotensin II signals the adrenal glands to secrete the hormone aldosterone. Aldosterone increases sodium reabsorption in the kidney, thus decreasing sodium excretion. These actions cause plasma sodium concentrations to increase, which is detected by the hypothalamus. The hypothalamus stimulates the pituitary gland to release antidiuretic hormone (ADH) that causes the kidneys to reabsorb water, decreasing water excretion. The net result is an increase in blood volume and blood pressure1<\/sup>.\r\n
\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"965\"]\"\" Figure 13.22 Response to decreased plasma volume and blood pressure[\/caption]\r\n\r\n<\/div>\r\n

2. Aids in monosaccharide and amino acid absorption<\/h3>\r\n\r\nGlucose and galactose are taken up into the enterocyte by sodium-glucose cotransporter 1 (SGLT1), which requires sodium to be transported along with glucose or galactose.\r\n
\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"1119\"]\"\" Figure 13.23 Carbohydrate Absorption[\/caption]\r\n\r\n<\/div>\r\nAmino acids are taken up and transported into circulation through a variety of amino acid transporters. Some of these transporters are sodium-dependent (require sodium to transport amino acids).\r\n
\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"1135\"]\"\" Figure 13.24 Protein absorption[\/caption]\r\n\r\n<\/div>\r\nSodium deficiency is rare, and is normally due to excessive sweating. Sweat loss must reach 2-3% of body weight before sodium losses are a concern1,2<\/sup>. This situation can occur in marathon runners and ultra-marathon runners who sweat for many hours straight (without proper liquid intake). Low blood sodium levels (hyponatremia) can result in1<\/sup>:\r\n\r\nHeadache\r\n\r\nNausea\r\n\r\nVomiting\r\n\r\nFatigue\r\n\r\nMuscle Cramps\r\n\r\nSodium is not toxic, but higher sodium intake increases the risk of developing high blood pressure. High sodium intake also increases calcium excretion, but studies haven't found an increased risk of osteoporosis. High sodium intake may also increase the risk of developing kidney stones (by increasing calcium excretion), because calcium oxalate is the most common form of kidney stone1<\/sup>.\r\n\r\n

References & Links<\/h3>\r\n\r\n1.\u00a0Byrd-Bredbenner C, Moe G, Beshgetoor D, Berning J. (2009) Wardlaw's perspectives in nutrition. New York, NY: McGraw-Hill.\r\n\r\n2. Gropper SS, Smith JL, Groff JL. (2008) Advanced nutrition and human metabolism. Belmont, CA: Wadsworth Publishing.\r\n\r\n3. https:\/\/en.wikipedia.org\/wiki\/ATPase#\/media\/File:Scheme_sodium-potassium_pump-en.svg\r\n\r\n<\/div>","rendered":"
\n

Salt (NaCl) contributes almost all the sodium that we consume. 75-85% of the salt we consume is from processed foods, 10% is naturally in foods, and added salt contributes 10-15% of total salt intake1<\/sup>.<\/p>\n

95-100% of consumed sodium is absorbed2. Sodium is taken up into the enterocyte through multiple mechanisms before being pumped out of the enterocyte by sodium-potassium (Na+\/K+) ATPase. Sodium-potassium ATPase is an active carrier transporter that pumps 3 sodium ions out of the cell and 2 potassium ions into the cell, as shown below.<\/p>\n

\n
\"\"<\/p>\n

Figure 13.21 Sodium-potassium ATPase (aka sodium-potassium pump), an active carrier transporter3<\/sup><\/p>\n<\/div>\n<\/div>\n

Sodium is the major cation in extracellular fluid.<\/p>\n

Sodium has 3 main functions1<\/sup>:<\/p>\n

1. Fluid balance<\/p>\n

2. Aids in monosaccharide and amino acid absorption<\/p>\n

3. Muscle contraction and nerve transmission (not discussed further below)<\/p>\n

Fluid balance<\/h3>\n

The body regulates sodium and fluid levels through a series of processes as shown below. A decrease in plasma volume and blood pressure signals the kidney to release the enzyme renin. Renin activates angiotensin that is converted to angiotensin II. Angiotensin II signals the adrenal glands to secrete the hormone aldosterone. Aldosterone increases sodium reabsorption in the kidney, thus decreasing sodium excretion. These actions cause plasma sodium concentrations to increase, which is detected by the hypothalamus. The hypothalamus stimulates the pituitary gland to release antidiuretic hormone (ADH) that causes the kidneys to reabsorb water, decreasing water excretion. The net result is an increase in blood volume and blood pressure1<\/sup>.<\/p>\n

\n
\"\"<\/p>\n

Figure 13.22 Response to decreased plasma volume and blood pressure<\/p>\n<\/div>\n<\/div>\n

2. Aids in monosaccharide and amino acid absorption<\/h3>\n

Glucose and galactose are taken up into the enterocyte by sodium-glucose cotransporter 1 (SGLT1), which requires sodium to be transported along with glucose or galactose.<\/p>\n

\n
\"\"<\/p>\n

Figure 13.23 Carbohydrate Absorption<\/p>\n<\/div>\n<\/div>\n

Amino acids are taken up and transported into circulation through a variety of amino acid transporters. Some of these transporters are sodium-dependent (require sodium to transport amino acids).<\/p>\n

\n
\"\"<\/p>\n

Figure 13.24 Protein absorption<\/p>\n<\/div>\n<\/div>\n

Sodium deficiency is rare, and is normally due to excessive sweating. Sweat loss must reach 2-3% of body weight before sodium losses are a concern1,2<\/sup>. This situation can occur in marathon runners and ultra-marathon runners who sweat for many hours straight (without proper liquid intake). Low blood sodium levels (hyponatremia) can result in1<\/sup>:<\/p>\n

Headache<\/p>\n

Nausea<\/p>\n

Vomiting<\/p>\n

Fatigue<\/p>\n

Muscle Cramps<\/p>\n

Sodium is not toxic, but higher sodium intake increases the risk of developing high blood pressure. High sodium intake also increases calcium excretion, but studies haven’t found an increased risk of osteoporosis. High sodium intake may also increase the risk of developing kidney stones (by increasing calcium excretion), because calcium oxalate is the most common form of kidney stone1<\/sup>.<\/p>\n

References & Links<\/h3>\n

1.\u00a0Byrd-Bredbenner C, Moe G, Beshgetoor D, Berning J. (2009) Wardlaw’s perspectives in nutrition. New York, NY: McGraw-Hill.<\/p>\n

2. Gropper SS, Smith JL, Groff JL. (2008) Advanced nutrition and human metabolism. Belmont, CA: Wadsworth Publishing.<\/p>\n

3. https:\/\/en.wikipedia.org\/wiki\/ATPase#\/media\/File:Scheme_sodium-potassium_pump-en.svg<\/p>\n<\/div>\n\n\t\t\t

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Candela Citations<\/h3>\n\t\t\t\t\t
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