What Is The Function Of Potassium In The Body – Potassium is an essential dietary mineral and electrolyte. The term electrolyte refers to a substance that dissociates into ions (charged particles) in solution, enabling it to conduct electricity. Normal physiological function depends on the tight regulation of potassium concentration both inside and outside cells (1).
) is the principal cation in the extracellular fluid. The concentration of potassium is 30 times higher inside than outside cells, while the concentration of sodium is 10 times higher than inside cells. The concentration difference between potassium and sodium across the cell membrane creates an electrochemical gradient known as the membrane potential. The cell membrane potential is maintained by ion pumps in the cell membrane, mainly Na
What Is The Function Of Potassium In The Body
ATPase pump. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium (Figure 1). Their activity is estimated to account for 20%-40% of the rest of the energy expenditure in a normal adult. The large fraction of energy devoted to maintaining the sodium/potassium concentration gradient emphasizes the importance of this function in sustaining life. Tight control of cell membrane potential is important for nerve impulse transmission, muscle contraction, and cardiac function (2-4).
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ATPase requires the presence of sodium and potassium. The presence of potassium is also essential for the activity of pyruvate kinase, an important enzyme in carbohydrate metabolism (5).
An abnormally low plasma potassium concentration is called hypokalemia. Hypokalemia is often the result of excess potassium loss, for example, due to prolonged vomiting or diarrhea, the use of certain diuretics and other drugs (see DRUG INTERACTIONS), some forms of kidney disease, or metabolic disorders. Symptoms of hypokalemia are associated with alterations in membrane potential and cellular metabolism (1). These include fatigue, muscle weakness and pain, and intestinal paralysis, which may cause bloating, constipation, and abdominal pain. Chronic hypokalemia is associated with hypertension and kidney stone formation (see Disease Prevention and Treatment). Severe hypokalemia can result in muscle paralysis or cardiac arrhythmias that can be fatal (1, 6).
Low dietary potassium intake alone does not usually result in hypokalemia. However, in patients at risk for hypokalemia, insufficient dietary potassium can precipitate hypokalemia (1).
In rare cases, the habitual consumption of large amounts of black licorice results in hypokalemia (7, 8). Licorice contains a compound (ie, glyceric acid) with physiological effects of aldosterone, a hormone that increases urinary excretion of potassium.
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Dietary Reference Intakes (DRIs) for potassium have recently been established by the Food and Nutrition Board (FNB) of the National Academy of Medicine. FNB found insufficient evidence to determine an Estimated Average Requirement (EAR) and derive a Recommended Dietary Allowance (RDA); Instead, they established an adequate intake (AI) based on the median intake in normally healthy individuals (Table 1) (9). FNB found insufficient evidence from human studies examining potassium intake in relation to chronic morbidity and mortality (recently reviewed by the Agency for Healthcare Research and Quality; 10) to inform DRIs for potassium (11). .
The diets of people living in Western industrialized countries are very different from those consumed before the agricultural revolution and the transition to consumption of highly refined, processed foods (12). Among other differences, the daily intake of sodium chloride (salt) in the modern diet is about three times higher than the daily intake of potassium, whereas salt intake in ancient cultures is seven times lower than potassium intake (13). The lack of dietary potassium and high sodium-to-potassium ratio in the modern diet may contribute to the development of certain chronic diseases.
Observational studies have consistently reported an increased risk of cardiovascular disease with high dietary sodium intake (14, 15). Several prospective cohort studies have also found an inverse relationship between potassium intake and stroke risk. A meta-analysis of nine prospective cohort studies showed that daily potassium intakes between 3,510 mg and 4,680 mg were associated with a 30% reduction in stroke (16). No association was found with coronary heart disease or total heart disease. In a more recent meta-analysis of 16 studies, the highest versus lowest dietary potassium intake was associated with a 13% lower risk after multiple adjustments (for blood pressure) (17). The lowest risk of stroke is a daily potassium intake of 3,500 mg. In subgroup analyses, the risk of ischemic stroke, but not hemorrhagic stroke, was reduced. Finally, in a recent meta-analysis of 16 observational studies, each 1-unit increase in dietary sodium-potassium ratio was found to be associated with a 22% higher risk of stroke (12).
Abnormally high urinary calcium (hypercalciuria) increases the risk of developing kidney stones. In individuals with a history of developing calcium-containing kidney stones, increased dietary acid load is significantly associated with urinary calcium excretion (18). Increase dietary potassium (and alkali) intake by increasing fruit and vegetable intake or by taking potassium bicarbonate (KHCO)
Potassium Sulfate Granular
) supplements have been found to reduce urinary calcium excretion. In contrast, potassium deprivation has been found to increase urinary calcium excretion (19, 20).
Three large US prospective cohort studies – the Health Professionals Follow-up Study and the Nurses’ Health Studies I and II – involving 193,676 participants, measured dietary potassium intake and the animal protein-to-potassium ratio (a marker of dietary acidity). load) in the diet in relation to the risk of developing kidney stones (21). In all three cohorts, dietary potassium intake was almost entirely derived from potassium-rich foods, such as fruits and vegetables. In all three groups, people with the highest intake of potassium were 33%-56% less likely to develop blood clots than those with the lowest intake. Additionally, a pooled analysis of data from all three cohorts showed that animals with the highest vs. the lowest protein-potassium ratio were 41% more likely to develop kidney stones (21).
Urine alkalinization with additional potassium citrate is used in stone forms to reduce the risk of recurrent stone formation (reviewed in 22). However, potassium citrate treatment should only be started under the supervision of a medical provider.
In a 2015 case-cohort study from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study, which included 5,319 people, dietary potassium intake (alone or in combination with magnesium intake) was associated with . with heel bone (calcaneus) broadband ultrasound attenuation (BUA) measurements (a predictor of accidental fracture risk) and hip fracture risk in women but not in men (23). More recently, a cross-sectional study in older Korean adults reported higher total hip and femur neck bone mineral density (BMD) in those with potassium intake (24). Although these observational studies suggest a link between potassium intake and bone health, they cannot establish a cause-and-effect relationship.
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The mechanisms by which potassium may affect bone health are poorly understood. Modern (Western) diets are relatively low in alkali sources (fruits and vegetables) and high in acid sources (fish, meat, and cheese) (25). When the amount of bicarbonate ions is insufficient to maintain a normal pH, the body is able to mobilize alkaline calcium salts from the bones to neutralize the acids consumed in the diet or metabolism (26). Because both fruits and vegetables are rich in potassium and are precursors of bicarbonate ions, increasing their consumption can help reduce the net acidic content of the diet and preserve calcium in bones that would otherwise be normal. Can be stimulated to maintain pH (see article on Fruits and Vegetables).
Alternatively, potassium bicarbonate supplementation may reduce urinary acid and calcium excretion and affect bone turnover – a small trial in postmenopausal women found that potassium bicarbonate supplementation increased bone formation. increases biomarkers and decreases biomarkers of bone resorption (7). A two-year randomized, double-blind, controlled trial in 201 older adults with osteoporosis (mean age, 69 years) found evidence of increased lumbar spine, hip, femoral neck, and total body BMD. radius and tibia, with additional potassium citrate (2, 340 mg/day) compared to placebo (28). Potassium citrate was also found to increase the serum concentration of the N-terminal propeptide of type I procollagen (PINP)–a marker of bone formation–and decrease the urinary concentration of the N-telopeptide of collagen type I (NTX). A trace of bone regeneration (28). Another three-month, randomized, placebo-controlled trial in 244 adults (≥50 years) examined the effect of oral potassium bicarbonate, either 39 mg/kg/day or 58.5 mg/kg/day, on bone turnover markers. At (29. ). Both dosing regimens resulted in reductions in serum PINP concentrations and urinary NTX concentrations, yet evidence of an effect was stronger with the lowest dose (median dose administered, 3, 160 mg/day) than with the highest dose (median dose administration, 4. 760 mg/day). In contrast, a two-year randomized controlled trial found that neither supplementation with potassium citrate (721 mg/day or 2,165 mg/day) nor increased fruit and vegetable intake (300 mg/day day) had an effect on the marks. Bone turnover or increased BMD in postmenopausal women (30). A 2015 meta-analysis of intervention studies found that supplemental potassium citrate or potassium bicarbonate
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