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Potassium And Insulin Relationship

Hypokalemia (low Potassium)

Hypokalemia (low Potassium)

What Is Hypokalemia? Hypokalemia is an electrolyte imbalance and is indicated by a low level of potassium in the blood. The normal adult value for potassium is 3.5-5.3 mEq/L. Potassium is one of many electrolytes in your body. It is found inside of cells. Normal levels of potassium are important for the maintenance of heart, and nervous system function. What Causes Hypokalemia? One way your body regulates blood potassium levels is by shifting potassium into and out of cells. When there is a breakdown or destruction of cells, the electrolyte potassium moves from inside of the cell to outside of the cell wall. This shift of potassium into the cells causes hypokalemia. Trauma or insulin excess, especially if diabetic, can cause a shift of potassium into cells (hypokalemia). Potassium is excreted (or "flushed out" of your system) by your kidneys. Certain drugs or conditions may cause your kidneys to excrete excess potassium. This is the most common cause of hypokalemia. Other causes of hypokalemia include: Increased excretion (or loss) of potassium from your body. Some medications may cause potassium loss which can lead to hypokalemia. Common medications include loop diuretics (such as Furosemide). Other drugs include steroids, licorice, sometimes aspirin, and certain antibiotics. Renal (kidney) dysfunction - your kidneys may not work well due to a condition called Renal Tubular Acidosis (RTA). Your kidneys will excrete too much potassium. Medications that cause RTA include Cisplatin and Amphotericin B. You may have hypokalemia from a loss of body fluids due to excessive vomiting, diarrhea, or sweating. Endocrine or hormonal problems (such as increased aldosterone levels) - aldosterone is a hormone that regulates potassium levels. Certain diseases of the endocrine system, s Continue reading >>

Hyperkalemia (high Blood Potassium)

Hyperkalemia (high Blood Potassium)

How does hyperkalemia affect the body? Potassium is critical for the normal functioning of the muscles, heart, and nerves. It plays an important role in controlling activity of smooth muscle (such as the muscle found in the digestive tract) and skeletal muscle (muscles of the extremities and torso), as well as the muscles of the heart. It is also important for normal transmission of electrical signals throughout the nervous system within the body. Normal blood levels of potassium are critical for maintaining normal heart electrical rhythm. Both low blood potassium levels (hypokalemia) and high blood potassium levels (hyperkalemia) can lead to abnormal heart rhythms. The most important clinical effect of hyperkalemia is related to electrical rhythm of the heart. While mild hyperkalemia probably has a limited effect on the heart, moderate hyperkalemia can produce EKG changes (EKG is a reading of theelectrical activity of the heart muscles), and severe hyperkalemia can cause suppression of electrical activity of the heart and can cause the heart to stop beating. Another important effect of hyperkalemia is interference with functioning of the skeletal muscles. Hyperkalemic periodic paralysis is a rare inherited disorder in which patients can develop sudden onset of hyperkalemia which in turn causes muscle paralysis. The reason for the muscle paralysis is not clearly understood, but it is probably due to hyperkalemia suppressing the electrical activity of the muscle. Common electrolytes that are measured by doctors with blood testing include sodium, potassium, chloride, and bicarbonate. The functions and normal range values for these electrolytes are described below. Hypokalemia, or decreased potassium, can arise due to kidney diseases; excessive losses due to heavy sweating Continue reading >>

The Power Of Potassium

The Power Of Potassium

We’ve talked about several different minerals in past blog entries. Potassium is the mineral of choice for this week’s post for several reasons, and it’s a mineral that people with kidney problems should be sure to pay close attention to. What potassium does in the body First, let’s explore what potassium does in the body. This mineral is often referred to as an “electrolyte.” Electrolytes are electrically charged particles, called ions, which our cells use to maintain voltage across our cell membranes and carry electrical impulses, such as nerve impulses, to other cells. (Bet you didn’t think you had all this electrical activity in your body, did you?) Some of the main electrolytes in our bodies, besides potassium, are sodium, chloride, calcium, and magnesium. Your kidneys help regulate the amount of electrolytes in the body. Potassium’s job is to help nerve conduction, help regulate your heartbeat, and help your muscles contract. It also works to maintain proper fluid balance between your cells and body fluids. The body is a fine-tuned machine in that, as long as it’s healthy and functioning properly, things will work as they should. This means that, as long as your kidneys are working up to par, they’ll regulate the amount of potassium that your body needs. However, people with diabetes who have kidney disease need to be especially careful of their potassium intake, as levels can get too high in the body when the kidneys don’t work as they should. Too much potassium is just as dangerous as too little. Your physician can measure the amount of potassium in your blood with a simple blood test. A normal, or “safe” level of potassium is between 3.7 and 5.2 milliequivalents per liter (mEq/L). Levels below or above this range are a cause for concer Continue reading >>

What Is The Connection Between Diabetes And Potassium?

What Is The Connection Between Diabetes And Potassium?

Usually, your body processes the food you eat and turns it into a sugar called glucose. Your body uses glucose for energy. Insulin is a hormone your pancreas produces. Your body uses the insulin to help move glucose into cells throughout your body. If you have diabetes, your body is unable to produce or use insulin efficiently. Type 1 diabetes isn’t preventable, but you can prevent type 2 diabetes. Type 2 diabetes, or adult-onset diabetes, usually occurs in people ages 35 and older. Potassium is an electrolyte and mineral that helps keep your bodily fluids at the proper level. Your body can do the following if your fluids are in check: contract your muscles without pain keep your heart beating correctly keep your brain functioning at its highest capability If you don’t maintain the right level of potassium, you can experience a variety of symptom that include simple muscle cramps to more serious conditions, such as seizures. According to recent research, there may be a link between type 2 diabetes and low potassium levels. Although people recognize that potassium affects diabetes, research is ongoing to determine why this may happen. Researchers in one study at Johns Hopkins University School of Medicine linked low levels of potassium with high levels of insulin and glucose in people who were otherwise healthy. Low levels of potassium with high levels of insulin and glucose are both traits doctors associate with diabetes. One 2011 study found that people taking thiazides to treat high blood pressure experienced a loss of electrolytes, such as potassium. Researchers noted that this loss might increase a person’s risk of developing diabetes. And along with that, researchers have also linked potassium levels to high blood pressure. Even though low potassium may incre Continue reading >>

Potassium As A Link Between Insulin And The Renin-angiotensin-aldosterone System.

Potassium As A Link Between Insulin And The Renin-angiotensin-aldosterone System.

Abstract PURPOSE: To focus on the interactions between insulin secretion, glucose tolerance and insulin sensitivity on the one hand and the renin-angiotensin-aldosterone system on the other. EFFECTS ON INSULIN: Insulin is a potent stimulus for hypokalaemia, sparing body potassium from urinary excretion by transporting it into cells. Potassium also appears to play a key role in the antinatriuretic effect of insulin. Insulin-induced hypokalaemia increases plasma renin and angiotensin II levels while decreasing the serum aldosterone concentration. In turn, the renin-angiotensin-aldosterone system affects glucose tolerance by modulating plasma potassium levels, which act as a stimulus for glucose-induced insulin release. EFFECTS OF ANGIOTENSIN CONVERTING ENZYME (ACE) INHIBITION: Interference with the renin-angiotensin-aldosterone system by ACE inhibition blunts the hypokalaemic response to insulin, thereby improving glucose-induced insulin release and oral glucose tolerance. ACE inhibition, however, does not cause major changes in insulin sensitivity. POTASSIUM AND BLOOD PRESSURE: Plasma potassium levels are inversely related to blood pressure, both in population surveys and in intervention studies. In addition, in patients with essential hypertension, the level of plasma potassium appears to predict the blood pressure response to ACE inhibition. SUMMARY: Potassium metabolism is an important link between carbohydrate metabolism and the renin-angiotensin-aldosterone system by way of a double-feedback mechanism. Through the potential effects on blood pressure control, plasma levels of potassium represent a link between insulin and blood pressure in humans. Continue reading >>

Insulin

Insulin

This article is about the insulin protein. For uses of insulin in treating diabetes, see insulin (medication). Not to be confused with Inulin. Insulin (from Latin insula, island) is a peptide hormone produced by beta cells of the pancreatic islets, and it is considered to be the main anabolic hormone of the body.[5] It regulates the metabolism of carbohydrates, fats and protein by promoting the absorption of, especially, glucose from the blood into fat, liver and skeletal muscle cells.[6] In these tissues the absorbed glucose is converted into either glycogen via glycogenesis or fats (triglycerides) via lipogenesis, or, in the case of the liver, into both.[6] Glucose production and secretion by the liver is strongly inhibited by high concentrations of insulin in the blood.[7] Circulating insulin also affects the synthesis of proteins in a wide variety of tissues. It is therefore an anabolic hormone, promoting the conversion of small molecules in the blood into large molecules inside the cells. Low insulin levels in the blood have the opposite effect by promoting widespread catabolism, especially of reserve body fat. Beta cells are sensitive to glucose concentrations, also known as blood sugar levels. When the glucose level is high, the beta cells secrete insulin into the blood; when glucose levels are low, secretion of insulin is inhibited.[8] Their neighboring alpha cells, by taking their cues from the beta cells,[8] secrete glucagon into the blood in the opposite manner: increased secretion when blood glucose is low, and decreased secretion when glucose concentrations are high.[6][8] Glucagon, through stimulating the liver to release glucose by glycogenolysis and gluconeogenesis, has the opposite effect of insulin.[6][8] The secretion of insulin and glucagon into the Continue reading >>

Insulin For The Treatment Of Hyperkalemia: A Double-edged Sword?

Insulin For The Treatment Of Hyperkalemia: A Double-edged Sword?

Insulin for the treatment of hyperkalemia: a double-edged sword? Please address correspondence to: Anitha Vijayan, MD, Professor of Medicine, Renal Division, Washington University in St. Louis, Box 8129, 660 S Euclid Ave, St. Louis, MO, 63110, Email: [email protected] , Tel: (314) 362-7211, Fax: (314) 747-3743 Search for other works by this author on: Clinical Kidney Journal, Volume 7, Issue 3, 1 June 2014, Pages 239241, Tingting Li, Anitha Vijayan; Insulin for the treatment of hyperkalemia: a double-edged sword?, Clinical Kidney Journal, Volume 7, Issue 3, 1 June 2014, Pages 239241, Potassium plays a critical role in cellular metabolism and normal neuromuscular function. Tightly regulated homeostatic mechanisms have developed in the process of evolution to provide primary defense against the threats of hyper- and hypokalemia. The kidney plays a primary role in potassium balance, by increasing or decreasing the rate of potassium excretion. Distribution of potassium between the intracellular and the extracellular fluid compartments is regulated by physiologic factors such as insulin and catecholamines which stimulate the activity of the Na+-K+ ATPase. Only about 10% of the ingested potassium is excreted via the gut under normal physiologic conditions [ 1 ]. End stage renal disease (ESRD) patients rely largely on extra-renal mechanisms and dialysis to maintain potassium homeostasis. Despite the availability of dialysis and the adaptive increase in colonic excretion of potassium in renal insufficiency, severe hyperkalemia (defined as serum potassium level > [6 mmol/L]) is observed in 5-10% of maintenance dialysis patients and is responsible for 0.7% of deaths in the dialysis population in the United States [ 24 ]. Several factors can explain the high incidence of hyp Continue reading >>

Insulin And Potassium

Insulin And Potassium

Insulin has a number of actions on the body besides lowering your blood glucose levels. Insulin suppresses the breakdown and buildup of glycogen, which is the storage form of glucose, it blocks fat metabolism and the release of fatty acids, and it puts potassium into the cells by activating the sodium-potassium cellular channels. Insulin stimulates the uptake of glucose and potassium in all cells of the body but primarily fuels the muscle cells as well as some of the fat cells. In type 2 diabetes or metabolic syndrome (a form of metabolic disease), insulin is not functioning up to its normal level. The cells of the body become resistant to insulin and the blood sugar levels are elevated. The serum potassium (K+) level is a reflection of the total body stores of potassium, although it can be inaccurate in some conditions that affect the distribution of potassium in the body’s cells. The plasma potassium level determines the resting potential of the cells of the body. A person can have low potassium (hypokalemia) or high potassium (hyperkalemia), both of which are asymptomatic conditions that can be serious as they both cause heart arrhythmias. The Relationship between Insulin and Potassium Shortly after insulin was discovered, scientists revealed that insulin had something to do with the potassium levels in both the cells and in the blood. The insulin is the hormone in the body that keeps the potassium level in the blood within the normal range. When insulin is decreased, the potassium level rises and can rise even further if you eat something high in potassium, such as salt substitutes and bananas. When the potassium level is high, it causes the pancreas to release insulin in order to counteract the effects of high potassium levels. When you eat something that is high Continue reading >>

Comparison Of Insulin Action On Glucose Versus Potassium Uptake In Humans

Comparison Of Insulin Action On Glucose Versus Potassium Uptake In Humans

Abstract Background and objectives Insulin has several physiologic actions that include stimulation of cellular glucose and potassium uptake. The ability of insulin to induce glucose uptake by cells is impaired in type 2 diabetes mellitus, but whether potassium uptake is similarly impaired is not known. This study examines whether the cellular uptake of these molecules is regulated in concert or independently. Design, setting, participants, & measurements Thirty-two nondiabetic and 13 type 2 diabetic subjects with normal GFR were given a similar, constant metabolic diet for 8 days. On day 9, they were subjected to a hyperinsulinemic euglycemic clamp for 2 hours. Serum and urinary chemistry were obtained before and during the clamp. Glucose disposal rate was calculated from glucose infusion rate during hyperinsulinemic euglycemia. Intracellular potassium and phosphate uptake were calculated by the reduction of extracellular potassium or phosphate content corrected for urinary excretion. Results Although glucose disposal rate tended to be lower in type 2 diabetics, cellular potassium uptake was similar between diabetics and nondiabetics. Additionally, although glucose disposal rate was lower with increasing body mass index (R2 = 0.362), cellular potassium (R2 = 0.052), and phosphate (R2 = 0.002), uptake rates did not correlate with body mass index. There was also no correlation between glucose disposal rate and potassium (R2 = 0.016) or phosphate uptake (R2 = 0.053). Conclusions Insulin-stimulated intracellular uptake of glucose and potassium are independent of each other. In type 2 diabetes, potassium uptake is preserved despite impaired glucose disposal. Introduction Insulin has a multitude of actions on a wide range of cellular processes. In terms of caloric and glucos Continue reading >>

Physiologic Effects Of Insulin

Physiologic Effects Of Insulin

Stand on a streetcorner and ask people if they know what insulin is, and many will reply, "Doesn't it have something to do with blood sugar?" Indeed, that is correct, but such a response is a bit like saying "Mozart? Wasn't he some kind of a musician?" Insulin is a key player in the control of intermediary metabolism, and the big picture is that it organizes the use of fuels for either storage or oxidation. Through these activities, insulin has profound effects on both carbohydrate and lipid metabolism, and significant influences on protein and mineral metabolism. Consequently, derangements in insulin signalling have widespread and devastating effects on many organs and tissues. The Insulin Receptor and Mechanism of Action Like the receptors for other protein hormones, the receptor for insulin is embedded in the plasma membrane. The insulin receptor is composed of two alpha subunits and two beta subunits linked by disulfide bonds. The alpha chains are entirely extracellular and house insulin binding domains, while the linked beta chains penetrate through the plasma membrane. The insulin receptor is a tyrosine kinase. In other words, it functions as an enzyme that transfers phosphate groups from ATP to tyrosine residues on intracellular target proteins. Binding of insulin to the alpha subunits causes the beta subunits to phosphorylate themselves (autophosphorylation), thus activating the catalytic activity of the receptor. The activated receptor then phosphorylates a number of intracellular proteins, which in turn alters their activity, thereby generating a biological response. Several intracellular proteins have been identified as phosphorylation substrates for the insulin receptor, the best-studied of which is insulin receptor substrate 1 or IRS-1. When IRS-1 is activa Continue reading >>

Does Insulin Raise Potassium Levels?

Does Insulin Raise Potassium Levels?

Insulin, a protein hormone secreted by the pancreas, promotes the entry of glucose into tissues as the body's primary energy source. Insulin encourages the liver to store glucose as glycogen, a form of starch. The result of insulin production lowers the amount of glucose in the blood and boosts the ability of cells to take up more potassium, magnesium and phosphate. The increase in potassium inside cells can have potential positive or negative side effects. Video of the Day Human insulin, one of three hormones produced in the pancreas, lowers sugar or glucose in the blood. The other two hormones are glucagon, which raises blood sugar, and somatostatin, which blocks the release of glucagon and insulin. Commercially prepared insulins are classified as rapid-acting, short-acting, intermediate-acting and long-acting insulins based on the onset of action, peak level of action and the duration of action. Insulin can be standard or purified and come from beef, pork or human sources. Diabetes is a chronic endocrine disease characterized by insulin production deficiency and problems with protein, carbohydrate and fat synthesis throughout the body. There are two types of diabetes: Type 1 diabetes or insulin-dependent and Type 2 diabetes or non-insulin dependent diabetes. Treatment for Type 1 includes insulin replacement while Type 2 is managed with diet, exercise and medications, and insulin may be required as the disease progresses. Monitoring blood sugar is part of the daily diabetes regimen. The most consistent life-threatening side effects with all insulin types are hypoglycemia,or low glucose, and anaphylaxis, an allergic reaction. Insulin increases the ability of the cells to draw more potassium into them from the fluid outside, thus lowering the amount of potassium in the Continue reading >>

Hyperkalemia In Emergency Medicine

Hyperkalemia In Emergency Medicine

Practice Essentials Hyperkalemia can be difficult to diagnose clinically because symptoms may be vague or absent. The fact, however, that hyperkalemia can lead to sudden death from cardiac arrhythmias requires that physicians be quick to consider hyperkalemia in patients who are at risk for it. See the electrocardiogram below. See also Can't-Miss ECG Findings, Life-Threatening Conditions: Slideshow, a Critical Images slideshow, to help recognize the conditions shown in various tracings. Signs and symptoms Patients with hyperkalemia may be asymptomatic, or they may report the following symptoms (cardiac and neurologic symptoms predominate): Evaluation of vital signs is essential for determining the patient’s hemodynamic stability and the presence of cardiac arrhythmias related to hyperkalemia. [1] Additional important components of the physical exam may include the following: Signs of renal failure, such as edema, skin changes, and dialysis sites, may be present Signs of trauma may indicate that the patient has rhabdomyolysis, which is one cause of hyperkalemia See Clinical Presentation for more detail. Diagnosis Laboratory studies The following lab studies can be used in the diagnosis of hyperkalemia: Potassium level: The relationship between serum potassium level and symptoms is not consistent; for example, patients with a chronically elevated potassium level may be asymptomatic at much higher levels than other patients; the rapidity of change in the potassium level influences the symptoms observed at various potassium levels Calcium level: If the patient has renal failure (because hypocalcemia can exacerbate cardiac rhythm disturbances) Urinalysis: To look for evidence of glomerulonephritis if signs of renal insufficiency without a known cause are present Cortisol a Continue reading >>

Hypokalemia And Hyperkalemia

Hypokalemia And Hyperkalemia

Physiology of Potassium Handling Potassium (K+) is the most abundant cation in the body. About 90% of total body potassium is intracellular and 10% is in extracellular fluid, of which less than 1% is composed of plasma. The ratio of intracellular to extracellular potassium determines neuromuscular and cardiovascular excitability, which is why serum potassium is normally regulated within a narrow range of 3.5 to 5.0 mmol/L. Dietary K+ intake is highly variable, ranging from as low as 40 mmol/day to more than 100 mmol/day.1, 2 Homeostasis is maintained by two systems. One regulates K+ excretion, or external balance through the kidneys and intestines, and the second regulates K+ shifts, or internal balance between intracellular and extracellular fluid compartments. Internal balance is mainly mediated by insulin and catecholamines. Cellular Shifts Ingested K+ is absorbed rapidly and enters the portal circulation, where it stimulates insulin secretion. Insulin increases Na+,K+-ATPase activity and facilitates potassium entry into cells, thereby averting hyperkalemia. β2-Adrenergic stimulation also promotes entry of K+ into cells through increased cyclic adenosine monophosphate (cAMP) activation of Na+,K+-ATPase. Renal Handling An increase in extracellular potassium concentration also stimulates aldosterone secretion (via angiotensin II), and aldosterone increases K+ excretion. In the steady state, K+ excretion matches intake, and approximately 90% is excreted by the kidneys and 10% in the stool. Renal K+ excretion is mediated by aldosterone and sodium (Na+) delivery (glomerular filtration rate [GFR]) in principal cells of the collecting ducts.3 K+ is freely filtered by the glomerulus, and almost all the filtered K+ is reabsorbed in the proximal tubule and loop of Henle (Fig. Continue reading >>

Role Of Glucoregulatory Hormones In Potassium Homeostasis - Sciencedirect

Role Of Glucoregulatory Hormones In Potassium Homeostasis - Sciencedirect

Volume 11, Issue 6 , June 1977, Pages 443-452 Role of glucoregulatory hormones in potassium homeostasis Author links open overlay panel James P.Knochel1 An incompletely defined interregulatory balance exists between potassium, insulin, and aldosterone. That potassium administration enhances and hypokalemia depresses aldoterone production is well known. It is not as well known that the same relationship exists between potassium and insulin. In a normal subject, acute hyperkalemia stimulates release of insulin from the pancreas. Potassium deficiency, on the other hand, may depress production of insulin. Both insulin and aldosterone, under appropriate conditions, may indirectly promote transfer of potassium ions from extracellular to intracellular fluid. In contrast, deficiency of either insulin or aldosterone, and expecially both, may favor development of hyperkalemia. Pharmacologically, glucagon, epinephrine, norepinephrine, and somatotropin may also influence transfer of potassium between extracellular and intracellular fluid. Their precise physiological roles in potassium homeostasis, however, are much less evident than that for insulin and aldosterone. It is the intention of this brief review to point out the salient effects and mechanisms whereby the foregoing substances affect potassium homeostasis and to point out physiologically important interrelationships wherever possible. Continue reading >>

A Critically Swift Response: Insulin-stimulated Potassium And Glucose Transport In Skeletal Muscle

A Critically Swift Response: Insulin-stimulated Potassium And Glucose Transport In Skeletal Muscle

It has been tempting to speculate that dietary glucose and potassium handling are coordinated in the postprandial state as a result of common molecular mechanisms that evolved in the distant past as a result of prolonged periods of fasting punctuated by less frequent episodes of feeding. The increase in insulin secretion by pancreatic β cells mediated by ATP-sensitive K+ channels (1) after a meal results in rapid skeletal muscle K+ and glucose uptake. However, the observed correlation between two processes may be the outward manifestation of pathways that have evolved to operate in parallel triggered by an initiating event (e.g., ingested meal) and does not establish that both are coordinated by a common pathway; cross-talk between pathways within a signaling network is as likely an explanation. Using the hyperinsulinemic-euglycemic insulin clamp technique, Nguyen et al. (2) show in this issue of CJASN that the reduced glucose uptake in skeletal muscle, characteristic of insulin resistance in patients with type 2 diabetes (3), is not associated with a parallel decrement in cellular potassium and phosphate uptake. Their work underscores limitations in our understanding regarding the relationship between insulin-mediated regulatory pathways for glucose and potassium handling both in health and in insulin-resistant states such as diabetes at a molecular level while at the same time providing further evidence that the pathways are discrete. It is well established that the long-term maintenance of potassium homeostasis results from the intricate regulation of renal K+ excretion ultimately mediated in large part by inward rectifier ROMK channels in the aldosterone-sensitive distal nephron (4,5). However, the major extrarenal mechanism for achieving K+ homeostasis on a moment Continue reading >>

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