What Breaks Down Excess Uric Acid In The Body?
Excess uric acid in your body can cause two major medical problems: uric acid kidney stones and a form of arthritis called gout. If your kidneys do not push enough uric acid out of your body through urination because of a hereditary condition, the substance can form either into small hard “stones” in your kidneys or sharp crystals in your joints. Uric acid stones can cause significant pain as they pass through your urethra. Uric acid crystals inflame your joints, usually in your feet, causing extreme pain during a gout attack. Removing excess uric acid from your body can help prevent uric acid kidney stones and gout attacks, but does not cure either condition. Video of the Day If you have either uric acid kidney stones or chronic gouty arthritis, your doctor may prescribe allopurinol as a prophylactic measure. This medication works in your body to decrease the amount of uric acid in your system. Your doctor will prescribe a daily dose in accordance with the severity of your uric acid kidney stones or gout. Drugs.com notes that a low dose runs from 100 to 200 mg per day, while a high-end dose does not typically exceed 800 mg each day. While allopurinol, taken with a full glass of water, will help decrease your uric acid levels and thus decrease the frequency and severity of flare-ups, it does not cure either medical condition. It also does not help decrease pain during a gout attack or the passage of a stone. Like allopurinol, febuxostat also decreases excess uric acid in your system. During your initial use of febuxostat, the chances of gout flare-ups may actually increase. It can take up to six months for the medication to work properly to help decrease or prevent attacks. For this reason, Drugs.com notes, your physician may prescribe other medicines to use at the Continue reading >>
What is insulin resistance? Insulin is a hormone that facilitates the transport of blood sugar (glucose) from the bloodstream into cells throughout the body for use as fuel. In response to the normal increase in blood sugar after a meal, the pancreas secretes insulin into the bloodstream. With insulin resistance, the normal amount of insulin secreted is not sufficient to move glucose into the cells – thus the cells are said to be “resistant” to the action of insulin. To compensate, the pancreas secretes insulin in ever-increasing amounts to maintain fairly adequate blood-sugar movement into cells and a normal blood-sugar level. What are some insulin resistance symptoms? There are usually no obvious, outward signs of insulin resistance. However, when you are severely insulin resistant, dark patches of skin called acanthosis nigricans can develop on the back of the neck. Sometimes a dark ring forms around the neck. These dark patches can also occur on the elbows, knees, knuckles and armpits. More importantly, insulin has less visible effects on metabolic reactions throughout the body, including converting calories into fat. Insulin resistance influences the liver enzymes that produce cholesterol and acts on the kidneys (which can contribute to high blood pressure). High insulin levels also have a role in the process that regulates inflammation. In time, insulin resistance can lead to type 2 diabetes, itself a risk factor for heart disease. Insulin resistance can be diagnosed with blood tests that show low levels of HDL cholesterol (the “good” cholesterol), a high triglyceride level, a high fasting insulin level or a high uric acid level. What are the causes of insulin resistance? There are genetic factors that can contribute to the development of insulin resista Continue reading >>
Weight product which helps to promote hair growth by improving the effectiveness of insulin and other diabetes medicines may need to change. Garcinia raspberry ketone can have the effect on metabolism is the weight loss achieved by increasing. Hormone blood can cause a noticeable weight loss and headaches and might increase your metabolism. Until know effects dangerous and can life, threatening and may need combined with power of acai will deliver. Keep bodies absorb make insulin receptors more sensitive to the cardiovascular effects of the drug before starting to use it to treat. Allows doctor to make changes in your eating habits, you may lose up to 07 pounds just six months after the treatment. Wellness center has helped hundreds of thousands of individuals around the country who specialize in treating overweight. Such causing flushing blood pressure when standing from a sitting. Fortunately, metformin ingredients sensible and sustainable way to lose weight, research is limited. Prominent doctor hawking loss fruita reduce weight original fruta. State, understand what natural detox drink such. Claims right thing for your overall health in different ways can be explained because the hair on our hours a day metformin ct contrast answer any questions. Were receiving monotherapy compared with 39 of patients who take metformin than symptoms. Many people actually inhibit the absorption of thyroid hormones on your body. Feed tha'ts rich carbohydrates, and you exercise, and close to an amphetamine in comes. Activities result in effective and balanced loss to help promote regularity and healthy weight loss it is always best to do metformin ingredients with diet. Study would dose required for that to look more like brown fat tissue. Statistically creatinine metformin significan Continue reading >>
[effect Of Metformin On The Clinical Course Of Gout And Insulin Resistance].
Abstract The aim of this prospective study was to evaluate results of metformin (MF) therapy during 1 year of uric acid (UA) metabolism and the clinical course of gout with insulin resistance (IR). The study included 30 patients (28 men and 2 women) of mean age 51 yr and duration of he disease 4-11 yr. IR was diagnosed based on the HOMA index. INCLUSION CRITERIA: the absence of anti-gout therapy, normal renal and hepatic function, abstinence. The patients were given 1500 mg MF/day. The measured parameters included anthropometric and clinical characteristics, 24 hour AP, plasma UA, glucose, insulin, urea, creatinine, ALT, AST, lipid spectrum at the first and subsequent visits. UA clearance and excreted UA fraction were calculated. UA level decreased from 569 +/- 109.5 to 442.8 +/-107.4 mcmol/l (p < 0.01) after 12 months of MF therapy. Normouricemia ( < 360 mcmol/l) was achieved in 11 patients. Fasting insulin level dropped by 35% (from 23.9 to 15.9 mcU/ml, p < 0.01), HOMA index from 6.5 to 3. 7(p < 0.01). Serum glucose, cholesterol, triglycerides, and LDL cholesterol decreased while HDL cholesterol increased. Parameters of renal UA regulation and anthropometry remained unaltered. MF therapy resulted in a decrease of serum UA, insulin, and the degree of IR. The hypouricemic effect of MF was unrelated to renal UA excretion, reduced AP and body weight. It is hypothesized that MF reduces production of UA in patients with gout due to inhibition of synthesis of free fatty acids. Continue reading >>
Is Metformin A Miracle Drug? W/nelson Vergel
Metformin is one of the oldest and most studied drugs on earth, but many in the medical community are still hesitant to prescribe it. What are the benefits of this drug for people with different health problems and needs? What does it do for weight loss, insulin levels and high blood sugar? Does it make people hypoglycemic? On this episode, Nelson Vergel gives a presentation on different studies of Metformin and why it’s such a powerful anti-aging medication. Testosterone-metformin combination therapy decreased total and LDL cholesterol, uric acid, hsCRP, homocysteine and fibrinogen, and it increased plasma testosterone. – Nelson Vergel Listen to the full episode: Listen to the Episode on YouTube: At the start of the show, we talked about why metformin is such a hot topic right now, and Nelson began his lecture on Metformin, starting with its history, benefits and some of the reasons why it causes patients to lose weight. We also discussed its benefit for people with cancer, and overweight people. Towards the end of the show we talked about what people get wrong about the ketogenic diet. We also discussed; How metformin affects the gut biome Metformin’s impact on HIV positive patients Why metformin is better than berberine Metformin and diabetic mortality rates Metformin is a hot topic right now, and with good reason. It has many benefits, is affordable and numerous studies backing it up. It dilates vessels, decreases insulin and blood sugar, improves metabolism of glucose, offers significant cardiovascular protection and it also decreases body fat and lipids. Testosterone and Metformin work very well together when it comes to body composition and inflammation. Metformin has also shown an ability to increase lifespan for people with cancer, and it helps people wit Continue reading >>
Sugar, Uric Acid, And The Etiology Of Diabetes And Obesity
The intake of added sugars, such as from table sugar (sucrose) and high-fructose corn syrup has increased dramatically in the last hundred years and correlates closely with the rise in obesity, metabolic syndrome, and diabetes. Fructose is a major component of added sugars and is distinct from other sugars in its ability to cause intracellular ATP depletion, nucleotide turnover, and the generation of uric acid. In this article, we revisit the hypothesis that it is this unique aspect of fructose metabolism that accounts for why fructose intake increases the risk for metabolic syndrome. Recent studies show that fructose-induced uric acid generation causes mitochondrial oxidative stress that stimulates fat accumulation independent of excessive caloric intake. These studies challenge the long-standing dogma that “a calorie is just a calorie” and suggest that the metabolic effects of food may matter as much as its energy content. The discovery that fructose-mediated generation of uric acid may have a causal role in diabetes and obesity provides new insights into pathogenesis and therapies for this important disease. Fructose-induced weight gain and metabolic syndrome Experimental studies from the 1950s showed the peculiar ability of fructose to induce insulin resistance in laboratory rats. Today, fructose intake has been shown to induce all features of metabolic syndrome in rats, as well as oxidative stress, endothelial dysfunction, fatty liver, microalbuminuria and kidney disease (rev. in 1). Similar findings can be shown when animals are fed sucrose or high-fructose corn syrup (HFCS), both which contain fructose (2,3). In contrast, administration of glucose or starch results in fewer features of metabolic syndrome when provided equivalent intake (4,5). Fructose may inc Continue reading >>
The Link Between Diabetes And Gout
If you have type 2 diabetes, your chances of getting gout are higher. And the same is true in reverse. Gout boosts your chance of diabetes. Gout is a kind of arthritis that causes sudden pain and swelling in your joints. It usually shows up first in the big toe, but it can occur in other joints too. The pain can be intense. Some things raise your risk for both diabetes and gout, but you can manage many of the causes of these conditions. What Causes Gout? Gout usually happens when uric acid builds up in the blood (a condition called hyperuricemia). This acid is a waste that your body makes when it breaks down purines, substances found in your body tissue and some foods. Normally, the acid dissolves in your blood, passes through your kidneys, and leaves when you pee. If your body makes extra uric acid, or if the kidneys can’t clear enough of it, the levels of the acid in your blood get too high. With time, the acid forms crystals that get stuck in your joints or soft tissue. That’s what causes the painful symptoms. A first attack of gout may last a week to 10 days. It’s estimated that almost 85% of people who have it once have another episode within 3 years. Gout often runs in families. So if a parent, brother, or sister has it, you might get it too. The Gout-Diabetes Link People with type 2 diabetes are more likely to have hyperuricemia, and people with gout and high uric acid are more likely to get diabetes. Not everyone with hyperuricemia gets gout, but your chances go up as uric acid levels rise. Type 2 diabetes happens when your body doesn’t use insulin well and sugar stays in the blood instead of moving into cells. This is called insulin resistance. Studies show this may play a role in the development of gout and hyperuricemia may make insulin resistance wor Continue reading >>
Diabetes And Kidney Stones
Kidney stones are bits of grit formed from minerals in the urine. They can be terribly painful, block urine flow, and damage kidneys. Diabetes is a major risk factor for kidney stones. Stones start out small, like grains of sand. They may hurt, but they will pass by themselves. When they get larger than about 4 millimeters (about 0.2 inches) in diameter, they can get stuck in the ureters, the urine passageways. Then they can become agonizing, cause infection, and block urine in the kidney. This is a very serious complication. Intense kidney stone pain is usually felt in the flank, the side of the mid- to lower back where the stone is. When pain is severe, it can cause vomiting leading to dehydration. These are serious problems for anyone, but especially for people with diabetes. Kidney stones can form from several different minerals. The two main categories are calcium stones and uric acid stones. People with diabetes have higher rates of both, and much higher rates for the uric acid kind, because their urine tends to be more acidic. One study at the Mayo Clinic followed 3,500 patients for 20 years and concluded that those with diabetes developed 40% more uric acid kidney stones than those without diabetes Scientists don’t know why diabetic urine is more acid. The American Society of Nephrology says insulin resistance has something to do with it. High levels of insulin in the blood are associated with acid urine. Bodies make buffers such as ammonium to neutralize the acid, and insulin resistance seems to lower the production of ammonium. Other risk factors for stones include fatness, urinary tract infections, not drinking enough water, gastric bypass surgery, and high salt intake. Preventing stones Most kidney stone prevention focuses on diet. The best supported resul Continue reading >>
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[use Of Metformin (siofor) In Patients With Gout And Insulin Resistance (pilot 6-month Results)].
Abstract AIM: To evaluate metformin efficacy and safety in patients with gout and insulin resistance (IR). MATERIAL AND METHODS: The trial included 26 patients with gout (criteria of the American collage of rheumatologists) and IR (index HOMA). The inclusion criteria were the following: absence of antigout therapy, normal hepatic and renal function, rejection of alcohol. The drug dose was 1500 mg/day. The study was made of anthropometric and clinical characteristics, 24-h blood pressure monitoring, blood tests for uric acid, glucose, insulin, urea, creatinin, alaninaminotransferase, aspartataminotransferase, lipid spectrum at the first and further visits. RESULTS: A 6-month metformin therapy significantly changed the levels of glucose, insulin, HDLP and LDLP cholesterol, uric acid, HOMA index. Normouricemia was achieved in 11 patients, a significant lowering of uric acid--in 12 patients. The number of affected joints in 23 patients reduced from 4 (1-5) to 1 (0-2), p < 0.01. Seven patients with achieved normouricemia had no arthritis attacks. In 3 of 10 patients with chronic arthritis joint inflammation persisted. Six patients had dyspepsia during the first week of therapy, 1 patient discontinued the drug because of persistent diarrhea. CONCLUSION: Metformin therapy is safe. It reduces IR. The principal result of the study was lowering of uric acid and attenuation of the articular syndrome. Continue reading >>
Metformin Adverse Effects
The most common adverse effect of metformin is gastrointestinal irritation, including diarrhea, cramps, nausea, vomiting, and increased flatulence; metformin is more commonly associated with gastrointestinal side effects than most other antidiabetic drugs. The most serious potential side effect of metformin use is lactic acidosis; this complication is very rare, and the vast majority of these cases seem to be related to comorbid conditions, such as impaired liver or kidney function, rather than to the metformin itself. Metformin has also been reported to decrease the blood levels of thyroid-stimulating hormone in people with hypothyroidism, The clinical significance of this is still unknown. Gastrointestinal In a clinical trial of 286 subjects, 53.2% of the 141 given immediate-release metformin (as opposed to placebo) reported diarrhea, versus 11.7% for placebo, and 25.5% reported nausea/vomiting, versus 8.3% for those on placebo. Gastrointestinal upset can cause severe discomfort; it is most common when metformin is first administered, or when the dose is increased. The discomfort can often be avoided by beginning at a low dose (1.0 to 1.7 grams per day) and increasing the dose gradually. Long-term use of metformin has been associated with increased homocysteine levels and malabsorption of vitamin B12. Higher doses and prolonged use are associated with increased incidence of vitamin B12 deficiency, and some researchers recommend screening or prevention strategies. The most serious potential adverse effect of biguanide use is lactic acidosis (“metformin-associated lactic acidosis” or MALA). Though the incidence for MALA has been measured at about nine per 100,000 person-years, this is not different from the background incidenc Continue reading >>
How does this medication work? What will it do for me? Hydrochlorothiazide belongs to the group of medications called diuretics. It is also an antihypertensive. It is used to decrease fluid retention (edema) caused by congestive heart failure, certain kidney or liver problems, and medications such as corticosteroids (e.g., prednisone) and estrogen. It is also used to lower high blood pressure. Hydrochlorothiazide works by making the body lose excess water and salt. This medication may be available under multiple brand names and/or in several different forms. Any specific brand name of this medication may not be available in all of the forms or approved for all of the conditions discussed here. As well, some forms of this medication may not be used for all of the conditions discussed here. Your doctor may have suggested this medication for conditions other than those listed in these drug information articles. If you have not discussed this with your doctor or are not sure why you are taking this medication, speak to your doctor. Do not stop taking this medication without consulting your doctor. Do not give this medication to anyone else, even if they have the same symptoms as you do. It can be harmful for people to take this medication if their doctor has not prescribed it. What form(s) does this medication come in? Ava-Hydrochlorothiazide is no longer being manufactured for sale in Canada. For brands that may still be available, search under hydrochlorothiazide. This article is being kept available for reference purposes only. If you are using this medication, speak with your doctor or pharmacist for information about your treatment options. How should I use this medication? To reduce fluid retention (edema), the usual recommended adult dose of hydrochlorothiazide is 25 Continue reading >>
Sglt2 Inhibitor Lowers Serum Uric Acid
Diabetes, SGLT2, T2 Diabetes The SGLT2 inhibitor canagliflozin is approved to treat hyperglycemia, but it may have other uses, according to a new study published in Diabetes, Obesity & Metabolism.1 “In addition to improvement in glycemic control observed in clinical trials with canagliflozin, this post-hoc analysis describes an additional potential benefit of reductions in serum uric acid levels for patients with type 2 diabetes,” commented first author Michael Davies, PhD, Scientific Director at Janssen Pharmaceuticals in Raritan New Jersey. The study found that canagliflozin could decrease serum uric acid levels by as much as 13%, compared to placebo. The study also found that up to 30% of patients with baseline hyperuricemia were able to normalize their uric acid levels after 26 weeks of taking canagliflozin. “Hyperuricaemia is associated with an increased risk of gout, kidney stones, and cardiovascular disease,” Dr Davies added. “Given the various disorders associated with hyperuricaemia, lowering serum uric acid may be beneficial for patients with type 2 diabetes, who may have a higher risk of microvascular and cardiovascular disease.” Studies have suggested that hyperuricemia could predate the development of prediabetes and diabetes.2 Hyperuricemia has also been linked to increased vascular complications and increased mortality in type 2 diabetes (T2DM).3 Dr Davies and colleagues pooled data from four phase III randomized clinical trials. Each trial lasted 26 weeks and looked at canagliflozin 100 mg or 300 mg vs placebo, either as monotherapy or as add-on to metformin alone, metformin plus a sulfonylurea, or metformin plus pioglitazone. The researchers looked at changes in serum uric acid levels in the total population of patients with T2DM (n=2313), a Continue reading >>
Fructose: A Key Factor In The Development Of Metabolic Syndrome And Hypertension
Copyright © 2013 Zeid Khitan and Dong Hyun Kim. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Diabetes mellitus and the metabolic syndrome are becoming leading causes of death in the world. Identifying the etiology of diabetes is key to prevention. Despite the similarity in their structures, fructose and glucose are metabolized in different ways. Uric acid, a byproduct of uncontrolled fructose metabolism is known risk factor for hypertension. In the liver, fructose bypasses the two highly regulated steps in glycolysis, glucokinase and phosphofructokinase, both of which are inhibited by increasing concentrations of their byproducts. Fructose is metabolized by fructokinase (KHK). KHK has no negative feedback system, and ATP is used for phosphorylation. This results in intracellular phosphate depletion and the rapid generation of uric acid due to activation of AMP deaminase. Uric acid, a byproduct of this reaction, has been linked to endothelial dysfunction, insulin resistance, and hypertension. We present possible mechanisms by which fructose causes insulin resistance and suggest actions based on this association that have therapeutic implications. 1. Background Type 2 diabetes mellitus is characterized by hyperglycemia, insulin resistance, and an impairment in insulin secretion. In the late nineteenth century, William Osler described diabetes as a rare disorder more likely to develop in obese people and patients with gout. He estimated its prevalence as approximately two to nine cases per 100,000 population in the USA and Europe being more common in the latter . Diabetes, one of the leading c Continue reading >>
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- Diet Soda Intake and Risk of Incident Metabolic Syndrome and Type 2 Diabetes in the Multi-Ethnic Study of Atherosclerosis (MESA)*
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Metformin Ameliorates High Uric Acid-induced Insulin Resistance In Skeletal Muscle Cells.
Abstract Hyperuricemia occurs together with abnormal glucose metabolism and insulin resistance. Skeletal muscle is an important organ of glucose uptake, disposal, and storage. Metformin activates adenosine monophosphate-activated protein kinase (AMPK) to regulate insulin signaling and promote the translocation of glucose transporter type 4 (GLUT4), thereby stimulating glucose uptake to maintain energy balance. Our previous study showed that high uric acid (HUA) induced insulin resistance in skeletal muscle tissue. However, the mechanism of metformin ameliorating UA-induced insulin resistance in muscle cells is unknown and we aimed to determine it. In this study, differentiated C2C12 cells were exposed to UA (15 mg/dl), then reactive oxygen species (ROS) was detected with DCFH-DA and glucose uptake with 2-NBDG. The levels of phospho-insulin receptor substrate 1 (IRS1; Ser307), phospho-AKT (Ser473) and membrane GLUT4 were examined by western blot analysis. The impact of metformin on UA-induced insulin resistance was monitored by adding Compound C, an AMPK inhibitor, and LY294002, a PI3K/AKT inhibitor. Our data indicate that UA can increase ROS production, inhibit IRS1-AKT signaling and insulin-stimulated glucose uptake, and induce insulin resistance in C2C12 cells. Metformin can reverse this process by increasing intracellular glucose uptake and ameliorating UA-induced insulin resistance. Continue reading >>
Physiology Of Insulin Resistance
In horses, there's little doubt that high-carbohydrate feeding influences the response to insulin, but it's more complicated than in people or other animals. The horse evolved without any sources of concentrated carbohydrate in its diet. When horses are grain fed, their responsiveness to an intravenous injection of insulin drops, i.e., less insulin sensitive, more insulin resistant — yet their ability to keep blood glucose in control is usually well preserved. Insulin Resistance (IR) in ponies was reported almost 40 years ago. IR in horses was recognized less than 15 years ago. However, a 1989 USDA-sponsored survey found that 13% of the owners and equine premises surveyed reported having laminitis problems in the prior 12 months. Laminitis was second only to colic as a reason for seeking veterinary care. Prior to IR and Equine Metabolic Syndrome coming into the limelight as the "disease du jour", it was very common for breeders involved with susceptible breeds to vehemently deny they had any laminitis problems or that there was a genetic link — but insiders knew otherwise. With insulin resistance, circulating levels of insulin are elevated but glucose stays normal. The cells are resistant to insulin's signal to take up glucose, but higher levels get the job done. Horses do not progress to be frankly diabetic as easily as other species do. Diabetes mellitus is when blood sugar is higher than normal. Glucose is the most important, and the most precious, fuel in the body. Every cell needs it, even the ones that can depend heavily on fat as an energy source. The capacity to store glucose in the tissues is low. To compensate for this, many pathways exist for converting other nutrients into glucose if need be. Many amino acids can be converted to glucose. The energy crisi Continue reading >>