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Effect Of Metformin On Uric Acid

[effect Of Metformin On The Clinical Course Of Gout And Insulin Resistance].

[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 >>

Insulin Resistance

Insulin Resistance

Insulin resistance is a condition in which the body produces insulin but does not use it properly, resulting in an excess of insulin and glucose in the blood stream. Insulin resistance increases the risk of developing prediabetes, type 2 diabetes, and cardiovascular disease (1). Metabolic syndrome consists of the co-occurrence of metabolic risk factors for type 2 diabetes and cardiovascular disease; including obesity, dyslipidemia (characterized by elevated levels of triglycerides and low levels of high-density lipoprotein cholesterol), hyperglycaemia, and hypertension. Abdominal obesity (53%), hypertension (40%), and hyperglycemia (39%) are the most frequently occurring risk factors for metabolic syndrome (2). Using criteria proposed by the National Cholesterol Education Program Adult Treatment Panel III, the 2003-2006 National Health and Nutrition Examination Survey (NHANES) data report the prevalence of metabolic syndrome in US adults greater than 20 years of age to be 34% (2). Identification of the syndrome warrants aggressive interventions known to prevent type 2 diabetes and cardiovascular disease, including weight reduction, increased physical activity, and control of hypertension and dyslipidemia. The prevalence of insulin resistance is estimated at 3% in the US (3) and will increase with the growing obesity epidemic. Endothelial dysfunction has been closely associated with obesity and insulin resistance (4). Years ago Rao et al reported that uric acid can induce vascular smooth muscle cell proliferation (5), and later the mechanism was shown to involve the uptake of uric acid via specific transporters with the activation of MAP kinases and other mediator systems (6,7). The raising of serum uric acid has also been shown to cause arteriolar disease in the kidney Continue reading >>

Use Of Metformin (siofor®) In Patients With Gout And Insulin Resistance (pilot 6-month Results)

Use Of Metformin (siofor®) In Patients With Gout And Insulin Resistance (pilot 6-month Results)

Abstract To evaluate metformin efficacy and safety in patients with gout and insulin resistance (IR). 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. 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. 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 >>

Effects Of Combined Resveratrol Plus Metformin Therapy In Db/db Diabetic Mice

Effects Of Combined Resveratrol Plus Metformin Therapy In Db/db Diabetic Mice

1CINDETEC A.C. Avenida Jurica, Industrial Park Querétaro, Querétaro, México 2Faculty of Pharmacy, Autonomous University of the State of Morelos, Cuernavaca, Morelos, México 3Nucitec, S. A. de C. V. Avenida Jurica, Industrial Park Querétaro, Querétaro, México Citation: Ángel DVM, Antonieta GSM, Rocio GC, Jorge RE, Rosado JL, et al. (2016) Effects of Combined Resveratrol Plus Metformin Therapy in db/db Diabetic Mice. J Metabolic Synd 5: 217. doi: 10.4172/2167-0943.1000217 Copyright: ©2016 Ángel DVM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Journal of Metabolic Syndrome Abstract Background: The worldwide prevalence of Type 2 diabetes mellitus is associated with other conditions that trigger metabolic syndrome. Although several studies on the benefits of resveratrol have been carried out, few have assessed this drug in combination with metformin. Objectives: This study looks at the effects that combined metformin/resveratrol therapy has on body weight gain and liver and renal damage of db/db diabetic mice. It also addresses biochemical findings. Method: Diabetic mice were treated with resveratrol (20 mg/kg/day), metformin (150 mg/kg/day) and combined metformin/resveratrol therapy for 5 weeks. Histopathological tissue analyses and biochemical parameters (glucose, insulin, triglycerides and cholesterol), functional liver enzymes (AP, AST and GGT) and renal parameters (urea and uric acid) were examined. Results: Our data clearly showed that combined metformin/resveratrol treatment reduced obesity, glucose and triglyceride levels, as w Continue reading >>

Have High Uric Acid ( Value= 8) Since Dec'12 , While The Fasting, Pp Values Are Under Control. Request Suggestions To Avoid Medicine

Have High Uric Acid ( Value= 8) Since Dec'12 , While The Fasting, Pp Values Are Under Control. Request Suggestions To Avoid Medicine

Have been on metformin for 8 years ( 500mg tablet after Breakfast and repeat after dinner) Started Ecospirin AV 75mg given family history of CAD Metformin is an oral diabetes medicine that helps control blood sugar levels. Metformin is for people with type 2 diabetes. Metformin is sometimes used in combination with insulin or other medications, but it is not for treating type 1 diabetes. This is a side effect of your drug which has resulted in high uric acid levels. Ask your doctor for any other alternative which is suitable as per your diabetic history . for lowering Uric Acid levels you may take chandraprabhavati tablets 3 times a days and also take Sansamani vati or Giloy Ghanvati . This will also helpful to you in lowering suger level. take sansamni vati with with cold water (Avoid refrigerator water) . Monitor your diabetes regularly. Continue reading >>

Metformin And Blood Uric Acid Increased - From Fda Reports

Metformin And Blood Uric Acid Increased - From Fda Reports

Blood uric acid increased is found among people who take Metformin, especially for people who are male, 60+ old , have been taking the drug for 1 - 2 years, also take medication Allopurinol, and have High blood pressure. This review analyzes which people have Blood uric acid increased with Metformin. It is created by eHealthMe based on reports of 199,020 people who have side effects when taking Metformin from FDA , and is updated regularly. What to expect? If you take Metformin and have Blood uric acid increased, find out what symptoms you could have in 1 year or longer. You are not alone! Join a support group for people who take Metformin and have Blood uric acid increased Personalized health information On eHealthMe you can find out what patients like me (same gender, age) reported their drugs and conditions on FDA since 1977. Our tools are simple to use, anonymous and free. Start now >>> * Approximation only. Some reports may have incomplete information. Continue reading >>

Gout A Painful Form Of Arthritis

Gout A Painful Form Of Arthritis

MAYO CLINIC HEALTH LETTER Gout is a form of arthritis that causes sudden, severe attacks of pain, tender- ness, redness, warmth and swelling in joints. It usually affects one joint at a time — typically the large joint of the big toe — and often at night. You may go to bed feeling fine, but then wake up in the middle of the night feeling like your big toe is on fire. The pain is so bad that you can’t even have a bed sheet covering it. Gout can also affect your ankles, knees, hands and wrists. Some people have just one attack of gout and never have another. Others have recurring attacks and may be at risk of additional problems. Medications and lifestyle changes can usually reduce or eliminate the attacks. Diet is only one factor Gout is caused by excess uric acid in the blood and tissues. Uric acid is a waste product that results from the breakdown of purines. The main source of uric acid is the breakdown of your body’s naturally occurring purines. But purines may also come from your diet. Gout was once known as the disease of kings because of its association with a diet rich in meat, seafood and alcohol — foods high in purines. However, anyone can get gout, and diet is only one factor. Why some people develop gout and others don’t is unclear, but its prevalence has been increasing over the last few decades, affecting more than 8 million Americans. The rise of conditions that often accompany gout — such as high blood pressure, obesity, diabetes, metabolic syndrome and Reliable Information for a Healthier Life Gout is a form of arthritis that causes sudden and severe attacks of pain, tenderness, redness, warmth and swelling in joints. Coming in May EYE REDNESS Beyond antibiotic eyedrops. ENDOMETRIAL CANCER Early signs can Continue reading >>

Address Correspondence To:

Address Correspondence To:

Hyperuricemia has been linked to metabolic syndrome, cardiovascular disease, and chronic kidney disease. Hyperuricemia and type 2 diabetes mellitus were inter-related, type 2 diabetes mellitus was more at risk of having a higher serum uric acid level, and also individuals with higher serum uric acid had higher risk of developing type 2 diabetes in the future. Insulin resistance seems to play an important role in the causal relationship between metabolic syndrome, type 2 diabetes, and hyperuricemia. Oral diabetic drugs that would have additional beneficial effects on reducing serum uric acid levels are of importance. Selective SGLT2 inhibitors were extensively studied in type 2 diabetes mellitus and were found to have improvement of glycemic control, in addition to their proven metabolic effects on weight and blood pressure. Additional beneficial effect of SGLT2 inhibitors on serum uric acid level reduction is investigated. Recently, data have been accumulating showing that they have additional beneficial effects on serum uric acid reduction. As for the postulated mechanism, serum uric acid decreased in SGLT2 inhibitor users as a result of the increase in the urinary excretion rate of uric acid, due to the inhibition of uric acid reabsorption mediated by the effect of the drug on the GLUT9 isoform 2, located at the collecting duct of the renal tubule. Continue reading >>

The Link Between Diabetes And Gout

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 >>

Effect Of Diacerein As An Add-on To Metformin In Patients With Type 2 Diabetes Mellitus And Inadequate Glycemic Control

Effect Of Diacerein As An Add-on To Metformin In Patients With Type 2 Diabetes Mellitus And Inadequate Glycemic Control

Objective To evaluate the effect of diacerein as an add-on to metformin in patients with type 2 diabetes mellitus (T2DM) and inadequate glycemic control. Materials and methods A randomized, double-blind, placebo-controlled clinical trial was carried out on 12 patients with T2DM and inadequate glycemic control [glycated hemoglobin A1c (A1C) ≥ 7%] with metformin as monotherapy (≥ 1500 mg per day) for at least the previous 90 days. Fasting and postprandial glucose were measured before and after the pharmacological intervention. A1C, lipid profile, creatinine and uric acid were also evaluated. After randomization, all patients continued with their dose of metformin. Six subjects received placebo and the other six volunteers took diacerein. Data were tested using the Wilcoxon signed-rank, Mann-Whitney U and chi-square tests. The Institutional Ethics Committee approved the study protocol. Results After 90 days of diacerein as an add-on to metformin, there was a significant decrease in fasting glucose (196 ± 79 vs. 149 ± 70 mg/dL, p < 0.05), postprandial glucose (262 ± 99 vs. 187 ± 70 mg/dlL, p < 0.05) and A1C (8.4 ± 2.0 vs. 6.7 ± 1.7 %, p < 0.05). Conclusions Diacerein as an add-on to metformin in patients with T2DM improved their glycemic control. Key words: Diacerein; metformin; glycemic control; type 2 diabetes mellitus Continue reading >>

Irq J Pharm Vol. Ù¡ù¡, No. Ù¢ù Ù¡ù¡ ,ù¡

Irq J Pharm Vol. Ù¡ù¡, No. Ù¢ù Ù¡ù¡ ,ù¡

Effects of glibenclamide and metformin on serum uric acid level in patients with type Ù¢ diabetes mellitus Najlaa Saadi Ismail Department of Pharmacology, Mosul College of Medicine, University of Mosul Received Accepted Ù£Ù .١١.٢٠١٠١٣.Ù§.Ù¢Ù Ù¡Ù ABSTRACT Objectives: To assess the effect of glibenclamide and metformin on serum uric acid level in patients with type Ù¢ diabetes. Study design: Case control study. Subjects and Methods: This study was conducted from March Ù¢Ù Ù Ù© to January Ù¢Ù Ù¡Ù . Fasting blood sugar and serum uric acid level were measured in patients suffering from type- Ù¢ diabetes mellitus who were referred to Al-Wafa Diabetic Center in Mosul City. Group ٣٢ :Ù¡ patients on glibenclamide therapy, group ٤٢ :Ù¢ patients on metformin therapy and group ٤٢ :Ù£ patients on combination therapy, group ٣٢ :Ù¤ patients on restricted diet, and ٢٣ apparently healthy volunteers, were taken as a control group. Results: The study showed a significant increase in the serum uric acid level of the diabetic patients as compared with the control. Glibenclamide and/or metformin showed no significant difference in the serum uric acid level in patients with type Ù¢ diabetes mellitus. Conclusion: Glibenclamide and/or metformin had no significant effect on serum uric acid level in patients with type Ù¢ diabetes mellitus. Keywords: Uric acid, hyperuricemia, type Ù¢ diabetes mellitus, glibenclamide, metformin. الخالصة Ù‰ وميتÙورمين ال عقار رتاثي لدراسة :اهدا٠البØØ« ÙŠ مصل المرضى مستوى Ø¹Ù‚Ø§Ø Continue reading >>

Metformin Activates Amp-kinase Through Inhibition Of Amp Deaminase

Metformin Activates Amp-kinase Through Inhibition Of Amp Deaminase

Abstract The mechanism for how metformin activates AMPK (AMP activated kinase) was investigated in isolated skeletal muscle L6 cells. A widely held notion is that inhibition of the mitochondrial respiratory chain is central to the mechanism. We also considered other proposals for metformin action. As metabolic pathway markers, we focused on glucose transport and fatty acid oxidation. We also confirmed metformin actions on other metabolic processes in L6 cells. Metformin stimulated both glucose transport and fatty acid oxidation. The mitochondrial Complex I inhibitor rotenone also stimulated glucose transport but it inhibited fatty acid oxidation, independently of metformin. The peroxynitrite generator 3-morpholinosydnonimine stimulated glucose transport, but inhibited fatty acid oxidation. Addition of the nitric oxide precursor arginine to cells did not affect glucose transport. These studies differentiate metformin from inhibition of mitochondrial respiration and from active nitrogen species. Knockout of adenylate kinase also failed to affect metformin stimulation of glucose transport. Hence, any means of increase in ADP appears not to be involved in the metformin mechanism. Knockout of LKB1, an upstream kinase and AMPK activator, did not affect metformin action. Having ruled out existing proposals, we suggest a new one: metformin might increase AMP through inhibition of AMP deaminase (AMPD). We found that metformin inhibited purified AMP deaminase activity. Furthermore, a known inhibitor of AMPD stimulated glucose uptake and fatty acid oxidation. Both metformin and the AMPD inhibitor suppressed ammonia accumulation by the cells. Knockout of AMPD obviated metformin stimulation of glucose transport. We conclude that AMPD inhibition is the mechanism of metformin action. Continue reading >>

Hypoglycemia And Reduced Feed Intake In Broiler Chickens Treated With Metformin

Hypoglycemia And Reduced Feed Intake In Broiler Chickens Treated With Metformin

C. M. Ashwell1 and J. P. McMurtry Growth Biology Laboratory, USDA-ARS, 10300 Baltimore Ave., Beltsville, Maryland 20705 ABSTRACT The bi-guanide metformin is used to treat noninsulin dependent diabetes in obese patients. In addi- tion to having antihyperglycemic effects, metformin is also anorectic and reduces BW. These studies were per- formed to determine if metformin possesses similar prop- erties in chickens. Metformin-HCl was administered to 14-day-old broiler chickens at either 300 or 600 mg/kg per day in the drinking water for 10 d while monitoring BW and feed intake. No changes in water intake were observed, while feed intake and daily gains were only significantly reduced by the 600 mg/kg dose. After oral administration of a single dose of 300 mg/kg metformin- HCl, feed intake was significantly reduced by 4 h and remained suppressed for greater than 24 h relative to (Key words: metformin, appetite, hypoglycemia, insulin, glucagons) 2003 Poultry Science 82:106–110 INTRODUCTION Metformin-HCl (Glucophage, Bristol-Meyers Squibb) is regarded as the first choice for therapy of type 2 diabetes that is generally characterized by insulin resistance or specifically obese patients with hyperinsulinaemia (Bray, 1999; Cusi and DeFronzo, 1998). By reducing blood glu- cose without inducing hypoglycemia and further hyper- insulinaemia, as well as reducing feed intake, metformin- HCl provides a suitable antidiabetic treatment (Lee and Morley, 1998; Rouru et al., 1992). Complications can occur with metformin-HCl induction of lactic acidosis (Stum- voll et al., 1995). High levels of fasting blood glucose, insulin resistance, and obesity are not just hallmarks of type 2 diabetes but are also normal physiologic conditions for chickens (Simon, 1989). The regulation of feed int Continue reading >>

Gout And Diabetes

Gout And Diabetes

Tweet Gout is a form of arthritis (inflammation of joints) caused by high levels of uric acid. Gout can be a painful condition but one that can be managed to reduce the frequency at which gout attacks occur. Gout is known to affect around 1 in 100 people in the UK and is around four times more common in men than in women. Research shows that people with gout are significantly more likely to develop type 2 diabetes than people without gout. Gout and diabetes A number of research papers have shown associations between gout and type 2 diabetes including a study from Harvard Medical School, published in 2014, which showed gout to be associated with a 70 increased risk of developing type 2 diabetes. A common medication for treating gout, allopurinol, has shown promise for reducing thickening of heart muscle and is currently undergoing testing as a possible medication for reducing risk of diabetic nephropathy (kidney disease). Symptoms of gout Gout is characterised by swelling of joints. The base of the big toe is most commonly affected by gout. More than one joint may be affected by gout in some people. Symptoms can come on quickly, with swelling occurring within a few hours. The swollen joint can be very painful and sensitive to touch. During swelling, skin covering the joint may typically turn red and shiny in appearance. The swelling and symptoms may occur for several days if not treated. Once the inflammation has subsided, the skin on the joint may become itchy and flaky. Causes of gout Gout occurs if high levels of uric acid in the blood leads to crystals of sodium urate forming in and around the joints. If these crystals spill into the joint space, this can cause the joint to become inflamed. Risk factors High levels of uric acid are more likely to build if you have an Continue reading >>

Starlix Side Effects Center

Starlix Side Effects Center

Starlix (nateglinide) is an oral diabetes medicine used together with diet and exercise to treat type 2 (non-insulin dependent) diabetes. Other diabetes medicines are sometimes used in combination with Starlix if needed. Starlix is available in generic form. Common side effects of Starlix include: weight gain, sneezing, cough, cold or flu symptoms, diarrhea, nausea, dizziness, or joint pain or stiffness. Starlix can cause low blood sugar (hypoglycemia). Tell your doctor if you have symptoms of low blood sugar such as: chills, dizziness, drowsiness, shaking, fast heartbeat, weakness, headache, tingling of the hands or feet, or hunger. Tell your doctor if you have serious side effects of Starlix including: The recommended starting and maintenance dose of Starlix, alone or in combination with metformin or a thiazolidinedione, is 120 mg three times daily before meals. Hyperglycemia (high blood sugar) may result if you take Starlix with drugs that raise blood sugar, such as: isoniazid, diuretics (water pills), steroids, phenothiazines, thyroid medicine, birth control pills and other hormones, seizure medicines, and diet pills, or medicines to treat asthma, colds or allergies. Hypoglycemia (low blood sugar) may result if you take Starlix with drugs that lower blood sugar, such as: non-steroidal anti-inflammatory drugs (NSAIDs), aspirin or other salicylates, sulfa drugs, monoamine oxidase inhibitors (MAOIs), beta-blockers, or probenecid. Tell your doctor all medications you use. During pregnancy, Starlix should be used only when prescribed. Pregnancy may cause or worsen diabetes. Discuss a plan with your doctor to manage blood sugar while pregnant. Your doctor may change diabetes treatment during your pregnancy. It is not known if this drug passes into breast milk. Consult you Continue reading >>

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