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Metformin Toxicology

Toxicology Brief: Metformin Overdose In Dogs And Cats

Toxicology Brief: Metformin Overdose In Dogs And Cats

Unlike the sulfonylurea medications (e.g. glyburide or glipizide), metformin does not increase pancreatic insulin secretion and, thus, even in overdose situations, does not cause substantial hypoglycemia. In people, acute ingestions of up to 85 g1,133 mg/kg for the average 165-lb (75-kg) persondid not result in hypoglycemia.11 However, in individuals with pre-existing malnutrition, with a history of excessive exercise coupled with inadequate food intake, or taking other glucose-lowering drugs concurrently, hypoglycemia may occur.1,8 While life-threatening lactic acidosis was a frequent adverse effect in people taking phenformin, an association between lactic acidosis and metformin used therapeutically or in cases of acute overdoses is rare. Lactic acidosis is usually associated with long-term use,6 and once it develops, it has been associated with a 50% to 75% mortality rate.4 Lactic acidosis in people receiving metformin has occurred primarily in diabetic patients with significant renal insufficiency. Additionally, patients with congestive heart failure who require pharmacologic management for hypoperfusion and hypoxemia are at increased risk of lactic acidosis. The threat of lactic acidosis increases with the extent of renal dysfunction and the patient's age.9 These conditions can result in decreased renal clearance of the drug, and, consequently, lactic acidosis can occur. The postulated mechanism is that metformin causes decreased hepatic production of glucose from lactate (via the Cori cycle). The net result is decreased conversion of lactate to glucose and subsequent lactic acidosis.2,8,9 No minimum toxic metformin dose for the development of lactic acidosis is established in people. In one case report, a 15-year-old healthy girl ingested 38.25 g (550 mg/kg) of m Continue reading >>

Severe Acidosis, Renal Failure And Metformin Toxicity

Severe Acidosis, Renal Failure And Metformin Toxicity

Severe Acidosis, Renal Failure and Metformin Toxicity The call comes in just after midnight. A 67 year old male has been brought to the Emergency Department. He had complained of lower back pain, feeling unwell, with two episodes of vomiting. He arrived in the Emergency Department, aggitated, complaining of severe pain and having already been given, 370mcg of Fentanyl by the ambulance.His past history is of Hypertension and Diabetes and he takes Amlodipine and Metformin. His vitals were: T 30.9, HR 60, Resp Rate 36, BP 100/35, GCS E1,V2,M4 =7 A rapid clinical examination demonstrated, clear lungs, a soft abdomen and a FAST scan of the abdomen was normal. The patient was intubated usingKetamine and Rocuronium and a size 7.5 endotracheal tube was passed. The airway was a Cormach Lehane grade 4. 100mmol of NaHCO3 was given intravenously to treat the low pH. A CT scan of the chest and abdomen was performed, looking for a cause for the patients back pain and high lactate ie., was there an ischaemic bowel, or a large aorta. The findings were some dependent atelectasis in the lungs and one atrophic kidney. Due to the atelectasis on CT, Ceftriaxone was given initially with anantivirals. Pip-tazidine was added iven that sepsis was the concern in this patient (even though he was not febrile) pip-tazidine was added. The patients Blood Pressure became somewhat volatile via a Non- Invasive Cuff and so an arterial line was inserted, reading a systolic BP of 80mmHg. Peripheral Metaraminol was used in 1mg boluses, to maintain blood pressure and a Metaraminol infusion was commenced. A further set of gases was taken without much improvement in acidosis. During this time the patients blood pressure continued to drop. A noradrenaline infusion was commenced. With very little improvement in Continue reading >>

6 Pearls About Metformin And Lactic Acidosis

6 Pearls About Metformin And Lactic Acidosis

Metformin accumulation: Lactic acidosis and high plasmatic metformin levels in a retrospective case series of 66 patients on chronic therapy. Vecchio S et al. Clin Toxicol 2014 Feb;52:129-135. Metformin is frequently used alone or in combination to treat type 2 diabetes. It lowers blood glucose by decreasing hepatic gluconeogenesis, predominantly by inhibiting mitochondrial respiratory chain complex I. The drug is eliminated mainly by the kidneys, and acute or chronic renal insufficiency may allow accumulation of the drug with increasing levels. A small percentage of patients on metformin develop severe lactic acidosis. There has been an ongoing controversy as whether this acidosis is metformin-associated or metformin-induced. This paper, from the Pavia Poison Control Centre in Northern Italy, helps shed light on this question. The authors retrospectively reviewed patients admitted to their toxicology unit over a 5-year period. Eligible patients were on chronic metformin therapy at the time of admission, had lactic acidosis (pH < 7.35, arterial lactate > 5 mmol/L), and elevated metformin levels (plasma metformin > 4 mcg/ml). Cases of acute overdose were excluded. The study objective was to correlate the metformin levels with measured pH, lactate levels, renal function, and mortality rate. Sixty-six eligible patients were identified. All patients presented with acute renal failure and severe lactic acidosis (mean pH 6.91, mean lactate 14.36 mmol/L). About half the patients had a pre-existing contraindication to metformin therapy, predominantly renal failure and/or heart disease. Approximately 75% presented after several days of a mild gastrointestinal prodrome with nausea, vomiting, and diarrhea; this may either have represented the initial manifestations of metformin po Continue reading >>

Metformin - National Library Of Medicine Hsdb Database

Metformin - National Library Of Medicine Hsdb Database

For more information, search the NLM HSDB database. IDENTIFICATION AND USE: Metformin is antihyperglycemic, not hypoglycemic agent. It does not cause insulin release from the pancreas and does not cause hypoglycemia, even in large doses. HUMAN EXPOSURE AND TOXICITY: Metformin is believed to work by inhibiting hepatic glucose production and increasing the sensitivity of peripheral tissue to insulin. It does not stimulate insulin secretion, which explains the absence of hypoglycemia. Metformin also has beneficial effects on the plasma lipid concentrations and promotes weight loss. Accumulation of metformin may occur in patients with renal impairment, and such accumulation rarely can result in lactic acidosis, a serious, potentially fatal metabolic disease. Lactic acidosis constitutes a medical emergency requiring immediate hospitalization and treatment; lactic acidosis is characterized by elevated blood lactate concentrations, decreased blood pH, electrolyte disturbances with an increased anion gap, and an increased lactate/pyruvate ratio. Lactic acidosis also may occur in association with a variety of pathophysiologic conditions, including diabetes mellitus, and whenever substantial tissue hypoperfusion and hypoxemia exist. Approximately 50% of cases of metformin-associated lactic acidosis have been reported to be fatal. No evidence of mutagenicity or chromosomal damage was observed in in vitro test systems, including human lymphocytes assay. ANIMAL STUDIES: No evidence of carcinogenic potential was seen in a 104-week study in male and female rats receiving metformin hydrochloride dosages up to and including 900 mg/kg daily or in a 91-week study in male and female mice receiving metformin hydrochloride at dosages up to and including 1500 mg/kg daily. Cancer preventive e Continue reading >>

Metformin Overdosage

Metformin Overdosage

Metformin is a biguanide used to treat type 2 diabetes mellitus and most commonly prescribed oral hypoglycemic agent. Metformin is now also used to treat polycystic ovary syndrome and some malignancies. Despite a good safety profile in a majority of patients with diabetes, the risk of metformin-associated lactic acidosis is genuine when safety guidelines are ignored. Overdoses with metformin are rare, but may result in serious consequences. Case reports and small case series of serious toxicity from metformin overdosage can be found in the medical literature, often with the portrayal of extracorporeal methods for the management of the subsequent severe lactic acidosis. Lactic acidosis can defined as a metabolic acidosis with a blood pH less than 7.35 and a serum lactate more than 2 mmol per liter. It can occur either with therapeutic metformin dosing (which is rare) or in overdose situations. 0.03 cases of lactic acidosis per 1000 patient-years occur within therapeutic dosing, with a majority of these cases among patients that have contraindications to metformin (such as renal insufficiency). In overdose situations, lactic acidosis is seen much more habitually, even though the precise incidence is unclear. Lactic acidosis has been observed in 1.6% of metformin exposures reported to poison control centers; nevertheless, merely 10% of these exposures were due to deliberate overdoses. The incidence of metformin-associated lactic acidosis was 12.8% in a review of poison control center inquiries from Germany. The minimum reported lethal dose was found in a 42 year-old patient who had a blood metformin level of 188 µg/ml (e.g. therapeutic range level is usually between 0.5–2.5 µg/ml). Although the intake of 35 g of metformin has shown to be lethal, the maximum reported to Continue reading >>

Emdocs.net Emergency Medicine Educationmetformin Associated Lactic Acidosis (mala): Ed-focused Management - Emdocs.net - Emergency Medicine Education

Emdocs.net Emergency Medicine Educationmetformin Associated Lactic Acidosis (mala): Ed-focused Management - Emdocs.net - Emergency Medicine Education

Metformin Associated Lactic Acidosis (MALA): ED-focused management Authors: Richard B. Moleno DO, MS (EM Resident Physician, UTSW/Parkland Memorial Hospital) and Ashley Haynes MD (Toxicology Fellow, UTSW/Parkland Memorial Hospital) // Edited by: Alex Koyfman MD (@EMHighAK) and Stephen Alerhand MD (@SAlerhand) A 43 year-old woman with a past medical history of depression, DM, and HTN presents to the Emergency Department 2.5 hours after a suicide attempt by prescription drug ingestion. She reports that feeling upset with her home situation and ingested a handful of Metformin 500mg tablets in addition to drinking three 40oz beers. Initial vitals are HR 109, BP 165/96, Temp 36.4 and SpO2 on RA of 98%. Review of pill count from the Metformin bottle provided by EMS is significant for 30 missing pills (15g of Metformin). Being the astute and vigilant resident physician that you are, you quickly ask the nurse to move the patient into a critical care booth, as you remember learning about the dangers of Metformin during your toxicology rotation. Nursing begrudgingly complies. What should be done next? Metformin, a biguanide derived from guanidine, was introduced in the 1950s as a treatment for diabetes, and remains widely used today with 40 million prescriptions filled worldwide in 2008 (1). Lactic acidosis is the primary toxicity of concern, with an estimated incidence of 0.03 per 1000 patients/year (2). Metformin-associated lactic acidosis may happen with therapeutic doses or after an acute overdose. Currently the data is mixed as to which situation leads to a more severe pattern of illness. Common initial symptoms are non-specific and include nausea, vomiting, diarrhea, abdominal pain, malaise, and decreased oral intake. In severe cases, altered mental status, tachypnea, hypo Continue reading >>

Metformin Litfl Life In The Fast Lane Medical Blog

Metformin Litfl Life In The Fast Lane Medical Blog

Metformin rarely causes hypoglycaemia but it can cause a profound lactic acidosis in overdose and in patients with renal failure. Used therapeutically to inhibit glucogenogenesis and stimulate peripheral glucose uptake, in toxic doses it causes a profound lactaemia. All the mechanisms are unclear but it is in part due to the inhibition of gluconeogenesis (which lactate is required). Therefore in healthy individuals there is some build up of lactate, this is normally excreted in the urine but at impaired renal function or an acute overdose there is excess lactate. It is not metabolised and excretion relies solely on renal excretion A lactic acidosis in the context of therapeutic metformin has a high mortality rate and an underlying cause (sepsis) needs to be managed Metformin overdose is usually benign but doses > 10 grams are concerning Lactic acidosis will occur in these individuals who are susceptible (renal, cardiac, respiratory failure) or in patients who have ingested co-ingestants or are on medications that impair cardiac and renal function Severe lactic acidosis usually manifests with non-specific symptoms several hours later but can progress to coma, shock and death Children: Unintentional ingestion of up to 1700mg is benign. Hypoglycaemia, if present can be managed with dextrose . Severe acidosis and hyperkalaemia may require the administration of sodium bicarbonate (1 2 mmol/kg). However, it is likely the patient is already hyperventilating to compensate for the metabolic acidosis, haemodialysis is the ultimate priority. If in a patient on therapeutic metformin, stop further administration and seek the underlying cause for their deterioration (sepsis, acute kidney injury) Screening: 12 lead ECG, BSL, Paracetamol level 50 grams of charcoal to the co-operative Continue reading >>

Fatal Metformin Overdose Presenting With Progressive Hyperglycemia

Fatal Metformin Overdose Presenting With Progressive Hyperglycemia

Go to: CASE REPORT A 29-year-old man ingested metformin in a suicide attempt. The patient consumed the entire remaining contents of his father’s prescription metformin bottle that originally contained 100 tablets of 850 mg each. The father stated that the bottle had contained at least three-quarters of its original contents, putting the ingested dose between 64 and 85 grams. The patient also consumed ethanol, but denied any other co-ingestants. The parents discovered the overdose around 6:30 a.m., about 5 ½ hours post-ingestion, when the patient began complaining of vomiting, diarrhea, thirst, abdominal pain and bilateral leg pain. Paramedics were called, who found the patient to be agitated with a fingerstick glucose level of 180 mg/dL. The patient had a history of psychosis and depression, including prior suicide attempts by drug ingestion. He was not taking any prescribed medications, having discontinued olanzapine and sertraline several months earlier. The patient had no personal history of diabetes, despite the family history of type II diabetes in his father, who was taking no other anti-diabetic medications than metformin. The patient admitted to daily ethanol and tobacco use, but denied any current or past use of illicit drugs. He had no surgical history or known allergies. Vital signs on arrival to the Emergency Department (ED) were temperature of 35.2°C (rectal), pulse of 113 beats/min, blood pressure of 129/59 mmHg, respirations at 28 breaths/min with 100% saturation via pulse oximetry on room air. The patient was awake and oriented x4, but agitated and slightly confused (GCS=14). Pupils were equal and reactive at 4mm and the oral mucous membranes were dry. Other than tachycardia, the heart and lung exams were unremarkable. The abdomen was mildly tender t Continue reading >>

Pharmacology And Toxicology: Treatment Of Poisons - Metformin Intoxication

Pharmacology And Toxicology: Treatment Of Poisons - Metformin Intoxication

Pharmacology and Toxicology: Treatment of Poisons - Metformin Intoxication Pharmacology and Toxicology: Treatment of Poisons - Metformin Intoxication Does this patient have metformin intoxication? Since its introduction to the US market in 1995, the biguinide, metformin has become one of the most prescribed oral hypoglycemics. It is now considered the first line agent to treat type 2 diabetes. Because of its similarity to the drug another biguinide, phenformin, there was concern that it might increase the risk of lactic acidosis as was seen in phenformin. This delayed its release in the United States and led to a number of safety studies in the 1990s. One such study compared the incidence of lactic acidosis in patients treated with metformin and found that among the 7,227 patients followed on metformin, there were no incidents of lactic acidosis reported. Following its introduction, there have been a number of comparative studies with other oral agents for diabetes showing that metformin has a superior safety profile and excellent efficacy. As per the manufacturer, metformin is contraindicated in patients with chronic kidney disease. This is defined as a creatinine 1.4 mg/dL in women and 1.5 mg/dL in men. There have been a number of studies in patients with diabetes and chronic kidney disease that show that metformin remains a very safe medication and a number of authors have argued that its use should no longer be restricted in chronic kidney disease. Other authors have argued that for consistency sake alone, metformin should be restricted by a creatinine clearance estimate as it is with most medications whose clearance depends on renal function rather than a serum creatinine. For the time being, this author recommends following the restricted use of metformin as desc Continue reading >>

Metformin Intoxication

Metformin Intoxication

Can we love Metformin? Need we to fear it? Or perhaps we must give it Machiavellis ultimate accolade, and love and fear the drug with equal weight? Why to love Metformin? It is endorsed in the US, UK and Europe as the initial drug treatment for adults with type 2 diabetes. It treats diabetes, does not cause weight gain, does not increase risk of hypoglycaemia, and might reduce heart attacks and strokes. One tablet costs about 0.20 ($0.29/0.26) and the drug has been widely used for upwards of 60 years. So, must the love be tempered by fear? Metformin inhibits the mitochondrial respiratory chain, driving anaerobic metabolism and increasing lactic acid production. The drug is excreted almost entirely unchanged in urine so reduced kidney function may lead to accumulation of both metformin and lactate and therefore, a metformin-associated lactic acidosis (MALA). Where ingestion of overdose doses of metformin is seen, acutely or intentionally, this may be termed metformin-induced lactic acidosis (MILA). Notoriously, a similar drug, Phenformin, was withdrawn in the late 1970s after catastrophic lactic acidosis occurred in patients. The fear of metformin has lingered ever since, despite the overall incidence of lactic acidosis in metformin users being somewhere between 3 and 10 cases per 100,000 patient years and generally indistinguishable from the base rate in diabetics. Admittedly, reliable data specifically in patients with CKD is hard to come by and UK and US recommendations are to review the dose and not start the drug at an eGFR <45ml/min and stop the drug at <30ml/min. If youve seen a case of MALA, it might have extinguished any love you had for metformin; mortality is 30-50%, serum lactate is often over 20mmol/l and pH can fall below 7. Those are frightening numbers. Continue reading >>

Survival Following A Metformin Overdose Of 63 G: A Case Report

Survival Following A Metformin Overdose Of 63 G: A Case Report

Survival Following a Metformin Overdose of 63 g: A Case Report Department of Clinical Pharmacology, Aarhus University Hospital, Aarhus Amtssygehus, DK8000 Aarhus C, Denmark Author for correspondence: Jrgen Rungby, Department of Endocrinology C, Aarhus University Hospital, Tage Hansensgade, DK8000 Aarhus C, Denmark (fax +45 8949 7659, Department of Clinical Pharmacology, Aarhus University Hospital, Aarhus Amtssygehus, DK8000 Aarhus C, Denmark Author for correspondence: Jrgen Rungby, Department of Endocrinology C, Aarhus University Hospital, Tage Hansensgade, DK8000 Aarhus C, Denmark (fax +45 8949 7659, Please review our Terms and Conditions of Use and check box below to share full-text version of article. I have read and accept the Wiley Online Library Terms and Conditions of Use. Use the link below to share a full-text version of this article with your friends and colleagues. Learn more. Metformin is a biguanide used in the treatment of type 2 diabetes mellitus. It lowers hepatic glucose production and peripheral insulin resistance. Hypoglycaemia is seen only after intake of toxic doses or in combination with other antidiabetic drugs or after prolonged fasting. As metformin is excreted by the kidneys, care must be taken in renal insufficiency or liver disease because of risk of lactic acidosis. Large overdoses of metformin can lead to lactic acidosis as well. Suicide with metformin is rare. Intake of 35 g of metformin has been shown to be lethal ( Teale et al. 1998 ). In the present paper we report on the treatment and outcome of a 70 year old man after ingestion of 63 g of metformin. Previously, survival after intake of up to 50 g has been described. A 70 year old man with type 2 diabetes mellitus who was being treated with metformin 850 mg twice daily and glimepiride Continue reading >>

Toxicity And Toxicokinetics Of Metformin In Rats

Toxicity And Toxicokinetics Of Metformin In Rats

Volume 243, Issue 3 , 15 March 2010, Pages 340-347 Toxicity and toxicokinetics of metformin in rats Get rights and content Metformin is a first-line drug for the treatment of type 2 diabetes (T2D) and is often prescribed in combination with other drugs to control a patient's blood glucose level and achieve their HbA1c goal. New treatment options for T2D will likely include fixed dose combinations with metformin, which may require preclinical combination toxicology studies. To date, there are few published reports evaluating the toxicity of metformin alone to aid in the design of these studies. Therefore, to understand the toxicity of metformin alone, Crl:CD(SD) rats were administered metformin at 0, 200, 600, 900 or 1200mg/kg/day by oral gavage for 13weeks. Administration of 900mg/kg/day resulted in moribundity/mortality and clinical signs of toxicity. Other adverse findings included increased incidence of minimal necrosis with minimal to slight inflammation of the parotid salivary gland for males given 1200mg/kg/day, body weight loss and clinical signs in rats given 600mg/kg/day. Metformin was also associated with evidence of minimal metabolic acidosis (increased serum lactate and beta-hydroxybutyric acid and decreased serum bicarbonate and urine pH) at doses 600mg/kg/day. There were no significant sex differences in mean AUC024 or Cmax nor were there significant differences in mean AUC024 or Cmax following repeated dosing compared to a single dose. The no observable adverse effect level (NOAEL) was 200mg/kg/day (mean AUC024=41.1g h/mL; mean Cmax=10.3g/mL based on gender average week 13 values). These effects should be taken into consideration when assessing potential toxicities of metformin in fixed dose combinations. Continue reading >>

The Toxicology Takedown #2 January 2015

The Toxicology Takedown #2 January 2015

The Toxicology Takedown #2 January 2015 A 15-Year-old female presents to the hospital 4 hours after ingestion of her diabetic fathers medication following a family dispute. Her family is unable to account for 75 x 5 mg glipizide and 29 x 500 mg metformin tablets. On arrival, she is vomiting and appears anxious and slightly sweaty with Glasgow Coma Score of 14/15. Her vital signs are pulse rate 90 bpm, blood pressure 110/75 mmHg, respiratory rate 18/min, and temperature of 36.8 C. A bedside blood glucose level is 54 mg/dl. Whats the immediate threat to life for this patient? Whats the mechanism of action of sulfonylurea medications, and how is it problematic in the management in toxicity? What are the antidotes for sulfonylurea toxicity? Whats concerning about metformin toxicity? What is the name of the syndrome that can develop in overdose and how it is managed? With respect to the ingestion of a potentially toxic amount of sulfonylureas, the immediate threat to life for this patient is hypoglycemia with potential progression to seizures and coma. This patient requires an IV line and administration of a bolus of 50 ml of 50% dextrose solution for correction of hypoglycemia and administration of another medication of minimize recurrent hypoglycemia. Glipizide is one of many sulfonylurea oral hypoglycemic agents. It exerts its effect by stimulating insulin release from the beta islet cells of the pancreas. All sulfonylureas inhibit ATP-sensitive K+ channels. This inhibition increases the membrane potential and depolarizes the cell. A subsequent influx of extracellular calcium ions through voltage-dependent calcium channels Occurs. An increase in the free intracellular calcium level is the signal, or second messenger, that triggers exocytosis and the release of insulin. F Continue reading >>

Metformin-associated Lactic Acidosis Following Intentional Overdose Successfully Treated With Tris-hydroxymethyl Aminomethane And Renal Replacement Therapy

Metformin-associated Lactic Acidosis Following Intentional Overdose Successfully Treated With Tris-hydroxymethyl Aminomethane And Renal Replacement Therapy

Metformin-Associated Lactic Acidosis following Intentional Overdose Successfully Treated with Tris-Hydroxymethyl Aminomethane and Renal Replacement Therapy Ngan Lam ,1,2 Gurbir Sekhon ,3and Andrew A. House 1,3 1Division of Nephrology, Department of Medicine, Western University, London, ON, Canada N6A 3K7 2London Health Sciences Centre, Kidney Clinical Research Unit, Victoria Hospital, Westminster Tower 800 Commissioners Road East, London, ON, Canada N6A 4G5 3Department of Medicine, Western University, London, ON, Canada N6A 3K7 Received 19 February 2012; Accepted 6 May 2012 Academic Editors: Y.Fujigaki, D.Packham, A.Papagianni, and H.Schiffl Copyright 2012 Ngan Lam et al. 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. A 43-year-old woman was brought to the hospital with severe metabolic acidosis (pH 6.56, bicarbonate 3 mmol/L, and lactate 18.4 mmol/L) and a serum creatinine of 162 mol/L with a serum potassium of 7.8 mmol/L. A delayed diagnosis of metformin-associated lactic acidosis was made, and she was treated with tris-hydroxymethyl aminomethane (THAM) and renal replacement therapy (RRT). Following a complete recovery, she admitted to ingesting 180 tablets (90 grams) of metformin. Her peak serum metformin concentration was 170 g/mL (therapeutic range 1-2 g/mL). Our case demonstrates an intentional metformin overdose resulting in lactic acidosis in a nondiabetic patient who was successfully treated with THAM and RRT. Metformin is an oral antihyperglycemic agent that is the first-line therapy for noninsulin-dependent diabetes mellitus [ 1 ]. Although the adverse event rate is 2030%, the majority of the Continue reading >>

Metformin Scavenges Methylglyoxal To Form A Novel Imidazolinone Metabolite In Humans

Metformin Scavenges Methylglyoxal To Form A Novel Imidazolinone Metabolite In Humans

Metformin Scavenges Methylglyoxal To Form a Novel Imidazolinone Metabolite in Humans Southwest Environmental Health Sciences Center, Department of Pharmacology and Toxicology, College of Pharmacy, Department of Chemical & Environmental Engineering, Department of Chemistry and Biochemistry, University of Arizona, Tucson, Arizona 85721, United States *E-mail: [emailprotected] . Tel: (313) 577-1574. Fax: (313) 577-0457. Cite this: Chem. Res. Toxicol. 2016, 29, 2, 227-234 Article Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days. Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts. The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Methylglyoxal (MG) is a highly reactive dicarbonyl compound involved in the formation of advanced glycation endproducts (AGE). Levels of MG are elevated in patients with type-2 diabetes mellitus (T2DM), and AGE have been implicated in the progression of diabetic complications. The antihyperglycemic drug metformin (MF) has been suggested to be a scavenger of MG. The present work examined and characterized unequivocally the resulting scavenged product from the metforminMG reaction. The primary product was characterized by 1H, 13C, 2D-HSQC, and HMBC NMR and tan Continue reading >>

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