![[full Text] Pharmacokinetic And Pharmacodynamic Interactions Between Metformin And | Dddt](https://diabetestalk.net/images/NYlAIOcyUohZJavR.jpg)
[full Text] Pharmacokinetic And Pharmacodynamic Interactions Between Metformin And | Dddt
Editor who approved publication: Professor Wei Duan Su-jin Rhee,1,* YoonJung Choi,1,* SeungHwan Lee,1,2 Jaeseong Oh,1 Sung-Jin Kim,3 Seo Hyun Yoon,1 Joo-Youn Cho,1 Kyung-Sang Yu1 1Department of Clinical Pharmacology and Therapeutics, Seoul National University Hospital, Seoul National University College of Medicine, Seoul, Republic of Korea; 2Clinical Trials Center, Seoul National University Hospital, Seoul, Republic of Korea; 3Department of Clinical Development, Dong-A ST Co., Ltd., Seoul, Republic of Korea *These authors contributed equally tothis work Abstract: Evogliptin is a newly developed dipeptidyl peptidase-4 (DPP-4) inhibitor, which is expected to be combined with metformin for treating type 2 diabetes mellitus. We investigated the potential pharmacokinetic and pharmacodynamic interactions between evogliptin and metformin. A randomized, open-label, multiple-dose, six-sequence, three-period crossover study was conducted in 36 healthy male subjects. All subjects received three treatments, separated by 7-day washout intervals: evogliptin, 5 mg od for 7 days (EVO); metformin IR, 1,000 mg bid for 7 days (MET); and the combination of EVO and MET (EVO + MET). After the last dose in a period, serial blood samples were collected for 24 hours for pharmacokinetic assessments. During steady state, serial blood samples were collected for 2 hours after an oral glucose tolerance test, and DPP-4, active glucagon-like peptide-1, glucose, glucagon, insulin, and C-peptide were measured to assess pharmacodynamic properties. EVO + MET and EVO showed similar steady state maximum concentration and area under the concentrationtime curve at steady state values for evogliptin; the geometric mean ratios (90% confidence interval) were 1.06 (1.011.12) and 1.02 (0.991.06), respectively. EV Continue reading >>
Metformin
Metformin, marketed under the trade name Glucophage among others, is the first-line medication for the treatment of type 2 diabetes,[4][5] particularly in people who are overweight.[6] It is also used in the treatment of polycystic ovary syndrome.[4] Limited evidence suggests metformin may prevent the cardiovascular disease and cancer complications of diabetes.[7][8] It is not associated with weight gain.[8] It is taken by mouth.[4] Metformin is generally well tolerated.[9] Common side effects include diarrhea, nausea and abdominal pain.[4] It has a low risk of causing low blood sugar.[4] High blood lactic acid level is a concern if the medication is prescribed inappropriately and in overly large doses.[10] It should not be used in those with significant liver disease or kidney problems.[4] While no clear harm comes from use during pregnancy, insulin is generally preferred for gestational diabetes.[4][11] Metformin is in the biguanide class.[4] It works by decreasing glucose production by the liver and increasing the insulin sensitivity of body tissues.[4] Metformin was discovered in 1922.[12] French physician Jean Sterne began study in humans in the 1950s.[12] It was introduced as a medication in France in 1957 and the United States in 1995.[4][13] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[14] Metformin is believed to be the most widely used medication for diabetes which is taken by mouth.[12] It is available as a generic medication.[4] The wholesale price in the developed world is between 0.21 and 5.55 USD per month as of 2014.[15] In the United States, it costs 5 to 25 USD per month.[4] Medical uses[edit] Metformin is primarily used for type 2 diabetes, but is increasingly be Continue reading >>
Metformin In The Treatment Of Adults With Type 2 Diabetes Mellitus
INTRODUCTION Two classes of oral hypoglycemic drugs directly improve insulin action: biguanides (only metformin is currently available) and thiazolidinediones (TZDs). In the absence of contraindications, metformin is considered the first choice for oral treatment of type 2 diabetes (table 1). A 2006 consensus statement from the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD), updated regularly, proposed that metformin therapy (in the absence of contraindications) be initiated, concurrent with lifestyle intervention, at the time of diabetes diagnosis [1-3]. The pharmacology, efficacy, and side effects of metformin for the treatment of diabetes will be reviewed here. A general discussion of initial treatment of type 2 diabetes and the role of metformin in the prevention of diabetes, in the treatment of polycystic ovary syndrome, and in gestational diabetes are reviewed separately. Continue reading >>
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Jci -role Of Amp-activated Protein Kinase In Mechanism Of Metformin Action
Metformin mediates AMPK activation in primary hepatocytes. (a) Metformin (black bars) and AICAR (A; 500 M) activate AMPK in rat primary hepatocytes. The treatments were 1 hour, 7 hours, and 39 hours, respectively. (b) Metformin (500 M) and AICAR (500 M) activated both AMPK1 and AMPK2 complexes demonstrated by immunoprecipitation-AMPK assay. DPM, disintegrations per minute. (c) Metformin (1 mM) and AICAR (500 M) stimulated AMPK Thr172 phosphorylation. (d) Metformin does not activate partially purified rat liver AMPK in vitro. (e) Metformin and AICAR (500 M) inactivate ACC in rat primary hepatocytes. (f) Metformin (500 M, 4 hours) and AICAR (500 M, 4 hours) stimulate hepatocyte fatty acid oxidation. C, vehicle control. Mean (n = 3 wells per treatment for 1 hour and 7 hours; for 39-hour treatment, n = 1215 wells per treatment) SEM values are shown. *P < 0.05, **P < 0.01, ***P < 0.001 vs. control medium (paired t test). AMP activates AMPK by promoting its phosphorylation at Thr 172 and by direct activation via an allosteric AMP site. Since enzyme activity shown in Figure 1 , a and b, was measured after precipitation from hepatocyte lysates and in the presence of AMP, it is likely that metformin promotes AMPK phosphorylation. In keeping with this notion, we observed that treatment of hepatocytes with either metformin or AICAR resulted in slower electrophoretic mobility of AMPK1 and AMPK2, which is consistent with increased Ser/Thr phosphorylation (data not shown). More specifically, both metformin and AICAR treatment induced AMPK Thr172 phosphorylation demonstrated by using antiphospho-AMPK Ab (Figure 1 c). Recent observations suggest that metformin can impair oxidative phosphorylation by inhibiting mitochondrial phosphorylation complex 1 ( 32 , 33 ). Although some have rep Continue reading >>
Potential Benefits Of Metformin Use In Sickle Cell Anemia | Umek | Journal Of Hematology
Potential Benefits of Metformin Use in Sickle Cell Anemia Sickle cell anemia (SCA) is one of the most important genetic disorders known to mankind. Even with the impressive advances in medical science, effective treatment and cure remain challenging. Currently available treatments including hydroxyurea, which is the only FDA approved drug for SCA, and hemopoietic stem cell transplantation all have significant limitations, so the search for new therapeutic options continues. Metformin, the traditional antidiabetic drug has recently gained novel attention from accumulating molecular evidence suggesting its pleiotropic effects and new potential applications. Our study of these new understandings of the pharmacodynamics and pleiotropic effects leads us to propose that the drug may be of potential therapeutic benefit in SCA. Our arguments are premised on a logical correlation of the interconnected pathophysiologic mechanisms in SCA with current information on the molecular pharmacodynamics of metformin. We reviewed existing evidence and deduced the diverse effects of metformin of relevant therapeutic significance in SCA, including enhancement of nitric oxide bioavailability, induction of fetal hemoglobin synthesis, attenuation of the inflammatory phenotype and beneficial effects in ischemia/reperfusion injury. Collectively, these considerations lead us to infer that there is reasonable evidence to support potential therapeutic adaptation of metformin in SCA. Continue reading >>
Pharmacokinetic And Pharmacodynamic Evaluation Of Floating Microspheres Of Metformin Hydrochloride
Pharmacokinetic and pharmacodynamic evaluation of floating microspheres of metformin hydrochloride Get access/doi/full/10.3109/03639045.2012.662503?needAccess=true Metformin hydrochloride (MH), a biguanide antidiabetic, is the drug of choice in obese patients. It is well absorbed from the upper part of gastrointestinal tract and has oral bioavailability of 50% to 60%. The objective of this study was to formulate MH into floating microspheres in order to increase its residence time at the site of absorption and thus improve its bioavailability; and to extend the duration of action along with possibilities of dose reduction. Microspheres were prepared by emulsion solvent evaporation method and evaluated for particle size, entrapment efficiency, buoyancy, and in vitro release; and further characterized by powder X-ray diffraction, Fourier transform infrared spectroscopy, scanning electron microscopy, and differential scanning calorimetry. The pharmacokinetic and pharmacodynamic evaluation of selected formulation was carried out in male Wistar diabetic rats. The data was statistically analyzed by unpaired t-test. A 3.5-fold increase in relative bioavailability was observed. The prolongation of half-life (t1/2) from 4.5 2.41 h to 14.12 4.81 h indicated extended duration of action. Oral glucose tolerance test (OGTT) was analyzed by one-way analysis of variance followed by Dunnet multiple comparison test, a significant decrease (p < 0.05) in the blood glucose levels was observed when formulations were compared with control rats. Hence, MH floating microspheres were tested at 50 mg/kg and 100 mg/kg body weight, OGTT data showed nonsignificant difference (p >0.05). In conclusion, an effective oral antidiabetics treatment can be achieved by formulating MH into floating microsphe Continue reading >>
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Metformin: An Old Drug For The Treatment Of Diabetes But A New Drug For The Protection Of The Endothelium
Abstract The anti-diabetic and oral hypoglycaemic agent metformin, first used clinically in 1958, is today the first choice or ‘gold standard' drug for the treatment of type 2 diabetes and polycystic ovary disease. Of particular importance for the treatment of diabetes, metformin affords protection against diabetes-induced vascular disease. In addition, retrospective analyses suggest that treatment with metformin provides therapeutic benefits to patients with several forms of cancer. Despite almost 60 years of clinical use, the precise cellular mode(s) of action of metformin remains controversial. A direct or indirect role of adenosine monophosphate (AMP)-activated protein kinase (AMPK), the fuel gauge of the cell, has been inferred in many studies, with evidence that activation of AMPK may result from a mild inhibitory effect of metformin on mitochondrial complex 1, which in turn would raise AMP and activate AMPK. Discrepancies, however, between the concentrations of metformin used in in vitro studies versus therapeutic levels suggest that caution should be applied before extending inferences derived from cell-based studies to therapeutic benefits seen in patients. Conceivably, the effects, or some of them, may be at least partially independent of AMPK and/or mitochondrial respiration and reflect a direct effect of either metformin or a minor and, as yet, unidentified putative metabolite of metformin on a target protein(s)/signalling cascade. In this review, we critically evaluate the data from studies that have investigated the pharmacokinetic properties and the cellular and clinical basis for the oral hypoglycaemic, insulin-sensitising and vascular protective effects of metformin. © 2015 S. Karger AG, Basel Introduction In his 1957 publication, Jean Sterne [1] was Continue reading >>
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An Error Occurred Setting Your User Cookie This site uses cookies to improve performance. If your browser does not accept cookies, you cannot view this site. There are many reasons why a cookie could not be set correctly. Below are the most common reasons: You have cookies disabled in your browser. You need to reset your browser to accept cookies or to ask you if you want to accept cookies. Your browser asks you whether you want to accept cookies and you declined. To accept cookies from this site, use the Back button and accept the cookie. Your browser does not support cookies. Try a different browser if you suspect this. The date on your computer is in the past. If your computer's clock shows a date before 1 Jan 1970, the browser will automatically forget the cookie. To fix this, set the correct time and date on your computer. You have installed an application that monitors or blocks cookies from being set. You must disable the application while logging in or check with your system administrator. This site uses cookies to improve performance by remembering that you are logged in when you go from page to page. To provide access without cookies would require the site to create a new session for every page you visit, which slows the system down to an unacceptable level. This site stores nothing other than an automatically generated session ID in the cookie; no other information is captured. In general, only the information that you provide, or the choices you make while visiting a web site, can be stored in a cookie. For example, the site cannot determine your email name unless you choose to type it. Allowing a website to create a cookie does not give that or any other site access to the rest of your computer, and only the site that created the cookie can read it. Continue reading >>
Efficacy Of Glyburide/metformin Tablets Compared With Initial Monotherapy In Type 2 Diabetes
Efficacy of Glyburide/Metformin Tablets Compared with Initial Monotherapy in Type 2 Diabetes Baylor College of Medicine and the Methodist Hospital (A.J.G.), Houston, Texas 77030; Address all correspondence and requests for reprints to: Alan J. Garber, M.D., Ph.D., Baylor College of Medicine and the Methodist Hospital, 6550 Fannin Street, Suite 1045, Houston, Texas 77030. Search for other works by this author on: Columbia University College of Physicians and Surgeons and Columbia-Presbyterian Medical Center (D.S.D.), New York, New York 10032; Search for other works by this author on: Millard Fillmore Gates Circle Hospital (P.D.), Buffalo, New York 14209; Search for other works by this author on: Bristol-Myers Squibb (S.B.), Princeton, New Jersey 08356 Search for other works by this author on: Baylor College of Medicine and the Methodist Hospital (A.J.G.), Houston, Texas 77030; Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 8, 1 August 2003, Pages 35983604, Alan J. Garber, Daniel S. Donovan, Paresh Dandona, Simon Bruce, Jong-Soon Park; Efficacy of Glyburide/Metformin Tablets Compared with Initial Monotherapy in Type 2 Diabetes, The Journal of Clinical Endocrinology & Metabolism, Volume 88, Issue 8, 1 August 2003, Pages 35983604, Many patients with type 2 diabetes fail to achieve or maintain the American Diabetes Associations recommended treatment goal of glycosylated hemoglobin levels. This multicenter, double-blind trial enrolled patients with type 2 diabetes who had inadequate glycemic control [glycosylated hemoglobin A1C (A1C), >7% and <12%) with diet and exercise alone to compare the benefits of initial therapy with glyburide/metformin tablets vs. metformin or glyburide monotherapy. Patients (n = 486) we Continue reading >>
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Safety, Pharmacokinetics And Pharmacodynamics Of Remogliflozin Etabonate, A Novel Sglt2 Inhibitor, And Metformin When Co-administered In Subjects With Type 2 Diabetes Mellitus
Safety, pharmacokinetics and pharmacodynamics of remogliflozin etabonate, a novel SGLT2 inhibitor, and metformin when co-administered in subjects with type 2 diabetes mellitus Hussey et al.; licensee BioMed Central Ltd.2013 The sodium-dependent glucose co-transporter-2 (SGLT2) is expressed in absorptive epithelia of the renal tubules. Remogliflozin etabonate (RE) is the prodrug of remogliflozin, the active entity that inhibits SGLT2. An inhibitor of this pathway would enhance urinary glucose excretion (UGE), and potentially improve plasma glucose concentrations in diabetic patients. RE is intended for use for the treatment of type 2 diabetes mellitus (T2DM) as monotherapy and in combination with existing therapies. Metformin, a dimethylbiguanide, is an effective oral antihyperglycemic agent widely used for the treatment of T2DM. This was a randomized, open-label, repeat-dose, two-sequence, cross-over study in 13 subjects with T2DM. Subjects were randomized to one of two treatment sequences in which they received either metformin alone, RE alone, or both over three, 3-day treatment periods separated by two non-treatment intervals of variable duration. On the evening before each treatment period, subjects were admitted and confined to the clinical site for the duration of the 3-day treatment period. Pharmacokinetic, pharmacodynamic (urine glucose and fasting plasma glucose), and safety (adverse events, vital signs, ECG, clinical laboratory parameters including lactic acid) assessments were performed at check-in and throughout the treatment periods. Pharmacokinetic sampling occurred on Day 3 of each treatment period. This study demonstrated the lack of effect of RE on steady state metformin pharmacokinetics. Metformin did not affect the AUC of RE, remogliflozin, or its ac Continue reading >>
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Membrane Physiology As A Basis For The Cellular Effects Of Metformin In Insulin Resistance And Diabetes - Em|consulte
MEMBRANE PHYSIOLOGY AS A BASIS FOR THE CELLULAR EFFECTS OF METFORMIN IN INSULIN RESISTANCE AND DIABETES [1]International Pharmacological Support, LIPHA S.A., 37, rue Saint Romain, 69379 Lyon Cedex 08, France. Many recent data provide new, original insights into the mechanisms of action of the antidiabetic Metformin. Careful selection of most relevant data in terms of dosage prompted this original review, largely devoted to the drug action at the cell level and whose hypotheses/conclusions are tentatively interpreted according to corresponding basic scientific knowledge. Metformin interferes with several processes linked to HGP (gluconeogenesis, glycogenolysis and their regulatory mechanisms), lowering glucose production and resensitizing the liver to insulin. The hepatic drug effect is largely favoured by prevailing glycemia. In peripheral tissues, metformin potentiates the effects of both hyperglycemia and hyperinsulinemia. Increase in glucose-mediated glucose transport is mainly mediated by an improvement in the glucose transporter's intrinsic activity. Potentiation of the hormone effect relates to an increase in insulin receptor tyrosine kinase activity. Both mechanisms (insulin signalling and glucose transport) result in the activation of glycogen synthase, a limiting enzyme in the causal defects of NIDDM. Exciting findings show that, conversely, priming cells with very low insulin concentrations also leads to full expression of metformin's antidiabetic activity. Specific investigations confirm a working hypothesis defining the site of action as the cell membrane level. Indeed metformin corrects membrane fluidity and protein configuration disturbed by the diabetic state and which interfere with normal protein-protein or protein-lipid interactions required for prope Continue reading >>
Pharmacodynamicpharmacokinetic Profiles Of Metformin Hydrochloride From A Mucoadhesive Formulation Of A Polysaccharide With Antidiabetic Property In Streptozotocin-induced Diabetic Rat Models
Volume 25, Issue 15 , July 2004, Pages 3041-3048 Pharmacodynamicpharmacokinetic profiles of metformin hydrochloride from a mucoadhesive formulation of a polysaccharide with antidiabetic property in streptozotocin-induced diabetic rat models Author links open overlay panel Michael U.Adikwu Get rights and content The antidiabetic property of a formulation containing metformin hydrochloride and detarium gum has been evaluated in streptozotocin model of experimental rats. Both the gum and metformin hydrochloride possess antidiabetic properties to varying degrees. The pharmacokinetics of metformin from the mucoadhesive dosage forms indicated that for metformin alone, the area under the curve (AUC) values were 125.6 and 135.6mgh/ml at 200 and 400mg/kg BW, respectively. For the mucoadhesive products using the same dose levels, the AUCs were modified to 102.4 and 150.2 in detarium gum and 59.9 and 80.4 in NaCMC. The results indicate that detarium gum is a good excipient for the formulation of metformin mucoadhesive delivery systems when compared with NaCMC. The gum also showed promising antidiabetic effect and should be cautiously used as it may lead to depressed blood-glucose levels beyond the desired levels. Continue reading >>
A Non-linear Pharmacokinetic-pharmacodynamic Relationship Of Metformin In Healthy Volunteers: An Open-label, Parallel Group, Randomized Clinical Study
A non-linear pharmacokinetic-pharmacodynamic relationship of metformin in healthy volunteers: An open-label, parallel group, randomized clinical study Hyewon Chung , Jaeseong Oh , Seo Hyun Yoon , Kyung-Sang Yu , Joo-Youn Cho , Jae-Yong Chung Affiliations: Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Korea, Department of Clinical Pharmacology and Toxicology, Korea University Guro Hospital, Seoul, Korea Affiliations: Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Korea, Department of Clinical Pharmacology and Therapeutics, Seoul National University Hospital, Seoul, Korea Affiliations: Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Korea, Department of Clinical Pharmacology and Therapeutics, Seoul National University Hospital, Seoul, Korea Affiliations: Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Korea, Department of Clinical Pharmacology and Therapeutics, Seoul National University Hospital, Seoul, Korea Affiliations: Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Korea, Department of Clinical Pharmacology and Therapeutics, Seoul National University Hospital, Seoul, Korea Affiliations: Department of Clinical Pharmacology and Therapeutics, Seoul National University College of Medicine, Seoul, Korea, Clinical Trials Center, Seoul National University Bundang Hospital, Seongnam, Korea The aim of this study was to explore the pharmacokinetic-pharmacodynamic (PK-PD) relationship of metformin on glucose levels after the administration of 250 mg and 1000 mg of metformin in he Continue reading >>
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Metformin Pathways: Pharmacokinetics And Pharmacodynamics
Metformin pathways: pharmacokinetics and pharmacodynamics aDepartment of Genetics, Stanford University Medical Center, Stanford University, Stanford bDepartment of Bioengineering, Stanford University Medical Center, Stanford University, Stanford aDepartment of Genetics, Stanford University Medical Center, Stanford University, Stanford bDepartment of Bioengineering, Stanford University Medical Center, Stanford University, Stanford cDepartment of Bioengineering and Therapeutic Sciences, University of California San Francisco, San Francisco, California, USA Correspondence to Teri E. Klein, PhD, Department of Genetics, Stanford University Medical Center, Stanford University, 1501 California Ave, Palo Alto, CA 94304, USA Tel: + 1 650 725 0659; fax: + 1 650 725 3863; [email protected] The publisher's final edited version of this article is available at Pharmacogenet Genomics See other articles in PMC that cite the published article. Metformin is a first-line therapy for type 2 diabetes mellitus (T2DM, formerly non-insulin-dependent diabetes mellitus), and is one of the most commonly prescribed drugs worldwide. As a biguanide agent, metformin lowers both basal and postprandial plasma glucose (PPG) [ 1 , 2 ]. It can be used as a monotherapy or in combination with other antidiabetic agents including sulfonylureas, -glucosidase inhibitors, insulin, thiazolidinediones, DPP-4 inhibitors as well as GLP-1 agonists. Metformin works by inhibiting the production of hepatic glucose, reducing intestinal glucose absorption, and improving glucose uptake and utilization. Besides lowering the blood glucose level, metformin may have additional health benefits, including weight reduction, lowering plasma lipid levels, and prevention of some vascular complications [ 3 ]. As the prevalence o Continue reading >>
Antidiabetic Drug Metformin Suppresses Endotoxin-induced Uveitis In Rats | Iovs | Arvo Journals
Immunology and Microbiology| June 2012 Antidiabetic Drug Metformin Suppresses Endotoxin-Induced Uveitis in Rats Department of Ophthalmology & Visual Sciences, Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas. Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, Texas. Corresponding author: Kota V. Ramana, Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX 77555; [email protected] . Investigative Ophthalmology & Visual Science June 2012, Vol.53, 3431-3440. doi:10.1167/iovs.12-9432 Antidiabetic Drug Metformin Suppresses Endotoxin-Induced Uveitis in Rats You will receive an email whenever this article is corrected, updated, or cited in the literature. You can manage this and all other alerts in My Account Nilesh M. Kalariya, Mohammad Shoeb, Naseem H. Ansari, Satish K. Srivastava, Kota V. Ramana; Antidiabetic Drug Metformin Suppresses Endotoxin-Induced Uveitis in Rats. Invest. Ophthalmol. Vis. Sci. 2012;53(7):3431-3440. doi: 10.1167/iovs.12-9432. ARVO (1962-2015); The Authors (2016-present) Purpose.: To investigate the therapeutic effects of metformin, a commonly used antidiabetic drug, in preventing endotoxin-induced uveitis (EIU) in rats. Methods.: EIU in Lewis rats was developed by subcutaneous injection of lipopolysaccharide (LPS; 150 g). Metformin (300 mg/kg body weight, intraperitoneally) or its carrier was injected either 12 hours before or 2 hours after LPS induction. Three and 24 hours after EIU, eyes were enucleate Continue reading >>
