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Effect Of Metformin On Muscles

Metformin

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 Side Effects And How To Deal With Them

Metformin Side Effects And How To Deal With Them

Metformin side effects include diabetic neuropathy, brain fog, and digestive issues. You can address them through diet, Vitamin B12, CoQ10, and exercise. Let us understand the drug Metformin in detail and study different forms of metformin, its uses and common metformin side effects along with how to deal with them. Metformin: What Is It Used For? Metformin is an old warhorse in the pharma battle against diabetes. It has been the mainstay in the treatment of Type 2 Diabetes for more than fifty years, often matching or outperforming newer drugs. In fact, many new combination drugs are often created with metformin as one of the main ingredients. Thanks to its long run in the pharmaceutical world, the side effects of Metformin are also well known. The Metformin-PCOS connection has been studied extensively since a majority of health complications associated with PCOS (polycystic ovarian syndrome) are due to hyperinsulinemia (high amounts of insulin in the blood stream). Metformin is known to reduce circulating insulin levels. The use of this drug in women with PCOS has shown highly encouraging results. RELATED: 10 Easy Breakfast Ideas For Diabetics Most Prescribed Names in Metformin Category Include: Fortamet: It is an extended-release formulation that contains metformin hydrochloride. The tablets are designed for once-a-day administration. They deliver either 500 mg or 1000 mg of metformin. The tablet is made using a patented technology called SCOTTM that delivers the active compound slowly and at a constant rate. Glucophage: Glucophage tablets contain metformin hydrochoride. They contain either 500 mg, 850 mg or 1000 mg of the active compound. Glucophage tablets do not contain any special covering and need to be taken multiple times a day until the prescribed dosage is me Continue reading >>

Differential Effects Of Metformin And Exercise On Muscle Adiposity And Metabolic Indices In Human Immunodeficiency Virus-infected Patients

Differential Effects Of Metformin And Exercise On Muscle Adiposity And Metabolic Indices In Human Immunodeficiency Virus-infected Patients

Differential Effects of Metformin and Exercise on Muscle Adiposity and Metabolic Indices in Human Immunodeficiency Virus-Infected Patients Program in Nutritional Metabolism (S.D.D., G.E.M., K.L., C.H., S.G.), Boston, Massachusetts 02114 Neuroendocrine Unit (S.D.D., G.E.M., K.L., C.H., A.K., S.G.), Boston, Massachusetts 02114 Search for other works by this author on: Program in Nutritional Metabolism (S.D.D., G.E.M., K.L., C.H., S.G.), Boston, Massachusetts 02114 Neuroendocrine Unit (S.D.D., G.E.M., K.L., C.H., A.K., S.G.), Boston, Massachusetts 02114 Search for other works by this author on: Program in Nutritional Metabolism (S.D.D., G.E.M., K.L., C.H., S.G.), Boston, Massachusetts 02114 Neuroendocrine Unit (S.D.D., G.E.M., K.L., C.H., A.K., S.G.), Boston, Massachusetts 02114 Search for other works by this author on: Program in Nutritional Metabolism (S.D.D., G.E.M., K.L., C.H., S.G.), Boston, Massachusetts 02114 Neuroendocrine Unit (S.D.D., G.E.M., K.L., C.H., A.K., S.G.), Boston, Massachusetts 02114 Search for other works by this author on: Division of Musculoskeletal Radiology (M.T.), Massachusetts General Hospital, Boston, Massachusetts 02114 Search for other works by this author on: Neuroendocrine Unit (S.D.D., G.E.M., K.L., C.H., A.K., S.G.), Boston, Massachusetts 02114 Search for other works by this author on: Department of Physical Medicine and Rehabilitation (W.R.F.), Spaulding Rehabilitation Hospital and Harvard Medical School, Boston, Massachusetts 02114 Search for other works by this author on: Program in Nutritional Metabolism (S.D.D., G.E.M., K.L., C.H., S.G.), Boston, Massachusetts 02114 Neuroendocrine Unit (S.D.D., G.E.M., K.L., C.H., A.K., S.G.), Boston, Massachusetts 02114 Address all correspondence and requests for reprints to: Steven Grinspoon, M.D. Continue reading >>

Metformin Protects The Skeletal Muscle Glycogen Stores Against Alterations Inherent To Functional Limitation

Metformin Protects The Skeletal Muscle Glycogen Stores Against Alterations Inherent To Functional Limitation

HUMAN AND ANIMAL HEALTH Paula Lima BosiI, *; Gabriel Delfino BorgesII; João Luiz Quagliotti DuriganII; Karina Maria CancellieroII; Carlos Alberto da SilvaII IRua Maestro Arthur Bosmans, 55 - Apto 1002; Belvedere; 30320-680; [email protected]; Belo Horizonte - MG - Brasil IIDepartamento de Fisioterapia; Universidade Metodista de Piracicaba - UNIMEP; Piracicaba - SP - Brasil ABSTRACT The aim of this study was to evaluate the glycogen content (GC) of the rat hind limb muscles submitted to joint immobilization, either associated with metformin treatment (M, 1,4mg.ml-1) or not. In the metformin group, there was a significant increase in the GC (soleus - S 65% , white gastrocnemius - WG 30.5%, red gastrocnemius- RG31.7%, extensor digitorum longus - EDL 44%, tibialis anterior- TA 77.4%). The immobilization significantly reduced the GC (S 31.6%, WG 56.6%, RG 39.1%, ELD 41.7%, TA 45.2%) and weight (S 34.2% and ELD 27%), whereas in the group immobilized with the metformin, there was an increase in the GC of all the muscles (S 177%, WG 290%, RG 172%,ELD 47%, TA 217%), in addition to minimizing the weight loss of S (29.6%) and ELD (27.8%). Key words: Muscle disuse, metformin, skeletal muscle, rehabilitation RESUMO O objetivo deste estudo foi avaliar o conteúdo de glicogênio (GLI) da musculatura da pata posterior de ratos submetidos à imobilização articular, associado ou não ao tratamento com metformina (MET, 1,4 mg.ml -1) no período de sete dias. No grupo metformina, houve elevação significativa nas RG (65% no sóleo - S, 30.5% no gastrocnêmio branco - GB, 31.7% no gastrocnêmio vermelho - GV , 44% no extensor longo dos dedos - EDL e de 77.4% no tibial anterior - TA ). A imobilização reduziu significativamente as RG (S 31,6%, GB 56,6%, GV 39,1%, ELD 41,7%, TA 45,2%) Continue reading >>

Metformin - Fountain Of Youth Or Muscle Destroyer?

Metformin - Fountain Of Youth Or Muscle Destroyer?

METFORMIN - Fountain of Youth or Muscle Destroyer? METFORMIN - Fountain of Youth or Muscle Destroyer? Metformin - Fountain of Youth or Muscle Destroyer? Metformin is one of the most effective drugs for the treatment of type 2 diabetes. This type of diabetes is the form where the body does not respond effectively to insulin, primarily because the insulin receptor has become desensitized. Since one of insulins primary functions is to shuttle sugar from the blood into the cell, the loss of insulin function seen in type 2 diabetics usually causes problematic increases in blood sugar. Metformin is able to combat this elevation in blood sugar by suppressing the production of glucose by the liver while also restoring the insulin response. Interestingly, metformin has also been shown to increase the life span in many different species such as worms and mice.1,2 Additional epidemiological data has shown that humans with type 2 diabetes who took metformin for an extensive period of time to treat their diabetes had a lower occurrence of many other life-threatening diseases, including heart disease and cancer.3 In fact, this data is so compelling that other scientific groups are going to see if metformin intake by individuals who dont have diabetes but have other health conditions, including cancer and heart disease, can forestall the progress of the diseases they already have. Of course, prevention of these diseases would likely increase the life span of each subject, giving metformin the remarkable capacity to function as a molecular Fountain of Youth. Increasing Insulin Action and Life Expectancy by Activating AMPK So, what is it about metformin that gives it the remarkable capacity to reestablish insulin signaling and increase life span? Well, this capability most certainly st Continue reading >>

The Role Of Metformin In Controlling Oxidative Stress In Muscle Of Diabetic Rats

The Role Of Metformin In Controlling Oxidative Stress In Muscle Of Diabetic Rats

Copyright © 2016 Danielle Diniz Vilela 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. Metformin can act in muscle, inhibiting the complex I of the electron transport chain and decreasing mitochondrial reactive oxygen species. Our hypothesis is that the inhibition of complex I can minimize damage oxidative in muscles of hypoinsulinemic rats. The present study investigated the effects of insulin and/or metformin treatment on oxidative stress levels in the gastrocnemius muscle of diabetic rats. Rats were rendered diabetic (D) with an injection of streptozotocin and were submitted to treatment with insulin (D+I), metformin (D+M), or insulin plus metformin (D+I+M) for 7 days. The body weight, glycemic control, and insulin resistance were evaluated. Then, oxidative stress levels, glutathione antioxidant defense system, and antioxidant status were analyzed in the gastrocnemius muscle of hypoinsulinemic rats. The body weight decreased in D+M compared to ND rats. D+I and D+I+M rats decreased the glycemia and D+I+M rats increased the insulin sensitivity compared to D rats. D+I+M reduced the oxidative stress levels and the activity of catalase and superoxide dismutase in skeletal muscle when compared to D+I rats. In conclusion, our results reveal that dual therapy with metformin and insulin promotes more benefits to oxidative stress control in muscle of hypoinsulinemic rats than insulinotherapy alone. 1. Introduction Oxidative stress reflects an imbalance between reactive oxygen species (ROS) production and the biological systems ability to detoxify the reactive intermediates. The antioxidant defense include Continue reading >>

Metformin And Muscle Growth

Metformin And Muscle Growth

by Mike Arnold Over the last few years insulin sensitizers, and metformin in particular, have become quite popular among bodybuilders due to their many positive effects, one of which is the ability to combat growth hormone/exogenous insulin induced insulin resistance. While their physique and health enhancing benefits are undeniable, many have begun utilizing these compounds indiscriminately, adhering to a more is better philosophy in terms of dose, frequency of use, and the number of compounds employed. This may be advantageous with some drugs, but is it true in this instance? Insulin sensitizers are rather unique in that many of their positive and negative effects are mediated through a single pathway; an enzyme known as adenosine monophosphate-activated protein kinase, or AMPK for short. Acting as a cellular energy regulator, AMPK is responsible for maintaining cellular energy homeostasis via the regulation of ATP levels. When the body is exposed to stresses that deplete ATP, such as heat shock, or much more commonly, low blood glucose and hypoxia as a result of diet and exercise, this enzyme is activated. As a result, processes which involve ATP consumption (fatty acid and cholesterol synthesis) are turned off, while processes which involve ATP production (fatty acid and glucose oxidation) are turned on in an attempt to replenish cellular energy levels. This has a number of beneficial effects. It improves insulin sensitivity (via improved insulin receptor function and increased Glut-4 translocation), increases glucose uptake into muscle tissue, simulates fat loss, improves cholesterol values, and results in an overall improvement in metabolic health. With such a diverse number of benefits and with all of them directly applicable to the goals/circumstances of a bodyb Continue reading >>

Should We All Take Metformin?

Should We All Take Metformin?

Metformin (Glucopage) is a wonderful drug that bodybuilders use for a very long time, nothing very spectacular just another drug in the bodybuilders toolbox. I wrote a few times before about this drug, in 2012 about its potential to burn fat and in general in 2014. But this drug is studied intensively and in 2015 this article in The Telegraph increased the interest in Metformins ability to increase life-span and improve quality of life. T he Food and Drug Administration (FDA) always maintained that aging is not a disease and most scientists have taken the same position. But because many studies confirmed that Metformin was able to slow down aging and prevent many conditions linked with aging, general consensus changed. Belgian researchers tested metformin on the tiny roundworm C.elegans the worms not only aged slower, but they also stayed healthier longer. They did not slow down or develop wrinkles. Mice treated with Metformin increased their lifespan by nearly 40 per cent and their bones were also stronger. Last year Cardiff University found that when patients with diabetes were given the drug metformin they in fact lived longer than others without the condition, even though they should have died eight years earlier on average. To analyze the advantage outside treatment of diabetes, the Food and Drug Administration has green-lighted a clinical trial in the U.S. for what has become known as the Targeting Aging with Metformin (TAME) study. The researchers will give Metformin to about 3.000 elderly people, who either suffer from or have a high risk of developing diseases like cancer, heart disease, or cognitive problems. They'll then track them over six years to see if the drug prevents aging-related diseases that were not pre-existing. They'll also be looking to see if i Continue reading >>

Metformin Increases Amp-activated Protein Kinase Activity In Skeletal Muscle Of Subjects With Type 2 Diabetes.

Metformin Increases Amp-activated Protein Kinase Activity In Skeletal Muscle Of Subjects With Type 2 Diabetes.

Metformin increases AMP-activated protein kinase activity in skeletal muscle of subjects with type 2 diabetes. Research Division, Joslin Diabetes Center, Brigham and Women's Hospital and Harvard Medical School, One Joslin Place, Boston, MA 02215, USA. [email protected] Metformin is an effective hypoglycemic drug that lowers blood glucose concentrations by decreasing hepatic glucose production and increasing glucose disposal in skeletal muscle; however, the molecular site of metformin action is not well understood. AMP-activated protein kinase (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of glucose uptake into skeletal muscle and the inhibition of liver gluconeogenesis. We recently reported that AMPK is activated by metformin in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production. In the present study, we evaluated whether therapeutic doses of metformin increase AMPK activity in vivo in subjects with type 2 diabetes. Metformin treatment for 10 weeks significantly increased AMPK alpha2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity. The increase in AMPK alpha2 activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after metformin treatment. Metformin-induced increases in AMPK activity were associated with higher rates of glucose disposal and muscle glycogen concentrations. These findings suggest that the metabolic effects of metformin in subjects with type 2 diabetes may be mediated by the activation of AMPK alpha2. Continue reading >>

Metformin And Muscle Pain

Metformin And Muscle Pain

Diabetes Forum The Global Diabetes Community Find support, ask questions and share your experiences. Join the community Hi, I am type 2, diagnosed before Xmas. On metformin 2 x 500g a day. The tops of my legs, hips and bum area go from slight numbness to painful especially when I lie down at night. Its like pressure points. Has anyone else experienced this. Not sure if I should persevere or ditch the pills. Any replies appreciated Rachox Type 2 (in remission!) Well-Known Member It sounds more like statin side effects. Are you on a statin by any chance? No, no statins. Doctor wasnt sure if I needed metformin or not as my levels not too high fbg 8.5 hbA1c 52 so might just stop taking them and see if symptoms ease. Thanks for reply Rachox Type 2 (in remission!) Well-Known Member No, no statins. Doctor wasnt sure if I needed metformin or not as my levels not too high fbg 8.5 hbA1c 52 so might just stop taking them and see if symptoms ease. Thanks for reply Many on here have reduced their HbA1c on diet alone, have you changed your diet? My HbA1c was higher at 70 on diagnosis and I do take Metformin, but I believe that the low carb diet I eat has reduced it more than the tablets. Hi, I am type 2, diagnosed before Xmas. On metformin 2 x 500g a day. The tops of my legs, hips and bum area go from slight numbness to painful especially when I lie down at night. Its like pressure points. Has anyone else experienced this. Not sure if I should persevere or ditch the pills. Any replies appreciated Was initially started just on Gliclazide when diagnosed T2 March last year. During an appointment with an Endocrinology consultant I had Metformin added to my medication. I experienced aches and pains in all my leg muscles after a few weeks on Gliclazide and Metformin. Had the Metformin sto Continue reading >>

Influence Of Metformin On Glucose Intolerance And Muscle Catabolism Following Severe Burn Injury

Influence Of Metformin On Glucose Intolerance And Muscle Catabolism Following Severe Burn Injury

Influence of Metformin on Glucose Intolerance and Muscle Catabolism Following Severe Burn Injury Copyright 2005 Lippincott Williams & Wilkins, Inc. This article has been cited by other articles in PMC. Hyperglycemia and accelerated muscle catabolism have been shown to adversely affect immune response and survival. The purpose of this study was to determine the effect of metformin on glucose kinetics and muscle protein metabolism in severely burned patients and assess any potential benefit of metformin in this clinical setting. In a double-blind, randomized manner, 8 adult burn patients received metformin (850 mg every 8 hours 7 days), while 5 burn patients received placebo. Infusions of 6,6d2 glucose, d5 phenylalanine, sequential muscle biopsies, and femoral arterial, venous blood sampling allowed determination of glucose and muscle protein kinetics. Measurements were obtained immediately prior and at the conclusion of 7 days of treatment (metformin versus placebo). All patients received enteral feeds of comparable amounts during study. Patients receiving metformin had a significant decrease in their plasma glucose concentration, the rate of glucose production, and an increase in glucose clearance. Metformin administration was also associated with a significant increase in the fractional synthetic rate of muscle protein and improvement in net muscle protein balance. Glucose kinetics and muscle protein metabolism were not significantly altered in the patients receiving placebo. Metformin attenuates hyperglycemia and increases muscle protein synthesis in severely burned patients, thereby indicating a metabolic link between hyperglycemia and muscle loss following severe injury. Therefore, therapies that improve glucose tolerance such as metformin may be of clinical value Continue reading >>

Stay Big While Getting Shredded With Metformin

Stay Big While Getting Shredded With Metformin

Stay big while getting shredded with Metformin By Matt Porter How many times have you heard people say when they are dieting for fat loss that they are flat, weak, losing muscle, or all of the above? Usually the people who say such things do not have a proper grasp on how to effectively construct a diet for extreme fat loss while maintaining muscle tissue. The same people also convince themselves that they cannot get lean without sacrificing substantial lean tissue in the process. I am here to tell you that if you diet right, supplement right, and train effectively, than you surely can keep your muscle tissue while incinerating your winter blubber from your holiday "bulking diet." In fact, when people get overly lenient with their dietary habits over the winter months, they oftentimes do not eat consistently and make poor food choices. They unknowingly set themselves up for the potential to gain a little muscle while getting shredded from diligent eating, supplementation, and consistent training. Once the dieter gets into the midst of their fat loss stage and has become fairly lean in the 8-9% body fat range, they can begin incorporating the oral anti-diabetic drug Metformin. This drug also goes by the name Glucophage and belongs to a class of drugs called biguanides. It is used for treating non-insulin dependent type 2 diabetics with insulin resistance. Metformin is generally well tolerated and is beneficial to the prolonged dieter attempting to retain muscle tissue while going from lean to shredded, which translates to -- going from 8-9% body fat to 4-5% body fat. When attempting to achieve extremely low levels of body fat, a cascade of hormonal events begin taking place, making will power, discipline and strong mental fortitude crucial to succeeding. Constant hunger Continue reading >>

Metformin Increases Amp-activated Protein Kinase Activity In Skeletal Muscle Of Subjects With Type 2 Diabetes

Metformin Increases Amp-activated Protein Kinase Activity In Skeletal Muscle Of Subjects With Type 2 Diabetes

Metformin is an effective hypoglycemic drug that lowers blood glucose concentrations by decreasing hepatic glucose production and increasing glucose disposal in skeletal muscle; however, the molecular site of metformin action is not well understood. AMP-activated protein kinase (AMPK) activity increases in response to depletion of cellular energy stores, and this enzyme has been implicated in the stimulation of glucose uptake into skeletal muscle and the inhibition of liver gluconeogenesis. We recently reported that AMPK is activated by metformin in cultured rat hepatocytes, mediating the inhibitory effects of the drug on hepatic glucose production. In the present study, we evaluated whether therapeutic doses of metformin increase AMPK activity in vivo in subjects with type 2 diabetes. Metformin treatment for 10 weeks significantly increased AMPK α2 activity in the skeletal muscle, and this was associated with increased phosphorylation of AMPK on Thr172 and decreased acetyl-CoA carboxylase-2 activity. The increase in AMPK α2 activity was likely due to a change in muscle energy status because ATP and phosphocreatine concentrations were lower after metformin treatment. Metformin-induced increases in AMPK activity were associated with higher rates of glucose disposal and muscle glycogen concentrations. These findings suggest that the metabolic effects of metformin in subjects with type 2 diabetes may be mediated by the activation of AMPK α2. Metformin is one of the most commonly used drugs for the treatment of type 2 diabetes. It is an effective hypoglycemic drug that also improves lipid profiles (1) and reduces cardiovascular risk (2). The Diabetes Prevention Program has recently shown that similar to diet and exercise, metformin treatment reduces the risk of developin Continue reading >>

Does Metformin Inhibit Recovery And Muscle Building?

Does Metformin Inhibit Recovery And Muscle Building?

Does Metformin inhibit recovery and muscle building? Does Metformin inhibit recovery and muscle building? My endocrinologist recommended that I take Metformin (an insulin sensitizer) to help lower my blood sugar and to help me lose weight (I'm 53yrs 5'9" 230lbs, at about 26% body fat). After taking it for six weeks I found that it was killing my progress and making me weaker. Is it true that Metformin inhibits muscle recovery? I stopped taking the Metformin 3 days ago. When could I expect the muscle recovery return to normal? Are there natural insulin sensitizers that could help my blood sugar levels without harming muscle recovery (such as Berberine, magnesium, and ginger)? Up to this point, I havent addressed metformin directly, but have referred to sensitizers in general. Heres where that changes. While the majority of sensitizers (including metformin) in use today work to increase insulin sensitivity via AMPK activation, metformin has other negative effects on androgen receptors which compound its negative effect on protein synthesis, the most problematic of which is its ability to reduce androgen receptor density. In other words, this stuff doesnt just have a suppressive effect on androgen receptor function, it actually gets rid of them! Being that androgen receptor signaling is the primary mechanism through which testosterone and other steroids stimulate muscle growth, anything which eliminates this critical mediator not only reduces the rate of muscle growth, but total growth potential as well. Metformin has also been proven to reduce endogenous testosterone production in both men and womensignificantly. this stuff doesnt just have a suppressive effect on androgen receptor function, it actually gets rid of them! According to the claim that metformin gets rid of Continue reading >>

Metformin Impairs Mitochondrial Function In Skeletal Muscle Of Both Lean And Diabetic Rats In A Dose-dependent Manner

Metformin Impairs Mitochondrial Function In Skeletal Muscle Of Both Lean And Diabetic Rats In A Dose-dependent Manner

Abstract Metformin is a widely prescribed drug for the treatment of type 2 diabetes. Previous studies have demonstrated in vitro that metformin specifically inhibits Complex I of the mitochondrial respiratory chain. This seems contraindicative since muscle mitochondrial dysfunction has been linked to the pathogenesis of type 2 diabetes. However, its significance for in vivo skeletal muscle mitochondrial function has yet to be elucidated. The aim of this study was to assess the effects of metformin on in vivo and ex vivo skeletal muscle mitochondrial function in a rat model of diabetes. Healthy (fa/+) and diabetic (fa/fa) Zucker diabetic fatty rats were treated by oral gavage with metformin dissolved in water (30, 100 or 300 mg/kg bodyweight/day) or water as a control for 2 weeks. After 2 weeks of treatment, muscle oxidative capacity was assessed in vivo using 31P magnetic resonance spectroscopy and ex vivo by measuring oxygen consumption in isolated mitochondria using high-resolution respirometry. Two weeks of treatment with metformin impaired in vivo muscle oxidative capacity in a dose-dependent manner, both in healthy and diabetic rats. Whereas a dosage of 30 mg/kg/day had no significant effect, in vivo oxidative capacity was 21% and 48% lower after metformin treatment at 100 and 300 mg/kg/day, respectively, independent of genotype. High-resolution respirometry measurements demonstrated a similar dose-dependent effect of metformin on ex vivo mitochondrial function. In conclusion, metformin compromises in vivo and ex vivo muscle oxidative capacity in Zucker diabetic fatty rats in a dose-dependent manner. Figures Citation: Wessels B, Ciapaite J, van den Broek NMA, Nicolay K, Prompers JJ (2014) Metformin Impairs Mitochondrial Function in Skeletal Muscle of Both Lean and Continue reading >>

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