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Metformin Intestinal Glucose Absorption

Oral Diabetes Medications

Oral Diabetes Medications

Oral diabetes medicines (taken by mouth) help control blood sugar (glucose) levels in people whose bodies still produce some insulin, such as some people with type 2 diabetes. These medicines are prescribed along with regular exercise and changes in the diet. Many oral diabetes medications may be used in combination with each other or with insulin to achieve the best blood glucose control. This guide provides general information about the different oral medicines for diabetes. It will help you learn more about your medication. Always take your medicine exactly as your doctor prescribes it. Discuss your specific questions and concerns with your health care provider. Sulfonylureas Glipizide (Glucotrol®, Glucotrol XL®,), Glimepride (Amaryl®), Glyburide (DiaBeta®, Glynase PresTab®, Micronase®) These medications lower blood glucose by causing the pancreas to release more insulin. Biguanides Metformin (Glucophage®, Glucophage XR®, Glumetza®, Fortamet®, Riomet®) These medications reduce how much glucose the liver produces. It also improves how insulin works in the body, and slows down the conversion of carbohydrates into sugar. Thiazolidinediones Pioglitozone (Actos®), rosiglitozone (Avandia®) These medications improve the way insulin works in the body by allowing more glucose to enter into muscles, fat, and the liver. Alpha-glucosidase inhibitors Acarbose (Precose®,) miglitol (Glyset®) These medications lower blood glucose by delaying the breakdown of carbohydrates and reducing glucose absorption in the small intestine. They also block certain enzymes in order to slow down the digestion of some starches. Meglitinide Repaglinide (Prandin®), nateglinide (Starlix®) These medications lower blood glucose by getting the pancreas to release more insulin. DPP-4 inhib Continue reading >>

Synjardy

Synjardy

Synjardy (empagliflozin/metformin hydrochloride) tablets (by Boehringer Ingelheim and Eli Lilly and Company) has received FDA approval for an expanded indication to include treatment-nave adults with type 2 diabetes (T2D). Synjardy is indicated as an adjunct to diet and exercise to improve glycemic control in adults with T2D when treatment with both empagliflozin and metformin is appropriate. The approval carries the limitation that Synjardy should not be used for the treatment of type 1 diabetes or diabetic ketoacidosis.1,2 Empagliflozin is a sodium-glucose co-transporter 2 (SGLT2) inhibitor that reduces renal reabsorption of filtered glucose and lowers the renal threshold for glucose, resulting in increased urinary glucose excretion. Metformin is a member of the biguanide class. It decreases hepatic glucose production, decreases intestinal glucose absorption, and improves insulin sensitivity by increasing peripheral glucose uptake and utilization.1 The starting dose of Synjardy should be individualized based on the patients current medication regimen, with a maximum daily dose of 12.5 mg empagliflozin/1000 mg metformin twice daily. To reduce the gastrointestinal side effects of metformin, the tablet should be taken with meals, with a gradual escalation in dose. Renal function should be assessed prior to initiation of treatment. Synjardy should not be used in patients with an eGFR below 45 ml/min/1.73m2. Discontinuation may be required at the time of, or prior to, iodinated contrast imagining procedures.1 The additional indication for Synjardy was based on a Phase III, double-blind, randomized, active-controlled study that evaluated the efficacy and safety of empagliflozin in combination with metformin as initial therapy compared with treatment with either empaglifloz Continue reading >>

Metformin And The Gastrointestinal Tract

Metformin And The Gastrointestinal Tract

Go to: Introduction Metformin—dimethylbiguanide—is an oral glucose-lowering agent. Its origins can be traced to Galega officinalis, also known as French lilac or goat’s rue [1]. In the early 20th century it was noted to lower blood glucose concentrations in animals, but it was not until the 1950s that Jean Sterne studied dimethylbiguanide and subsequently developed ‘Glucophage’ [2]. Over the last 15 years, metformin has become the first-line agent for the treatment of type 2 diabetes, as noted in several international guidelines, including the ADA-EASD guidelines [3]. Metformin has had a chequered history—it was initially eclipsed by phenformin, which was withdrawn in the late 1970s after it was discovered to be associated with lactic acidosis [4]. The lower propensity of metformin for hyperlactataemia [5] and success in several large randomised controlled clinical trials, such as the UK Prospective Diabetes Study (UKPDS) [6], confirmed its clinical benefit. It is widely recognised that metformin improves glycaemic control with a good safety profile, weight neutrality or weight loss, lack of associated hypoglycaemia, reduced cardiovascular mortality and low cost [3]. However, a large proportion of patients cannot tolerate the medication in adequate amounts because of its associated side effects. Up to 25% of patients suffer metformin-associated gastrointestinal (GI) side-effects, with approximately 5% unable to tolerate metformin at all [7]. In addition to this interindividual variation in side effects, there is variability in the efficacy of metformin. There are likely to be a number of factors to account for this variability in efficacy, for example, our group (Zhou et al) recently established that the glycaemic response to metformin is moderately heritabl Continue reading >>

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Mechanism(s): Inhibits amylase and functions via three additional mechanisms to internally regulate glucose and triglyceride metabolism.29-31 Mechanism(s): Inhibits the lipase digestive enzyme used to break down fatty foods and boosts internal utilization of glucose by boosting resting metabolic rate.32,33 We suggest taking a powdered drink mix containing these ingredients before the two heaviest meals of the day. For those whose glucose levels remain unacceptably high despite taking the powdered drink mix, there are encapsulated nutrients that work to specifically block the sucrase and glucosidase digestive enzymes. Sucrase breaks down sucrose to fructose and glucose, and glucosidase catalyzes the hydrolysis of the glycosidic linkage to all carbohydrates to release smaller sugars. Blocking these enzymes reduces the amount of glucose absorbed from dietary sources. One capsule containing L-arabinose and a special brown seaweed extract should be taken before eating sucrose (table sugar)-containing foods.34-36 Aging causes a loss of insulin sensitivity, which means that glucose that would normally be utilized by energy-producing cells instead either remains in the blood or converts to storage as triglycerides (in blood and fat cells) or glycogen in the liver. A cinnamon extract has been developed to enhance the ability of insulin to drive blood glucose into muscle cells. This cinnamon compound that enhances insulin sensitivity is combined with brown seaweed extract (to inhibit the glucosidase enzyme) to provide additive control over glucose levels.36-42 An anti-diabetic drug that Life Extension suggests normal aging people consider taking to lower glucose is metformin (refer to article on page 56 of this months issue about metformin and cancer risk reduction). It is avail Continue reading >>

Metformin Reduces The Rate Of Small Intestinal Glucose Absorption In Type 2diabetes.

Metformin Reduces The Rate Of Small Intestinal Glucose Absorption In Type 2diabetes.

1. Diabetes Obes Metab. 2017 Feb;19(2):290-293. doi: 10.1111/dom.12812. Epub 2016Nov 21. Metformin reduces the rate of small intestinal glucose absorption in type 2diabetes. Wu T(1)(2), Xie C(1)(2)(3), Wu H(1)(2)(3), Jones KL(1)(2), Horowitz M(1)(2),Rayner CK(1)(2). (1)Discipline of Medicine, University of Adelaide, Adelaide, South Australia, Australia. (2)Centre of Research Excellence in Translating Nutritional Science to Good Health, University of Adelaide, Adelaide, South Australia, Australia. (3)Medical School, Southeast University, Nanjing, China. In rodents, metformin slows intestinal glucose absorption, potentially increasingexposure of the distal gut to glucose to enhance postprandial glucagon-likepeptide-1 (GLP-1) secretion. We evaluated the effects of metformin on serum3-O-methylglucose (3-OMG; a marker of glucose absorption) and plasma total GLP-1 concentrations during a standardized intraduodenal infusion of glucose and 3-OMG in patients with type 2 diabetes. A total of 12 patients, treated with metformin 850 mg twice daily or placebo for 7 days each in a double-blind, randomized,crossover design (14 days' washout between treatments), were evaluated on days 5 or 8 of each treatment (6 subjects each). On each study day, 30 minutes afteringesting 850 mg metformin or placebo, patients received an infusion of glucose(60 g + 5 g 3-OMG, dissolved in water to 240 mL) via an intraduodenal catheterover the course of 120 minutes. Compared with placebo, metformin was associatedwith lower serum 3-OMG ( P < .001) and higher plasma total GLP-1 ( P = .003)concentrations. The increment in plasma GLP-1 after metformin vs placebo wasrelated to the reduction in serum 3-OMG concentrations ( P = .019). Accordingly, metformin inhibits small intestinal glucose absorption, which m Continue reading >>

Insulin And Intestinal Sugar Absorption

Insulin And Intestinal Sugar Absorption

Harvard Medical School and Beth Israel Hospital, 330 Brookline Avenue, Boston, Massachusetts 02215 Search for other works by this author on: The American Journal of Clinical Nutrition, Volume 22, Issue 3, 1 March 1969, Pages 311314, DAVID FROMM; Insulin and Intestinal Sugar Absorption, The American Journal of Clinical Nutrition, Volume 22, Issue 3, 1 March 1969, Pages 311314, 1) Insulin has been shown to increase glucose absorption from isolated rat small intestine in vivo; this effect was proportional to the dose of insulin. An effect of insulin has not been demonstrated with intubation-perfusion studies in man. Fundamental differences in methodology, however, prevent a direct comparison of these conflicting results. 2) Insulin has been shown to increase sugar transport in vitro across small intestine from normal animals. 3) There is no convincing evidence that the enhanced sugar absorption in vivo and in vitro of diabetes mellitus is altered by insulin. 4) The physiological significance of the enhancement of intestinal sugar absorption by insulin in normal animals is not clear. Copyright 1969 by The American Society for Clinical Nutrition, Inc Continue reading >>

The Use Of Metformin For The Treatment Of Equine Metabolic Syndrome

The Use Of Metformin For The Treatment Of Equine Metabolic Syndrome

Home Equinews The Use of Metformin for the Treatment of Equine Metabolic Syndrome The Use of Metformin for the Treatment of Equine Metabolic Syndrome Metformin is a human drug prescribed for the treatment of type II diabetes mellitus. In humans, metformin reduces glucose absorption from the intestine and decreases the amount of glucose produced by the liver (gluconeogenesis). Metformin has been used in horses to counteract the effects of equine metabolic syndrome. However, some studies have shown that intestinal absorption of metformin in horses is poor, and metformin may not improve insulin sensitivity in ponies. Nine horses were given a feed containing glucose, and their blood concentrations of insulin and glucose were measured for 240 minutes afterward. The test was performed with and without administration of metformin. The horses were treated with a high dose of metformin (30 mg/kg). Results of the study showed that administration of metformin significantly decreased intestinal absorption of glucose and the corresponding insulin response. This study indicates that metformin may be useful for the treatment of equine metabolic syndrome. For best results, medical therapy should be combined with management practices such as reducing obesity, feeding lower carbohydrate feeds, controlling pasture grazing, and increasing exercise. Durham, A.E., D.I. Rendle, F. Rutledge, et al. 2012. The effects of metformin hydrochloride on intestinal glucose absorption and use of tests for hyperinsulinaemia. In: Proceedings. Am. Coll. Vet. Intern. Med. 281. Continue reading >>

Metformin And Digestive Disorders

Metformin And Digestive Disorders

Digestive disorders (diarrhoea, vomiting) represent the most common metformin side-effects (around 30%) with this first-line drug treatment for type 2 diabetes. In healthy individuals, metformin affects glucose, vitamin B12 and the digestive uptake of bile salts. In the colon, it acts locally by modifying glucose cell metabolism. Different pathophysiological hypotheses have been proposed to explain the metformin-induced diarrhoea and vomiting, which can sometimes cause the patient to stop an effective treatment. These theories include stimulation of intestinal secretion of serotonin, changes in incretin and glucose metabolism, and bile-salt malabsorption. However, none of these hypotheses can be considered an adequate pathophysiological explanation of metformin digestive side-effects. In addition, there is a lack of experimental data to explain these highly patient-dependent adverse effects. The full text of this article is available in PDF format. Les troubles digestifs (diarrhée, vomissements) sous metformine représentent l’effet indésirable le plus fréquent (environ 30 %) pour le médicament de référence du diabète de type 2. Chez l’individu non diabétique, la metformine agit sur l’absorption digestive du glucose, de la vitamine B12 et des sels biliaires. Pour le côlon, elle agit localement en modifiant le métabolisme cellulaire. Différentes hypothèses physiopathologiques peuvent expliquer les diarrhées et vomissements qui peuvent obliger le patient à cesser un traitement efficace: stimulation de la sécrétion intestinale de sérotonine, modification des incrétines et du métabolisme du glucose ou malabsorption des sels biliaires. Aucune de ces hypothèses ne peut être considérée comme l’explication physiopathologique des effets secondaires Continue reading >>

Mechanism Of Metformin: A Tale Of Two Sites

Mechanism Of Metformin: A Tale Of Two Sites

Metformin (dimethylbiguanide) features as a current first-line pharmacological treatment for type 2 diabetes (T2D) in almost all guidelines and recommendations worldwide. It has been known that the antihyperglycemic effect of metformin is mainly due to the inhibition of hepatic glucose output, and therefore, the liver is presumably the primary site of metformin function. However, in this issue of Diabetes Care, Fineman and colleagues (1) demonstrate surprising results from their clinical trials that suggest the primary effect of metformin resides in the human gut. Metformin is an orally administered drug used for lowering blood glucose concentrations in patients with T2D, particularly in those overweight and obese as well as those with normal renal function. Pharmacologically, metformin belongs to the biguanide class of antidiabetes drugs. The history of biguanides can be traced from the use of Galega officinalis (commonly known as galega) for treating diabetes in medieval Europe (2). Guanidine, the active component of galega, is the parent compound used to synthesize the biguanides. Among three main biguanides introduced for diabetes therapy in late 1950s, metformin (Fig. 1A) has a superior safety profile and is well tolerated. The other two biguanides, phenformin and buformin, were withdrawn in the early 1970s due to the risk of lactic acidosis and increased cardiac mortality. The incidence of lactic acidosis with metformin at therapeutic doses is rare (less than three cases per 100,000 patient-years) and is not greater than with nonmetformin therapies (3). Major clinical advantages of metformin include specific reduction of hepatic glucose output, with subsequent improvement of peripheral insulin sensitivity, and remarkable cardiovascular safety, but without increasi Continue reading >>

An Error Occurred Setting Your User Cookie

An Error Occurred Setting Your User Cookie

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 >>

Metformin: An Old Drug For The Treatment Of Diabetes But A New Drug For The Protection Of The Endothelium

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 >>

How Much Do You Know About Metformin?

How Much Do You Know About Metformin?

Metformin is a drug commonly used in the treatment of Type 2 diabetes. It is sold as a generic and under several brand names, including Glucophage, Glumetza, Riomet, and Fortamet. Both the American Diabetes Association (ADA) and the American Association of Clinical Endocrinologists (AACE) recommend metformin as a cornerstone of therapy for Type 2 diabetes when exercise and dietary changes aren’t enough to keep blood glucose levels in target range. The low cost of the generic forms along with a long history of use make it a good choice for many individuals with Type 2 diabetes. Although metformin has helped many people lower their blood glucose levels, it does have some potential side effects that are worth knowing about. Understanding the risks and benefits of metformin is key to using it successfully. Take this quiz to test your knowledge of this popular diabetes medicine. (You can find the answers later in the article.) Q 1. How does metformin work to lower blood glucose levels? A. It stimulates the pancreas to make more insulin. B. It decreases the amount of glucose produced by the liver and makes it easier for cells to accept glucose from the bloodstream. C. It slows the digestive system’s breakdown of carbohydrates into glucose, allowing more time for insulin to work. D. It suppresses appetite, slows stomach emptying, and inhibits the release of glucagon (a hormone that raises blood glucose levels). 2. In addition to lowering blood glucose, metformin sometimes causes moderate weight loss. TRUE FALSE 3. In research studies, metformin use was associated with which of the following benefits in people with Type 2 diabetes? A. Reduced risk of morning high blood glucose. B. Reduced neuropathy (nerve damage). C. Reduced retinopathy (damage to the retina, a membrane in Continue reading >>

[11c]metformin

[11c]metformin

Metformin Metformin (1,1-dimethylbiguanide) is an orally administered drug, used as an insulin sensitizer in the treatment of type II diabetes (Nesti & Natali, 2017). Liver is the main site of metformins positive effects: metformin indirectly inhibits gluconeogenesis in the liver and reduces the concentration of glucose in blood. Oral dosing induces stronger and longer response than intravenous administration, since the gastrointestinal tract is an important target for metformin, affecting also liver via nervous system (Foretz and Viollet, 2015). Metformin increases glucose uptake and anaerobic metabolism in the gut, leading to increased lactate concentration in the intestine and plasma. Metformin also increases GLP-1 plasma concentration and expression of GLP-1 receptors in the pancreas. Metformin reduces absorption of bile acids in ileum, leading to increased bile acid pool within intestine; this may be one of the reasons for reduced blood cholesterol levels, and altered microbiome (McCreight et al., 2016). Metformin is a strong base and it is positively charged under physiological pH. Its uptake in the gut is mostly transporter-dependent, and saturable, affected by inhibitors and other substrates of the transporters. Metformin is a substrate (and competitive inhibitor) for several transporters, such as organic cation transporters (OCT1, OCT2, OCT3), plasma membrane monoamine transporter (PMAT), multidrug and toxin extrusion proteins (MATE1 and MATE2), serotonin transporter (SERT), choline transporter (CHT) (McCreight et al., 2016), OCTN1, and thiamine transporter THTR-2. Genetic polymorphism of transporter genes affect the pharmacokinetics and effects of metformin. OCT1 is expressed in the liver and gut. OCT2 is expressed mainly in the kidneys, and with MATE1 is r Continue reading >>

Metformin And The Intestine

Metformin And The Intestine

To the Editor: The antihyperglycaemic effect of metformin is generally attributed to a decrease in hepatic glucose output, with some additional effects that increase peripheral glucose uptake and utilisation [ 1 ]. The intestine also makes an important contribution to the glucose-lowering effect of metformin, but this is often overlooked because of a paucity of clinical data [ 2 ]. Animal studies indicate that metformin can cause intestinal glucose absorption to be delayed and occur more distally along the tract [ 3 , 4 ]. However, animal studies have also shown that metformin increases glucose utilisation by the intestine, particularly anaerobic glucose metabolism [ 5 , 6 , 7 ], and this contributes to an apparent shortfall in the passage of glucose from the luminal to the serosal side of the intestine [ 3 ]. Extra lactate delivered into the portal vein is at least partly converted into glucose, increasing glucose turnover after administration of metformin [ 5 , 7 , 8 ]. We demonstrate here that metformin increases lactate production in human intestinal mucosa, similar to reports in animal studies. Animal studies have long established that very high concentrations of metformin accumulate in the wall of the intestine [ 9 ], which may at least partly explain the increase in anaerobic metabolism. We provide confirmatory evidence herein that similarly high concentrations of metformin accumulate in the human intestinal mucosa. In the present study, eight recently diagnosed, drug-naive, obese type 2 diabetic patients [five men, three women; age 55 3years (mean SEM); BMI 33 1kg/m2] attended on three occasions after an overnight fast. Patients gave informed consent, and ethical approval was granted by the research ethics committee. A venous blood sample was taken for plasma g Continue reading >>

Inhibitory Effect Of Metformin On Intestinal Glucose Absorption In The Perfused Rat Intestine.

Inhibitory Effect Of Metformin On Intestinal Glucose Absorption In The Perfused Rat Intestine.

Biochem Pharmacol. 2000 Apr 1;59(7):887-90. Inhibitory effect of metformin on intestinal glucose absorption in the perfused rat intestine. The Department of Medical Technology, Tottori University College of Medical Care Technology, Yonago, Japan. [email protected] To investigate the effect of metformin on intestinal glucose absorption, a perfusion study of the intestine was performed in the rat. Male Wistar albino rats (8 weeks old) were used in the present study. The glucose absorption by the perfused intestine (788.1+/-81.9 micromol/30 min) was not changed significantly by the direct addition of metformin (90 microg/mL) to the perfusing medium (737.0+/-118.2 micromol/30 min) or by intraduodenal metformin (250 mg/kg in saline solution) infusion (772.8+/-106.3 micromol/30 min). In rats orally administered metformin (250 mg/kg) for 5 days, glucose absorption by the perfused intestine (375.0+/-164.3 micromol/30 min) was significantly (P<0.001) lower than that in control rats (811.0+/-83.1 micromol/30 min). These results indicate that metformin had a significant effect on the digestive tract, and that metformin treatment exerted an inhibitory effect on intestinal glucose absorption in the rat. Continue reading >>

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