Metformin, Cancer And Glucose Metabolism
1Department of Internal Medicine (DIMI), University of Genova, Viale Benedetto XV/6, 16132 Genova, Italy 2IRCCS Azienda Ospedaliera Universitaria San Martino IST Istituto Nazionale per la Ricerca sul Cancro, 16132 Genova, Italy 3Department of Experimental, Diagnostic and Specialty Medicine (DIMES), Alma Mater Studiorum, University of Bologna, Bologna, Italy 4CNR Institute of Organic Synthesis and Photoreactivity (ISOF), 40129 Bologna, Italy 5CNR Institute of Molecular Bioimaging and Physiology (IBFM), 16132 Genova, Italy 6Department of Health Science (DISSAL), University of Genova, 16132 Genova, Italy Correspondence should be addressed to D Maggi; Email: davide.maggi{at}unige.it Metformin is the first-line treatment for type 2 diabetes. Results from several clinical studies have indicated that type 2 diabetic patients treated with metformin might have a lower cancer risk. One of the primary metabolic changes observed in malignant cell transformation is an increased catabolic glucose metabolism. In this context, once it has entered the cell through organic cation transporters, metformin decreases mitochondrial respiration chain activity and ATP production that, in turn, activates AMP-activated protein kinase, which regulates energy homeostasis. In addition, metformin reduces cellular energy availability and glucose entrapment by inhibiting hexokinase-II, which catalyses the glucose phosphorylation reaction. In this review, we discuss recent findings on molecular mechanisms that sustain the anticancer effect of metformin through regulation of glucose metabolism. In particular, we have focused on the emerging action of metformin on glycolysis in normal and cancer cells, with a drug discovery perspective. Made available online as an Accepted Preprint 1 October 2014 Copyrig Continue reading >>
- Exercise and Glucose Metabolism in Persons with Diabetes Mellitus: Perspectives on the Role for Continuous Glucose Monitoring
- ‘Type 3 diabetes’: New links emerge between poor glucose metabolism and Alzheimer’s disease
- Effect of Probiotics on Glucose and Lipid Metabolism in Type 2 Diabetes Mellitus: A Meta-Analysis of 12 Randomized Controlled Trials
Metformin Use In Pcos Pregnancies Increases The Risk Of Offspring Overweight At 4 Years Of Age; Follow-up Of Two Rcts
Metformin use in PCOS pregnancies increases the risk of offspring overweight at 4 years of age; follow-up of two RCTs Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Correspondence: Liv Guro Engen Hanem, Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, PO Box 8905 MTFS, NO-7491 Trondheim, Norway, Tel +47 98652774, Email [email protected] Search for other works by this author on: Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Departement of Obstetrics and Gynecology, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway Search for other works by this author on: Department of Clinical Science, University of Bergen, Bergen, Norway Search for other works by this author on: Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Search for other works by this author on: Department of Public Health and Primary Care, KU Leuven - University of Leuven, Belgium Search for other works by this author on: Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Departement of Endocrinology, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway Search for other works by this author on: Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Childrens clinic, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway Search for other works by this auth Continue reading >>
Effect Of Metformin On Metabolic Improvement And Gut Microbiota
Effect of Metformin on Metabolic Improvement and Gut Microbiota aCenter for Human and Environmental Microbiome, School of Public Health, Seoul National University, Seoul, South Korea bN-Bio, Seoul National University, Seoul, South Korea Metformin is commonly used as the first line of medication for the treatment of metabolic syndromes, such as obesity and type 2 diabetes (T2D). Recently, metformin-induced changes in the gut microbiota have been reported; however, the relationship between metformin treatment and the gut microbiota remains unclear. In this study, the composition of the gut microbiota was investigated using a mouse model of high-fat-diet (HFD)-induced obesity with and without metformin treatment. As expected, metformin treatment improved markers of metabolic disorders, including serum glucose levels, body weight, and total cholesterol levels. Moreover, Akkermansia muciniphila (12.44% 5.26%) and Clostridium cocleatum (0.10% 0.09%) abundances increased significantly after metformin treatment of mice on the HFD. The relative abundance of A. muciniphila in the fecal microbiota was also found to increase in brain heart infusion (BHI) medium supplemented with metformin in vitro. In addition to the changes in the microbiota associated with metformin treatment, when other influences were controlled for, a total of 18 KEGG metabolic pathways (including those for sphingolipid and fatty acid metabolism) were significantly upregulated in the gut microbiota during metformin treatment of mice on an HFD. Our results demonstrate that the gut microbiota and their metabolic pathways are influenced by metformin treatment. Metformin is a common antidiabetic agent in the biguanide class and is known to suppress glucose production in the liver, increase insulin sensitivity, an Continue reading >>
Metformin: The Sweet Link Between Tumor Genetics And Metabolism?
(1) Department of Radiation Oncology, Kimmel Cancer Center and Jefferson Medical College of Thomas Jefferson, Philadelphia PA (2) Department of Radiation Oncology, University of Pittsburgh Cancer Institute, Pittsburgh, PA Epidemiological studies have shown a correlation between insulin resistance, a marker of impaired glucose metabolism and metabolic syndrome, and malignancy development. Insulin resistance leads to a hyperinsulinemic state, which is thought to promote carcinogenesis via the direct effect of insulin on the insulin like growth factor 1 (IGF-1), an increase in IGF-1 synthesis, modulation of sex hormone availability, and finally through the resultant elevated glucose levels that promote inflammation and aid glycolysis in cancer cells. In addition to an increased incidence of cancer induction, insulin resistance has also been correlated with worse prognosis in cancer patients undergoing active treatment. Metformin is an oral agent that is widely used in the treatment of diabetes as it has been shown to sensitize cells to the effects of insulin. Several epidemiologic studies show a potential protective effect of metformin in diabetic patients. Preclinical studies have shown a direct inhibitory effect of metformin on cancer cell lines both in vitro and in vivo. This is thought to be mediated through multiple mechanisms, including effects on cellular metabolism via the AMP-activated protein kinase (AMPK) pathway, effects on cell cycle progression, and decreased cellular oxygen consumption. Though the data is conflicting, several retrospective studies suggest an antitumor benefit of metformin in cancer patients undergoing active treatment. Several prospective studies examining the role of metformin as an adjunctive antineoplastic agent are currently ongoing. Th Continue reading >>
Metforminmode Of Action And Clinical Implications For Diabetes And Cancer
Metforminmode of action and clinical implications for diabetes and cancer Mrta Korbonits, MD, PhD is Professor of Endocrinology and Metabolism at Queen Mary University of London. Her primary research interests are the hormonal regulation of AMPK, pituitary diseases and familial pituitary adenomas. Nature Reviews Endocrinology volume 10, pages 143156 (2014) Metformin has been the mainstay of therapy for diabetes mellitus for many years; however, the mechanistic aspects of metformin action remained ill-defined. Recent advances revealed that this drug, in addition to its glucose-lowering action, might be promising for specifically targeting metabolic differences between normal and abnormal metabolic signalling. The knowledge gained from dissecting the principal mechanisms by which metformin works can help us to develop novel treatments. The centre of metformin's mechanism of action is the alteration of the energy metabolism of the cell. Metformin exerts its prevailing, glucose-lowering effect by inhibiting hepatic gluconeogenesis and opposing the action of glucagon. The inhibition of mitochondrial complex I results in defective cAMP and protein kinase A signalling in response to glucagon. Stimulation of 5-AMP-activated protein kinase, although dispensable for the glucose-lowering effect of metformin, confers insulin sensitivity, mainly by modulating lipid metabolism. Metformin might influence tumourigenesis, both indirectly, through the systemic reduction of insulin levels, and directly, via the induction of energetic stress; however, these effects require further investigation. Here, we discuss the updated understanding of the antigluconeogenic action of metformin in the liver and the implications of the discoveries of metformin targets for the treatment of diabetes mell Continue reading >>
Metformin Use In Pcos Pregnancies Increases The Risk Of Offspring Overweight At 4 Years Of Age: Follow-up Of Two Rcts
The Journal of Clinical Endocrinology & Metabolism Metformin Use in PCOS Pregnancies Increases the Risk of Offspring Overweight at 4 Years of Age: Follow-Up of Two RCTs Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Correspondence and Reprint Requests: Liv Guro Engen Hanem, MD, Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, PO Box 8905 MTFS, NO-7491 Trondheim, Norway. E-mail: [email protected] . Search for other works by this author on: Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Department of Obstetrics and Gynecology, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway Search for other works by this author on: Department of Clinical Science, University of Bergen, Bergen, Norway Search for other works by this author on: Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Search for other works by this author on: Department of Public Health and Primary Care, KU Leuven-University of Leuven, Leuven, Belgium Search for other works by this author on: Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Department of Endocrinology, St. Olavs Hospital, Trondheim University Hospital, Trondheim, Norway Search for other works by this author on: Department of Clinical and Molecular Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway Childrens Clinic, St. Olavs Hospital, Trondheim Universi Continue reading >>
Breast Cancer Metabolism And Mitochondrial Activity: The Possibility Of Chemoprevention With Metformin
Breast Cancer Metabolism and Mitochondrial Activity: The Possibility of Chemoprevention with Metformin Division of Cancer Prevention and Genetics, European Institute of Oncology, 20141 Milan, Italy Received 27 May 2015; Revised 11 September 2015; Accepted 7 October 2015 Copyright 2015 Massimiliano Cazzaniga and Bernardo Bonanni. 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. Metabolic reprogramming refers to the ability of cancer cells to alter their metabolism in order to support the increased energy request due to continuous growth, rapid proliferation, and other characteristics typical of neoplastic cells. It has long been believed that the increase of metabolic request was independent of the mitochondrial action but recently we know that mitochondrial activity together with metabolism plays a pivotal role in the regulation of the energy needed for tumor cell growth and proliferation. For these reasons the mitochondria pathways could be a new target for therapeutic and chemopreventive intervention. Metformin in particular is actually considered a promising agent against mitochondrial activity thanks to its ability to inhibit the mitochondrial complex I. Although breast cancer is considered a genetic disease in which several mutations and genome dynamic changes are present [ 1 ], recent research endeavors are geared to try and understand other mechanisms contributing to the (formation) development and progression of the disease. In this regard, the evidence of the changes affecting cancer cells metabolism has proved to be one of the most promising features and it has influenced several studies on this Continue reading >>
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 >>
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 >>
Beneficial Effects Of Metformin On Energy Metabolism And Visceral Fat Volume Through A Possible Mechanism Of Fatty Acid Oxidation In Human Subjects And Rats
Click through the PLOS taxonomy to find articles in your field. For more information about PLOS Subject Areas, click here . Beneficial effects of metformin on energy metabolism and visceral fat volume through a possible mechanism of fatty acid oxidation in human subjects and rats Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Division of Endocrinology and Metabolism, Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan Affiliation Institute of Animal Experimentation, Kurume University School of Medicine, Kurume, Japan Continue reading >>
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 >>
Effect Of Metformin On Metabolic Improvement And Gut Microbiota
Effect of Metformin on Metabolic Improvement and Gut Microbiota aCenter for Human and Environmental Microbiome, School of Public Health, Seoul National University, Seoul, South Korea bN-Bio, Seoul National University, Seoul, South Korea Metformin is commonly used as the first line of medication for the treatment of metabolic syndromes, such as obesity and type 2 diabetes (T2D). Recently, metformin-induced changes in the gut microbiota have been reported; however, the relationship between metformin treatment and the gut microbiota remains unclear. In this study, the composition of the gut microbiota was investigated using a mouse model of high-fat-diet (HFD)-induced obesity with and without metformin treatment. As expected, metformin treatment improved markers of metabolic disorders, including serum glucose levels, body weight, and total cholesterol levels. Moreover, Akkermansia muciniphila (12.44% 5.26%) and Clostridium cocleatum (0.10% 0.09%) abundances increased significantly after metformin treatment of mice on the HFD. The relative abundance of A. muciniphila in the fecal microbiota was also found to increase in brain heart infusion (BHI) medium supplemented with metformin in vitro. In addition to the changes in the microbiota associated with metformin treatment, when other influences were controlled for, a total of 18 KEGG metabolic pathways (including those for sphingolipid and fatty acid metabolism) were significantly upregulated in the gut microbiota during metformin treatment of mice on an HFD. Our results demonstrate that the gut microbiota and their metabolic pathways are influenced by metformin treatment. Metformin is a common antidiabetic agent in the biguanide class and is known to suppress glucose production in the liver, increase insulin sensitivity, an Continue reading >>
Metformin Influences Nitrogen And Urea Metabolism
Follow all of ScienceDaily's latest research news and top science headlines ! Metformin influences nitrogen and urea metabolism Helmholtz Zentrum Muenchen - German Research Centre for Environmental Health The most frequently prescribed oral antidiabetic drug metformin significantly affects metabolic pathways, report scientists. Metformin is a widespread oral medication to increase insulin sensitivity in patients with type 2 diabetes (T2D). According to a number of studies, it additionally reduces the risk of cardiovascular complications. The most frequently prescribed oral antidiabetic drug metformin significantly affects metabolic pathways. This was reported by scientists from the Helmholtz Zentrum Mnchen together with colleagues from the German Diabetes Center (DDZ) in Dsseldorf. The underlying study was conducted with further scientists of the German Center for Diabetes Research (DZD). These results have now been published in the journal 'Diabetes'. Metformin is a widespread oral medication to increase insulin sensitivity in patients with type 2 diabetes (T2D). According to a number of studies, it additionally reduces the risk of cardiovascular complications. Last year, a team led by Dr. Rui Wang-Sattler discovered that metformin intake lowers the levels of the harmful LDL cholesterol by activating the AMPK protein complex. Dr. Wang-Sattler is head of the "Metabolism" research group in the Research Unit of Molecular Epidemiology at the Institute of Epidemiology II at the Helmholtz Zentrum Mnchen. Her group aims to understand the molecular mechanisms that underlie the activity of metformin. Metformin intake changes metabolite profiles in population-based KORA* study In the present work, the interdisciplinary team of scientists was able to explain a further feature of Continue reading >>
Metformin And Pancreatic Cancer Metabolism
Metformin and Pancreatic Cancer Metabolism By Mary Jo Cantoria, Hitendra Patel, Laszlo G. Boros and Emmanuelle J.Meuillet 5. Chemotherapeutic properties of metformin Figure 3. Metformin impairs signaling molecules for cancer survival. Metformin and Pancreatic Cancer Metabolism Mary Jo Cantoria1, 2, Hitendra Patel2, 3, Laszlo G. Boros4, 5 and Emmanuelle J. Meuillet2, 6 [1] Department of Nutritional Sciences, The University of Arizona, Tucson, USA [2] The University of Arizona Cancer Center, Tucson, AZ, USA [3] College of Medicine, The University of Arizona, Tucson, USA [5] Department of Pediatrics, Los Angeles Biomedical Research, USA [6] Institute at the Harbor-UCLA Medical Center, Torrance, CA, USA [7] Department of Nutritional Sciences, The University of Arizona, Tucson, USA Numerous epidemiological studies have reported that metformin, a well-known and widely used anti-diabetic drug, may provide protective benefits in decreasing pancreatic cancer risk among the diabetic population. Following a brief introduction regarding metformins history and pharmacological properties, this book chapter presents epidemiological findings showing how metformin is associated with protection against pancreatic cancer. We also introduce the anti-cancer effects of metformin through AMPK-independent and AMPK-dependent manners [ 1 - 6 ]. These mechanisms include its inhibitory effects on the insulin growth factor-1 (IGF-1), G protein-coupled receptor (GPCR) and mTORC1 signaling pathways [ 3 - 10 ]. We then discuss the metabolic effects of metformin in cancer. For example, metformin has been shown to inhibit glycolysis in various cancer cell lines [ 11 - 13 ]. Metformin is a known inhibitor of complex I of the electron transport chain [ 14 - 18 ], potentially limiting the intact oxidative Continue reading >>
Long-term Effects Of Metformin On Metabolism And Microvascular And Macrovascular Disease In Patients With Type 2 Diabetes Mellitus
Background We investigated whether metformin hydrochloride has sustained beneficial metabolic and (cardio) vascular effects in patients with type 2 diabetes mellitus (DM2). Methods We studied 390 patients treated with insulin in the outpatient clinics of 3 hospitals in a randomized, placebo-controlled trial with a follow-up period of 4.3 years. Either metformin hydrochloride, 850 mg, or placebo (1-3 times daily) was added to insulin therapy. The primary end point was an aggregate of microvascular and macrovascular morbidity and mortality. The secondary end points were microvascular and macrovascular morbidity and mortality, as separate aggregate scores. In addition, effects on hemoglobin A1c (HbA1c), insulin requirement, lipid levels, blood pressure, body weight, and body mass index were analyzed. Results Metformin treatment prevented weight gain (mean weight gain, −3.07 kg [range, −3.85 to −2.28 kg]; P < .001), improved glycemic control (mean reduction in HbA1c level, 0.4% percentage point [95% CI, 0.55-0.25]; P < .001) (where CI indicates confidence interval), despite the aim of similar glycemic control in both groups, and reduced insulin requirements (mean reduction, 19.63 IU/d [95% CI, 24.91-14.36 IU/d]; P < .001). Metformin was not associated with an improvement in the primary end point. It was, however, associated with an improvement in the secondary, macrovascular end point (hazard ratio, 0.61 (95% CI, 0.40-0.94; P = .02), which was partly explained by the difference in weight. The number needed to treat to prevent 1 macrovascular end point was 16.1 (95% CI, 9.2-66.6). Conclusions Metformin, added to insulin in patients with DM2, improved body weight, glycemic control, and insulin requirements but did not improve the primary end point. Metformin did, howeve Continue reading >>
- Association of Glycemic Variability in Type 1 Diabetes With Progression of Microvascular Outcomes in the Diabetes Control and Complications Trial
- ‘Type 3 diabetes’: New links emerge between poor glucose metabolism and Alzheimer’s disease
- Effect of Probiotics on Glucose and Lipid Metabolism in Type 2 Diabetes Mellitus: A Meta-Analysis of 12 Randomized Controlled Trials
