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Does Metformin Lower Insulin

Wait Times: How Long Until Your Med Begins Working

Wait Times: How Long Until Your Med Begins Working

Photography by Mike Watson Images/Thinkstock There are many type 2 medications, and each drug class works in the body in a different way. Here’s a quick guide to help you understand how long each drug will generally take to work: These short-acting oral medications, taken with meals, block the breakdown of complex sugars into simple sugars in the gastrointestinal (GI) tract. “Simple sugars are more easily absorbed and cause the blood sugar to ultimately go up,” Sam Ellis, PharmD, BCPS, CDE, associate professor in the Department of Clinical Pharmacy at the University of Colorado says. These drugs are minimally absorbed into the blood, so a certain blood level concentration is not necessary for them to work. You will see the effect immediately with the first dose. “You take it before a meal, and with that meal you see the effect,” says George Grunberger, MD, FACP, FACE, President of the American Association of Clinical Endocrinologists. While researchers aren’t exactly sure how these oral medications work, it’s likely that the meds block some absorption of glucose in the GI tract. “You’ll see most of the effect in the first week with these drugs,” says Ellis. alogliptin, linagliptin, saxagliptin, sitagliptin These drugs work to block the enzyme responsible for the breakdown of a specific gut hormone that helps the body produce more insulin when blood glucose is high and reduces the amount of glucose produced by the liver. Take a DPP-4 inhibitor (they come in pill form) and it’ll work pretty fast—you’ll see the full effect in about a week. “It’s blocking that enzyme after the first dose a little bit, but by the time you get out to dose five, you’re blocking the majority of that enzyme,” Ellis says. albiglutide, dulaglutide, exenatide, exe Continue reading >>

9 Ways To Lower Insulin Levels

9 Ways To Lower Insulin Levels

Chromium supplements may help to enhance insulin's effectiveness, which might help to lower insulin levels. Some studies have supported the use of supplements in reducing insulin levels. One study , published in the Annals of Nutrition & Metabolism, found that overweight women taking a dietary supplement that consisted of 125 milligrams (mg) of green tea , 25 mg of capsaicin, and 50 mg of ginger extract twice daily resulted in a greater decrease in body weight and insulin levels than those who took a placebo . Another supplement that has been widely studied for its insulin-lowering benefits is chromium, which is a trace mineral found in the human body. Supplements of chromium may help enhance insulin's effectiveness, which ideally, would help with lowering insulin levels overall. Chromium supplements are available to buy online . Studies have not definitively proven chromium's benefits in lowering insulin, yet. However, one study published in The Journal of Nutrition found that taking chromium supplements lowered the risk of having type 2 diabetes by helping reduce blood glucose and insulin levels. Sometimes, doctors will prescribe a medication known as Metformin. This medicine makes the body more sensitive to insulin, which can help to lower insulin levels because the body uses it more. According to the Center for Young Women's Health , women with PCOS who were overweight, practiced a healthful lifestyle, and took metformin were more likely to lose weight than those women who adopted a healthful lifestyle alone. However, side effects of taking metformin exist, so it is not always the best solution for women with PCOS or those with similar medical conditions. Excess insulin in the body is known to affect how the body works. For example, excess insulin triggers the body Continue reading >>

Multiple Benefits Of Metformin | Life Extension Magazine

Multiple Benefits Of Metformin | Life Extension Magazine

As the type II diabetic condition progresses, many people gain weight and develop more fat cells.2 Treating type II diabetes with insulin-enhancing therapy increases the risk of cardiovascular complications, induces weight gain, and fails to correct the underlying cause of the disease. Many type II diabetics produce too much insulin in a futile attempt to drive glucose into insulin-resistant cells. When doctors prescribe insulin-enhancing drugs to these type II diabetics, a temporarily reduction of serum glucose may occur, but the long-term effects of this excess insulin can be devastating. An ideal anti-diabetic drug would enhance cellular insulin sensitivity, inhibit excess intestinal absorption of sugar, reduce excess liver production of glucose, promote weight loss and reduce cardiovascular risk factors. Metformin (Glucophage) is the one drug that does all of this and more. Metformin works by increasing the number of muscle and adipocyte (fat cell) insulin receptors and the attraction for the receptor. It does not increase insulin secretion, it only increases insulin sensitivity. Therefore, metformin is not associated with causing hypoglycemia. This activity reduces insulin levels by increasing the sensitivity of peripheral tissues to the effects of insulin by rejuvenating the response, and restoring glucose and insulin to younger physiological levels that may cause weight loss and most certainly a decrease in the body's total fat content.3-7 In an study published by the American Diabetes Association, metformin was found to decrease the fasting plasma glucose concentration by -60 to -70mg/dl in patients with non-insulin dependent type II diabetes.1 Metformin also reduced hemoglobin A1C levels, a blood measurement of glycosylation. One of the most devastating conseq Continue reading >>

Metformin: Improving Insulin Sensitivity

Metformin: Improving Insulin Sensitivity

Metformin is the only medication in the biguanides category of blood glucose-lowering drugs approved by the U.S. Food and Drug Administration (FDA). Metformin has been available in the United States since the mid-1990s, when it received FDA approval. You may also know it by its brand name when it was under patent, Glucophage. Metformin is now widely available as a relatively inexpensive generic medication. Metformin’s main action is to decrease the overproduction of glucose by the liver, a common problem in prediabetes and type 2 diabetes. The action of metformin helps lower blood sugar levels particularly during the night to keep fasting glucose levels under control, but it also helps control blood glucose throughout the day. Metformin also increases the uptake of glucose by your muscles. Overall, metformin decreases insulin resistance and improves insulin sensitivity, thereby helping the insulin your body still makes work more effectively. People with prediabetes and in the early years of type 2 diabetes often continue to make some insulin, just not enough to control blood sugar levels alone. Metformin is not formally approved for use in prediabetes, and any use to treat prediabetes is considered off-label by providers. Since its approval, metformin has become the most commonly recommended blood glucose-lowering medication to treat type 2 diabetes. In recent years it has significantly replaced sulfonylureas, such as glipizide and glyburide. Today both the American Diabetes Association (ADA), the European Association for the Study of Diabetes (EASD), and the American Association of Clinical Endocrinologists (AACE) generally recommend that people with type 2 diabetes start taking metformin when they are diagnosed to help treat insulin resistance and maximize insulin s Continue reading >>

Insulin Resistance

Insulin Resistance

What medical conditions are associated with insulin resistance? While the metabolic syndrome links insulin resistance with abdominal obesity, elevated cholesterol, and high blood pressure; several other medical other conditions are specifically associated with insulin resistance. Insulin resistance may contribute to the following conditions: Type 2 Diabetes: Overt diabetes may be the first sign insulin resistance is present. Insulin resistance can be noted long before type 2 diabetes develops. Individuals reluctant or unable to see a health-care professional often seek medical attention when they have already developed type 2 diabetes and insulin resistance. Fatty liver: Fatty liver is strongly associated with insulin resistance. Accumulation of fat in the liver is a manifestation of the disordered control of lipids that occurs with insulin resistance. Fatty liver associated with insulin resistance may be mild or severe. Newer evidence suggests fatty liver may even lead to cirrhosis of the liver and, possibly, liver cancer. Arteriosclerosis: Arteriosclerosis (also known as atherosclerosis) is a process of progressive thickening and hardening of the walls of medium-sized and large arteries. Arteriosclerosis is responsible for: Other risk factors for arteriosclerosis include: High levels of "bad" (LDL) cholesterol Diabetes mellitus from any cause Family history of arteriosclerosis Skin Lesions: Skin lesions include increased skin tags and a condition called acanthosis nigerians (AN). Acanthosis nigricans is a darkening and thickening of the skin, especially in folds such as the neck, under the arms, and in the groin. This condition is directly related to the insulin resistance, though the exact mechanism is not clear. Acanthosis nigricans is a cosmetic condition strongly Continue reading >>

Effects Of Metformin On Insulin Secretion, Insulin Action, And Ovarian Steroidogenesis In Women With Polycystic Ovary Syndrome

Effects Of Metformin On Insulin Secretion, Insulin Action, And Ovarian Steroidogenesis In Women With Polycystic Ovary Syndrome

Hyperinsulinemia contributes to the ovarian androgen overproduction and glucose intolerance of polycystic ovary syndrome (PCOS). We sought to determine whether metformin would reduce insulin levels in obese, nondiabetic women with PCOS during a period of weight maintenance and thus attenuate the ovarian steroidogenic response to the GnRH agonist leuprolide. All subjects (n = 14) had an oral glucose tolerance test, a GnRH agonist (leuprolide) test, a frequently sampled iv glucose tolerance test, graded and oscillatory glucose infusions, and a dual energy x-ray absorptiometry scan before and after treatment with metformin (850 mg, orally, three times daily for 12 weeks). With weight maintenance (body mass index: pretreatment, 39.0 7.7 kg/m2; posttreatment, 39.1 7.9 kg/m2), oral glucose tolerance, insulin sensitivity (Si; 0.87 0.82 vs. 0.74 0.63 105 min1/pmolL), and the relationship between Si and first phase insulin secretion (AIRg vs. Si) were not improved by metformin. The insulin secretory response to glucose, administered in both graded and oscillatory fashions, was likewise unaltered in response to metformin. Free testosterone levels remained about 2-fold elevated (pretreatment, 26.6 12.7 pg/mL; posttreatment, 22.4 9.8 pg/mL). Both basal and stimulated LH and FSH levels were unaffected by metformin. The mean responses to leuprolide of 17-hydroxyprogesterone (pretreatment, 387 158 ng/dL; posttreatment, 329 116 ng/dL) as well as those of the other ovarian secretory products (androstenedione, dehydroepiandrosterone, progesterone, and estradiol) were not attenuated by metformin. We conclude that hyperinsulinemia and androgen excess in obese nondiabetic women with PCOS are not improved by the administration of metformin. HYPERINSULINEMIA appears to play a key pathogeneti Continue reading >>

Reducing Insulin Resistance With Metformin: The Evidence Today.

Reducing Insulin Resistance With Metformin: The Evidence Today.

Abstract Insulin resistance, defined as the inability of insulin to exert a normal biological action at the level of its target tissues, is one of the principal pathogenetic defects of type 2 diabetes. Metformin, the most widely-prescribed insulin-sensitizing agent in current clinical use, improves blood glucose control mainly by improving insulin-mediated suppression of hepatic glucose production, and by enhancing insulin-stimulated glucose disposal in skeletal muscle. Experimental studies show that metformin-mediated improvements in insulin sensitivity may be associated with several mechanisms, including increased insulin receptor tyrosine kinase activity, enhanced glycogen synthesis, and an increase in the recruitment and activity of GLUT4 glucose transporters. In adipose tissue, metformin promotes the re-esterification of free fatty acids and inhibits lipolysis, which may indirectly improve insulin sensitivity through reduced lipotoxicity. The improved glycaemia with metformin is not associated with increased circulating levels of insulin, and the risk of hypoglycaemia with metformin is minimal. The therapeutic profile of metformin supports its use for the control of blood glucose, in diabetic patients and for the prevention of diabetes in subjects with impaired glucose tolerance. Moreover, the improvement by metformin of cardiovascular risk factors associated with the dysmetabolic syndrome may account for the significant improvements in macrovascular outcomes observed in the UK Prospective Diabetes Study. Continue reading >>

Insulin Resistance And The Use Of Metformin: Effects On Body Weight

Insulin Resistance And The Use Of Metformin: Effects On Body Weight

by Ruchi Mathur, MD, FRCPC Dr. Mathur is Assistant Professor of Medicine, Cedars Sinai Medical Center, University of California, Los Angeles, California. Bariatric Times. 2011;8(1):10–12 Abstract Metformin is a widely perscribed drug for the treatment of diabetes and is often used off label for the treatment of prediabetes and insulin resistance. In addition to its primary use, metformin has often been cited as having weight loss benefits. This article reviews the concept of insulin resistance as it pertains to body weight and the effects of meformin on body weight in subgroups of patients with and without diabetes. Introduction Insulin is an anabolic storage hormone produced by the beta cells in both a basal and a pulsatile fashion in response to food intake. Insulin is fundamental in allowing cells to uptake and use glucose. Insulin also regulates gluconeogenesis along with processes, such as protein synthesis and lipogenesis. When we were evolving, the theory is that insulin was necessary because we lived a life of feast and famine. Those who could store calories had a survival benefit, thus insulin had a significant evolutionary role. So, where and when did insulin become a bad thing? Likely, at the same time our evolutionary environment took a bit of a turn. These days, it is usual to go three hours without eating, and certainly not three days! Thus, what was once adaptive is now maladaptive as we continue to store as our ancestors did. Our environment has changed faster than our genetics. Insulin resistance is an impaired response to endogenous or exogenous insulin in cells, tissues (especially skeletal muscle and adipose tissue), the liver, or the whole body.[1,2] Many investigators believe that insulin resistance is an important factor in the development of th Continue reading >>

Metformin Alone Or Combined With Insulin Does Not Improve Or Preserve Beta-cell Function In Youth With Impaired Glucose Tolerance Or Newly Diagnosed Type 2 Diabetes

Metformin Alone Or Combined With Insulin Does Not Improve Or Preserve Beta-cell Function In Youth With Impaired Glucose Tolerance Or Newly Diagnosed Type 2 Diabetes

Metformin Alone or Combined with Insulin Does Not Improve or Preserve Beta-Cell Function in Youth with Impaired Glucose Tolerance or Newly Diagnosed Type 2 Diabetes Restoring Insulin Secretion (RISE) Pediatric Medication Study shows that youth have markedly reduced insulin sensitivity and respond differently to medications According to recent research, the insulin resistance and pancreatic beta-cell (-cell) dysfunction associated with type 2 diabetes (T2D) was unresponsive to treatment with metformin alone or metformin combined with insulin glargine in youth with impaired glucose tolerance (IGT), which is an element of prediabetes, or early T2D. Additionally, youth with IGT and T2D, compared to adults, are more insulin resistant, and thus their insulin is less effective in lowering blood glucose levels in their bodies. These findings from the Restoring Insulin Secretion (RISE) programs Pediatric Medication Study were presented today at the American Diabetes Associations (ADAs) 78th Scientific Sessions at the Orange County Convention Center. T2D is increasing in prevalence in youth and adults in the U.S., and increases the risk of early morbidity and mortality, as well as long-term complications. T2D and its precursor, prediabetes, are characterized by insulin resistance and beta-cell dysfunction in youth and adults, and prediabetes includes IGT. However, research has suggested that T2D in youth might represent a more severe and rapidly progressive condition than in adults. Given the increased recognition of the critical role of pancreatic -cell function (-cells store and release insulin in the body) in the pathogenesis of T2D, research efforts have begun to focus on prevention of the loss of insulin secretion among individuals at high risk for T2D or in early stages of Continue reading >>

Metformin And Insulin Resistance

Metformin And Insulin Resistance

About a year ago, my endocrinologist determined that I was exhibiting signs of insulin resistance. In short, my body requires more than the average amount of insulin to cover carbohydrate. She suggested that I start taking metformin, noting that it would do two things for me: It would decrease the amount of insulin I need to take and it would help curb my appetite, thus resulting in weight loss. When I first got on it, I thought it was great. My blood sugar levels improved, my appetite was in fact curbed, and all seemed wonderful — until I stopped taking my metformin. As a high school senior, I had atrocious sleeping habits! That, coupled with the fact that taking metformin was really killing my appetite, was causing me to become exhausted and get some pretty severe headaches. Looking back on it now, it’s very clear that the metformin wasn’t the problem, it was me. However, as a stubborn senior in high school, I was determined to maintain my sleeping habits, as I deemed them completely normal and in accordance with the typical behavior exhibited by my peers (boy, how I’ve changed…). So, I stopped the metformin. The last three weeks or so, I’ve been back on metformin regularly. I decided to start it up again after my last appointment with my CDE. Thus far, it’s really been working wonders and my blood sugars have decreased substantially! Where my 30-day average was hovering around 190 just a few weeks ago, it has now dropped to 137! I was seriously shocked when I saw how much my average fell. For the most part, my blood sugar levels are in range, but I have had my fair share of lows as well. Managing metformin really is a science that can change on a daily basis depending on my activity level. For example, the first two weeks that I was back on metformin, I Continue reading >>

Ask The Experts - How Does Metformin Affect Insulin Resistance?

Ask The Experts - How Does Metformin Affect Insulin Resistance?

How Does Metformin Affect Insulin Resistance? What is the role of metformin in managing insulin resistance and obesity in people with diabetes? How does metformin affect the obese nondiabetic patient? Response from Mary Anne Dumas, PhD, RN, CFNP, FAANP In order to understand the role of metformin in insulin resistance and obesity, it is essential to understand the pathophysiology of both clinical problems and the pharmacologic mechanisms of metformin. Insulin resistance occurs when there is an impairment of insulin transport at either the prereceptor, receptor, or postreceptor sites. Insulin resistance occurs in obese individuals, usually at the postreceptor site, where there is an apparent failure to activate the postreceptor tyrosine kinase.[ 1 ] (Type II diabetes reportedly is related to a postreceptor abnormality.[ 1 ]) Failure of the cellular transport of insulin results in hyperglycemia, requiring greater amounts of insulin to maintain euglycemia (normal level of sugar in the blood). Euglycemia may be maintained for a long period by hyperinsulinemia; however, insulin levels are not able to sustain control glucose levels, and hyperglycemia results.[ 1 , 2 ] Metformin is a biguanide (a hypoglycemia-inducing drug) that has been demonstrated to decrease hepatic glucose production and improve peripheral insulin sensitivity. Metformin benefits individuals with diabetes by: Reducing lipid levels (eg, triglycerides); Facilitating postreceptor transport of insulin; and Continue reading >>

Metformin And Pregnancy: Is This Drug Safe?

Metformin And Pregnancy: Is This Drug Safe?

Whether you're expecting your first child or expanding your family, a safe and healthy pregnancy is crucial. This is why you take precautions before and during pregnancy to keep your unborn child healthy and reduce the risk of birth defects. In every pregnancy, there’s a 3 to 5 percent risk of having a baby with a birth defect, according to the Organization of Teratology Information Specialist (OTIS). Some birth defects can’t be prevented. But you can lower your child’s risk by taking prenatal vitamins, maintaining a healthy weight, and maintaining a healthy lifestyle. Your doctor might recommend that you don’t take certain medications while pregnant. This is because certain medications can cause birth defects. If you're taking the prescription drug metformin, you might have concerns about how the drug will affect your pregnancy and the health of your unborn child. What Is Metformin? Metformin is an oral medication used to treat type 2 diabetes and polycystic ovary syndrome (PCOS). Type 2 diabetes is a condition that increases blood sugar levels. PCOS is an endocrine disorder that occurs in women of reproductive age. It’s important to maintain a healthy blood sugar level while pregnant. This is one way to reduce the risk of birth defects and complications. Although metformin can control blood sugar, you may question whether this drug is safe to take during pregnancy. Before we get into this, let’s discuss how metformin is beneficial prior to pregnancy. Metformin Before Conception If you took metformin before getting pregnant, you might know that this drug can be a godsend — especially if you’ve had difficulty conceiving. Having PCOS makes it harder to become pregnant. This condition can cause missed or irregular periods, and small cysts can grow on your Continue reading >>

Reducing Insulin Resistance With Metformin: The Evidence Today

Reducing Insulin Resistance With Metformin: The Evidence Today

Tirés à part : S Del Prato Keywords: Insulin resistance , Type 2 diabetes , Metabolic syndrome , Cardiovascular risk factors Although overt hyperglycaemia does not develop until ?-cell failure develops, insulin resistance is a main feature of type 2 diabetes. The term insulin resistance identifies the inability of insulin to exert a normal biological action at the level of its target tissues. Though insulin exerts a variety of effects, in the current clinical use, insulin resistance refers to the inability of circulating insulin to promote glucose utilisation in the skeletal muscle and adipose tissue, and to properly suppress endogenous glucose production (mainly in the liver). As such insulin resistance not only characterises type 2 diabetes [1]but it is very common in pre-diabetic patients [2]as well as in individuals with central obesity, dyslipidaemia, hypertension, endothelial dysfunction, hyperuricemia, and microalbuminuria [3]. Moreover, insulin resistance is considered central to the metabolic syndrome [4], while more recent epidemiological studies have indicated that insulin resistance may be an independent risk factor for cardiovascular mortality both in the general [5]and diabetic [6]population. Therefore, the comprehension of the mechanisms responsible for impaired insulin action is fundamental in the attempt to ameliorate insulin resistance and to account for the favourable effects of insulin sensitisers. Among these compounds, metformin has the largest clinical use. Employed for almost 50 years in Europe, it has been more recently introduced in the United States. The drug exerts an antihyperglycaemic effect, with minimal risk of hypoglycaemia. The initial observation that metformin reduces plasma glucose levels without increasing, and sometime decreasing Continue reading >>

New Information On How Metformin Works

New Information On How Metformin Works

Not only has new research told us how metformin really works, but a new biomarker was found that can determine the optimal dose of metformin that should be used to get the best results for each patient. Research from the Johns Hopkins Children’s Center reveals that the drug most commonly used in Type 2 diabetics who don’t need insulin works on a much more basic level than once thought, treating persistently elevated blood sugar — the hallmark of Type 2 diabetes — by regulating the genes that control its production. investigators say they have zeroed in on a specific segment of a protein called CBP made by the genetic switches involved in overproduction of glucose by the liver that could present new targets for drug therapy of the disease. In healthy people, the liver produces glucose during fasting to maintain normal levels of cell energy production. After people eat, the pancreas releases insulin, the hormone responsible for glucose absorption. Once insulin is released, the liver should turn down or turn off its glucose production, but in people with Type 2 diabetes, the liver fails to sense insulin and continues to make glucose. The condition, known as insulin resistance, is caused by a glitch in the communication between liver and pancreas. Metformin, introduced as frontline therapy for uncomplicated Type 2 diabetes in the 1950s, up until now was believed to work by making the liver more sensitive to insulin. The Hopkins study shows, however, that metformin bypasses the stumbling block in communication and works directly in the liver cells. Senior investigator, Fred Wondisford, M.D., who heads the metabolism division at Hopkins Children’s, tells us that, "Rather than an interpreter of insulin-liver communication, metformin takes over as the messenger itself Continue reading >>

Pcos: Insulin And Metformin

Pcos: Insulin And Metformin

Young women with PCOS often have elevated insulin levels and are more likely to develop diabetes. Metformin is a medication often prescribed for women with PCOS to help prevent diabetes. A lifestyle that includes healthy nutrition and daily exercise is the most important part of a PCOS treatment plan. What is insulin? Insulin is a hormone made by an organ in the body called the pancreas. The food you eat is broken down into simple sugar (glucose) during digestion. Glucose is absorbed into the blood after you eat. Insulin helps glucose enter the cells of the body to be used as energy. If there’s not enough insulin in the body, or if the body can’t use the insulin, sugar levels in the blood become higher. What is insulin resistance? If your body is resistant to insulin, it means you need high levels of insulin to keep your blood sugar normal. Certain medical conditions such as being overweight or having PCOS can cause insulin resistance. Insulin resistance tends to run in families. What can insulin resistance do to me? High insulin levels can cause thickening and darkening of the skin (acanthosis nigricans) on the back of the neck, axilla (under the arms), and groin area. In young women with PCOS, high insulin levels can cause the ovaries to make more androgen hormones such as testosterone. This can cause increased body hair, acne, and irregular or few periods. Having insulin resistance can increase your risk of developing diabetes. How can I lower my insulin levels? You can help lower your insulin levels naturally by eating fewer starches and sugars, and more foods that are high in fiber and low in refined carbohydrates. Low glycemic foods, on the other hand, don’t raise your blood sugar or insulin levels as much as foods that are high in sugar or refined carbohydr Continue reading >>

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