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Insulin And Leptin Relationship

Insulin, Leptin, And Blood Sugar – Why Diabetic Medication Fails

Insulin, Leptin, And Blood Sugar – Why Diabetic Medication Fails

This Week's Health Podcast > Type 2 diabetes is a difficult metabolic problem. It is a national embarrassment that so many of our young people are becoming type 2 diabetic. It is a national disgrace that millions of type 2 diabetic patients are being injured with commonly used diabetic medications that are known to make their metabolic situation worse. An overwhelming body of science demonstrates that insulin resistance leads to obesity and vice versa. Once this problem sets in, a person is on a path of ever worsening metabolic control as diabetes related issues, cholesterol problems, and heart disease risk factors pile up. If nothing is done, very poor health, and early death are certain. The Big Pharma blood sugar remedies, however, turn out to be really bad for health – they actually complicate rather than improve the patient's health. Even when the drugs aren't directly damaging in a major way, they fail to address the actual reasons for diabetes and typically have the net result of making the factors that cause diabetes worse. I know that may seem hard to believe, but it is true, and I will explain it shortly. On December 17, 2008 the New England Journal of Medicine1 put the nail in the coffin on another dismal year for the theory of drugs to treat disease, reporting that aggressive use of blood sugar lowering medication to prevent heart disease was a complete failure. Its not that lowering blood sugar in this patient population didn't do anything; it made the patients heavier and more hypoglycemic. This newer study followed equally dismal results from the ACCORD trial (Action to Control Cardiovascular Risk in Diabetes), which earlier in 2008 found a 22 percent increased rate of death in diabetic patients who were aggressively treated with medications. Some of th Continue reading >>

How Does Insulin Affect Leptin?

How Does Insulin Affect Leptin?

Leptin is a hormone produced by your fat cells. Measuring how much leptin is in your body tells your brain, specifically the hypothalamus, if enough fat is currently stored. From this, your hypothalamus is able to regulate how hungry you feel, whether or not you need to conserve energy/fat, and even if you should feel satisfied. It’s an important part of our body’s natural tendency towards healthy eating and energy levels. Insulin has two primary jobs: transferring energy (in the form of glucose) to our cells and storing excess energy as fat. When we become insulin resistant or don’t use insulin efficiently, our bodies are forced to create extra insulin to compensate. With too much insulin in your bloodstream, the hypothalamus is unable to gauge leptin levels properly, creating a range of problems: Your body makes more fat: Because your brain can’t detect the leptin as well, it assumes you don’t have enough, i.e., you need to eat more, particularly more sugar and more fat. Your body gets locked into a sort of loop in which it wants to take in more food and expend less energy (do less), so as a result it makes more fat instead. You crave unhealthy food: When we are low on specific nutrients, our brains create a hunger for certain foods, a behavior often seen in the seemingly random cravings of pregnant women. It’s generally a great way to regulate our diets and maintain a healthy variety. However, when your brain falsely thinks you are low on sugar and fat, you end up feeling hungry for exactly the kinds of foods you should be avoiding! You don’t feel satisfied: Eating and other activities beneficial to the body, like sex, result in the release of reward chemicals (dopamine) that make us feel good and help us associate pleasure with activities. When you’r Continue reading >>

Leptin Therapy, Insulin Sensitivity, And Glucose Homeostasis

Leptin Therapy, Insulin Sensitivity, And Glucose Homeostasis

Leptin therapy, insulin sensitivity, and glucose homeostasis Department of Translational Medicine, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia Department of Translational Medicine, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia Department of Translational Medicine, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia Department of Translational Medicine, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia Department of Translational Medicine, The John Curtin School of Medical Research, The Australian National University, Canberra, Australia Corresponding Author: Dr. Gilberto Paz-Filho, The John Curtin School of Medical Research, The Australian National University, Garran Rd, Building 131, Acton ACT, 0200, Australia. E-mail: [email protected] Author information Copyright and License information Disclaimer Copyright : Indian Journal of Endocrinology and Metabolism This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. This article has been cited by other articles in PMC. Glucose homeostasis is closely regulated not only by insulin, but also by leptin. Both hormones act centrally, regulating food intake and adiposity in humans. Leptin has several effects on the glucose-insulin homeostasis, some of which are independent of body weight and adiposity. Those effects of leptin are determined centrally in the hypothalamus and peripherally in the pancreas, muscles and Continue reading >>

Leptin And Diabetes Are You Leptin Resistant?

Leptin And Diabetes Are You Leptin Resistant?

Leptin and Diabetes Are You Leptin Resistant? We know insulin resistance contributes to Type 2 diabetes. But resistance to another hormone called leptin also contributes big time. Fortunately, we may be able to turn down both kinds of resistance. Leptin helps regulate body fat, in part by telling the brain what level of fat is in the body and how that level is changing. When fat stores are sufficient, it lets the brain know, Were full. We have enough food now. So stop eating. Some Indian scientists put it in more technical terms : The net action of leptin is to inhibit appetite, stimulate thermogenesis [heat production], [burn up fatty acids], decrease glucose, and reduce body weight and fat. Those are good things for most of us. We want that. But many people, especially fat people, are leptin resistant. Talking to the UK newspaper Daily Mail, anti-sugar crusader Robert Lustig, MD, said, This means thebrainno longer reads the signals saying the body is full, but instead assumes it is starving no matter how much food you continue to eat. So leptin resistance (LR) contributes to fatness in much the same way that insulin resistance (IR) contributes to Type 2 diabetes. In fact, the two frequently go together. Not always as we know, most fat people dont have diabetes, and many people with Type 2 are thin. But a huge number of people have both types of resistance, which is why fat people are more likely to get diabetes, and diabetes gets wrongly blamed on fat. In fact, Dr. Lustig believes insulin resistance triggers LR . Insulin blocks leptins fullness signals in the brain. His studies have found that lowering insulin levels stops cravings and helps people get control of their food consumption, presumably because leptin is working again. Scientists used to think increasing l Continue reading >>

Clinical Scientist Sets The Record Straight On Hazards Of Sugar

Clinical Scientist Sets The Record Straight On Hazards Of Sugar

The conventional wisdom is that people are eating too much and exercising too little. However, groundbreaking research suggests obesity is primarily related to a high-sugar diet In order for you to significantly gain weight, you must first become leptin resistant. Leptin resistance blocks the sensation of being full, making you eat more than you need. Energy metabolism also falls, due to a reduction inimpairs your body’s ability to oxidize fat, causing a low-energy state Sugar, and fructose in particular, is exceptionally effective at causing leptin resistance in animals, and it’s very effective at blocking the burning of fat Fructose stimulates weight gain through its effects on your appetite and by blocking the burning of fat. It also changes your body composition to increase body fat even when you are on a caloric restriction If you are insulin or leptin resistant, it would be prudent for you to restrict your fructose consumption to about 15 to 25 grams of fructose per day from all sources By Dr. Mercola Dr. Richard Johnson is the head of nephrology at the University of Colorado and is actively engaged in clinical research. Over the past 25 years, much of his research (which is funded by the National Institutes of Health) has focused on fructose and obesity-related diseases. Not only has he published some 500 papers in the peer-reviewed literature, he’s also authored books along the way. His latest book, The Fat Switch, is a really intriguing book that shatters many of our age-old myths about diet and weight loss. His hypothesis is that, rather than being driven by eating too many calories and lack of exercise, obesity is primarily driven by eating too much refined sugar, particularly fructose. According to Dr. Johnson: “The conventional wisdom is that people Continue reading >>

Secrets You Need To Know About Insulin, Cortisol & Leptin To Get And Stay Lean

Secrets You Need To Know About Insulin, Cortisol & Leptin To Get And Stay Lean

We really don’t want to change careers and become endocrinologists, and I’m guessing that you don’t, either. But when we began researching the role that hormones play in not only losing but gaining body fat, we couldn’t wait to share it with you. The latest research is clear: It’s not only our diet and strength training that helps us manage our weight, but our levels of certain hormones — specifically insulin, cortisol and leptin — that can make or break our ability to get lean and stay lean. By simply educating yourself about how to eat so that you consciously optimize the levels of three hormones, you can easily take control of a hidden hormonal powerhouse right inside your own body. Here’s the skinny on the big three that you really need to know: Insulin What is it, exactly? This amazing hormone does a lot for you, but the simplest explanation is that it’s released from your pancreas in response to blood sugar levels to help you store nutrients from the foods that you eat. High Levels of Insulin = High Levels of Fat Storage Want to gain a lot of body fat? Then you’ll want to keep your insulin levels high all day long. Wondering how you would accomplish this? Easy. Just eat lots of food that turns into sugar the second it hits your mouth. Aren’t sure what these foods are? Think highly processed foods like cereals, cakes, Dunkin’ Donuts and most white carbohydrates, like rice or potatoes. When you reach for these foods, your blood sugar levels skyrocket and as a response, your poor pancreas lets loose a volume of insulin. Your body is now primed to store that food as pure body fat. Lower Levels of Insulin = The Ability to Lose Body Fat Want to lose body fat? Your body can’t burn body fat if your insulin levels are too high. You can train twice Continue reading >>

The Hormones Of Fat: Leptin And Insulin

The Hormones Of Fat: Leptin And Insulin

Hormones tell your body whether to burn fat and lose weight or to store fat and gain weight or to find balance and weight maintenance in between. When it comes to your body “deciding” what state to be in, there are two key hormones that regulate food intake and energy balance: the adipocyte hormone leptin and the pancreatic hormone insulin. While there are many other hormone players with complex interactions between them, understanding these two hormones (which you could think of as the hormones of fat) will give you important insight into how the diet and lifestyle choices you make can help you achieve and maintain a healthy weight. The hormone insulin, which is released by the pancreas in response to increased blood sugar, facilitates the transport of glucose into the cells of your body and signals to the liver to convert glucose into glycogen for storage. When glycogen stores are maxed out, increased insulin levels stimulate conversion of glucose into triglycerides (fat) for long-term storage in adipocytes (fat cells) 1. But beyond this important action for the metabolism of fuels, insulin has an additional role as an adiposity signal to the brain, i.e., it tells the brain whether or not you should eat and informs the brain about the energy status of your body. The AIP Lecture Series is a 6-week video-based, self-directed online course that will teach you the scientific foundation for the diet and lifestyle tenets of the Autoimmune Protocol. The major stimulant of insulin secretion is an increase of blood glucose levels, as detected by the pancreas (blood glucose levels go up when you eat carbohydrates). Circulating insulin enters the brain (proportionally to the amount that is circulating in the blood) where it binds to receptors in the hypothalamus region of th Continue reading >>

Original Article Relationships Between Changes In Leptin And Insulin Resistance Levels In Obese Individuals Following Weight Loss

Original Article Relationships Between Changes In Leptin And Insulin Resistance Levels In Obese Individuals Following Weight Loss

Abstract Obesity can augment insulin resistance (IR), leading to increased risk of diabetes and heart disease. Leptin, ghrelin, and various fatty acids present in the cell membrane may modulate IR. In this study, we aimed to investigate the impact of weight loss on IR, serum leptin/ghrelin levels, and erythrocyte fatty acids, and studied the associations between changes in these variables. A total of 35 obese (body mass index ≥ 27) adults participated in a weight loss program for 3 months. IR was assessed using homeostasis model assessment for insulin resistance (HOMA-IR). The obese participants had a mean weight loss of 5.6 ± 3.8 kg followed by a 16.7% and 23.3% reduction in HOMA-IR and leptin (p < 0.001) levels, and an 11.3% increase in ghrelin levels (p = 0.005). The level of erythrocyte saturates decreased by 2.8%, while the level of n–3 polyunsaturates increased by 16.8% (all p < 0.05). The changes in leptin levels (−5.63 vs. −1.57 ng/mL) were significantly different (p = 0.004) in those with improved IR (changes in HOMA-IR < 0) than those without improvement (changes in HOMA-IR ≥ 0), though there were no differences in the changes of ghrelin (p = 0.120) and erythrocyte fatty acids (all p > 0.05) levels. After adjusting for age, gender, changes in ghrelin, and body fat, we found a significant correlation between decreases in leptin and less risk of no improvement in HOMA-IR levels [odds ratio (OR) = 0.69, p = 0.039]. In conclusion, a moderate weight reduction in obese participants over a short period significantly improved IR. This weight reduction concomitantly decreased serum leptin, increased ghrelin, and elevated some erythrocyte unsaturates. Only leptin correlated independently with IR improvement upon multivariable logistic regression analysis, whi Continue reading >>

Drop In Both Insulin And Leptin Needed For Fat Burning To Occur

Drop In Both Insulin And Leptin Needed For Fat Burning To Occur

Drop in both insulin and leptin needed for fat burning to occur Drop in both insulin and leptin needed for fat burning to occur Ketogenic diet improves metabolic syndrome in multiple ways 18 December 2017 Researchers have found that metabolism moves from using glucose to burning fat when there is a drop in both insulin and leptin levels. The study has been led by Gerald I. Shulman, professor of medicine, cellular and molecular physiology, and physiological chemistry at Yale University. The research could point towards improved understanding of how best to lose weight which could benefit many people with diabetes. Prior to the study, it was known that mammals can switch from burning carbohydrates , like glucose, for energy towards burning fat instead. This allows mammals to get energy without breaking down muscle mass. It was thought that a decrease in insulin levels is all that was needed to help the switch to burning fat occur. However, the new research has identified that a reduction in leptin levels is also needed. Insulin and leptin are both hormones. Insulin works to decrease blood sugar levels by moving glucose out of the blood and into neighbouring cells where it can be used directly as fuel or stored as body fat. A higher level of insulin also prevents fat from being broken down for energy. Leptin is a hormone which is linked to appetite and plays a key role in energy regulation. In their study, the researchers from Yale investigated the rate of carbohydrate and fat metabolism as rats went from a fed to a fasted state. The researchers observed that as the rats fasted, leptin levels decreased and activated a pathway that led to fat burning rather than carbohydrate burning. During fasting, the rats' use of stored glucose went down and sugar levels decreased as a Continue reading >>

Insulin-stimulated Increase In Serum Leptin Levels Precedes And Correlates With Weight Gain During Insulin Therapy In Type 2 Diabetes

Insulin-stimulated Increase In Serum Leptin Levels Precedes And Correlates With Weight Gain During Insulin Therapy In Type 2 Diabetes

The Journal of Clinical Endocrinology & Metabolism Insulin-Stimulated Increase in Serum Leptin Levels Precedes and Correlates with Weight Gain during Insulin Therapy in Type 2 Diabetes Departments of Nutrition and Dietetics (A.-M.A.) Aker University Hospital, 0514 Oslo, Norway University of Oslo, Faculty Division Aker (A.-M.A., K.F.H., J.P.B., P.M.T., K.I.B.), Aker University Hospital, 0514 Oslo, Norway Address all correspondence and requests for reprints to: Anne-Marie Aas, Department of Nutrition and Dietetics, Aker University Hospital, Trondheimsveien 235, 0514 Oslo, Norway. Search for other works by this author on: Endocrinology (K.F.H., J.P.B., P.M.T., K.I.B.) Aker University Hospital, 0514 Oslo, Norway University of Oslo, Faculty Division Aker (A.-M.A., K.F.H., J.P.B., P.M.T., K.I.B.), Aker University Hospital, 0514 Oslo, Norway Search for other works by this author on: Endocrinology (K.F.H., J.P.B., P.M.T., K.I.B.) Aker University Hospital, 0514 Oslo, Norway University of Oslo, Faculty Division Aker (A.-M.A., K.F.H., J.P.B., P.M.T., K.I.B.), Aker University Hospital, 0514 Oslo, Norway Search for other works by this author on: Endocrinology (K.F.H., J.P.B., P.M.T., K.I.B.) Aker University Hospital, 0514 Oslo, Norway University of Oslo, Faculty Division Aker (A.-M.A., K.F.H., J.P.B., P.M.T., K.I.B.), Aker University Hospital, 0514 Oslo, Norway Search for other works by this author on: Endocrinology (K.F.H., J.P.B., P.M.T., K.I.B.) Aker University Hospital, 0514 Oslo, Norway University of Oslo, Faculty Division Aker (A.-M.A., K.F.H., J.P.B., P.M.T., K.I.B.), Aker University Hospital, 0514 Oslo, Norway Search for other works by this author on: The Journal of Clinical Endocrinology & Metabolism, Volume 94, Issue 8, 1 August 2009, Pages 29002906, Anne-Marie Aas, Krist Continue reading >>

Leptin Resistance & Insulin Resistance -hormones Making You Fat

Leptin Resistance & Insulin Resistance -hormones Making You Fat

Is Leptin Resistance the new Insulin Resistance? How Hormones Are Making You Fat The topic of discussion today is resistance! Vive la resistance! Okay, so maybe not that kind of resistance, but rather the body resistance to certain hormones. Most of us have heard about insulin resistance but what about its sister-hormone, leptin resistance? Both are driven by sugar intake, and both are linked to weight gain and loss. Lets take a closer look. Insulin is produced by the pancreas beta cells and is the key to unlocking our cells to let glucose (aka. sugar or carbohydrates we eat) in so they give us energy to do things. In healthy people, insulin is tightly regulated via feedback loops, but can be out of whack as is in the case of diabetes. Leptin is known as the satiety hormone (meaning, its released when weve had enough to eat) but it has been consistently linked to obesity . For years, science has perhaps oversimplified the weight loss equation to a simple caloric deficit equation, but we now know that the regulatory mechanisms are not well understood. Instead of obesity seen as the bodys lack of weight regulation (resulting in extreme overweight), it may be more appropriate to view obesity as a defense of an elevated body weight. In other words, our body tends to protect its preferred weight . (To be) Obese or not obese, that is the question! [ATTENTION Fat Shamers] Please take note that research suggests that gaining weight is way more than just a lack of will power (find out why fat shaming doesnt work here ). You may want to stop reading if you refuse to let your current views on fatness get challenged. Keep reading to find out why! There are various factors that influence obesity. Simply saying theyre too fat because they eat too much is a) super rude and b) quite m Continue reading >>

Appetite Control: Understanding Your Hunger Hormones

Appetite Control: Understanding Your Hunger Hormones

Imagine you are out to dinner with a friend and the bread arrives at your table. You are not very hungry, but you think, “l’ll just have one little piece.” A few minutes later, you realize you have eaten three slices before your meal even arrives. What’s going on here? Even though you are not physically hungry, your body gave you the signal to eat. That’s the work of three hormones in your body that control hunger — insulin, ghrelin and leptin. They are important because the way these balance can impact your weight and health. Insulin Insulin is made in the pancreas and allows cells to take sugar or glucose from the blood stream to use as energy. Approximately one-third of the population inherits a resistance to respond properly to insulin, which prompts the pancreas to secrete more insulin if you eat a meal high in refined or “simple” carbohydrates such as white pasta or white bread. When the insulin does not respond normally — allowing sugars to enter the cells of the body — you can experience insulin resistant hunger. Rather than being physically hungry, you might experience it as a “gnawing” desire to eat. If you consume meals high in refined carbohydrates on a regular basis, that are not balanced with respect to protein and good fat, you may continually crave carbohydrates. “Just One...” Think back to the restaurant example with the bread, or perhaps a recent party where you have helped yourself to a few chips, only to find that you ate a good portion of the bowl. Again, even though you were not physically hungry, your body gave you the signal to eat. In these situations, you know what you are “supposed” to be eating, but your body continues to give you the signal to eat more carbohydrates. Running on Empty The more refined carbohydr Continue reading >>

Role Of Ghrelin, Leptin And Insulin Resistance In Development Of Metabolic Syndrome In Obese Patients

Role Of Ghrelin, Leptin And Insulin Resistance In Development Of Metabolic Syndrome In Obese Patients

1Department of Internal Medicine, Faculty of Medicine, Taif University and Tanta University, Egypt 2Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz and Tanta University, Egypt 3Department of Clinical Pathology, Faculty of Medicine, Azhar University, Egypt Citation: Mohamed WS, Hassanien MA, Sayed Abokhosheim KEL (2014) Role of Ghrelin, Leptin and Insulin Resistance in Development of Metabolic Syndrome in Obese Patients. Endocrinol Metab Synd 3:122. doi: Copyright: © 2014 Mohamed WS, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Visit for more related articles at Endocrinology & Metabolic Syndrome Abstract Objective: Obesity and its complications including metabolic syndrome (MetS) have been increased in children and adolescents recently. Leptin is known to play an important role in the pathogenesis of obesity. The objective of this study was to evaluate the relationship between Leptin, Ghrelin and Insulin resistance in the development of metabolic syndrome in obese persons. Methods: this study was carried out on fifty obese persons. All patients have BMI ≥ 30 Kg/m2. Twenty of them have metabolic syndrome. Body Mass Index (BMI), Waist Circumference (WC), and blood pressure were measured. Fasting Plasma Glucose (FBG), two hours Post Prandial Blood Glucose (PPBG), Glycated hamoglobin A1C (HbA1c), triglyceride (TG), Total Cholesterol (TC), high and low density lipoprotein cholesterol (HDL-C and LDL-C), serum Leptin, Ghrelin and Insulin were done. HOMA-IR and HOMA- β were calculated. Results: SBP, DBP, FBS, PPBG, HbA1c, HOMA-IR and HOMA-β were signific Continue reading >>

Relationship Between Leptin, Insulin, Body Composition And Liver Steatosis In Non-diabetic Moderate Drinkers With Normal Transaminase Levels

Relationship Between Leptin, Insulin, Body Composition And Liver Steatosis In Non-diabetic Moderate Drinkers With Normal Transaminase Levels

Objective: Obesity and insulin resistance play a major role in the development of liver steatosis (LS), but also relative leptin resistance has been reported to correlate with LS in humans. Our objective was to investigate the relationship between serum leptin, insulin, obesity and LS in non-diabetic males (n = 74) and postmenopausal females (n = 50) with normal transaminase levels and low-to-moderate alcohol intake. Methods: A medical history to retrieve information about health status, current medications, alcohol consumption and history of viral or toxic hepatitis; a physical examination including height, weight, waist circumference and blood pressure; a fasting blood draw for the determination of glucose, insulin, leptin, lipid profile, transaminases and uric acid; an oral glucose tolerance test to exclude type 2 diabetes; a dual-energy X-ray absorptiometry scan to assess fat mass (FM) and lean body mass (LBM), and an echography of the liver to assess LS. Results: Fasting leptin and insulin were highly correlated with FM in men (R = 0.767 and R = 0.495 respectively, P < 0.001) and women (R = 0.713 and R = 0.526 respectively, P < 0.001). After correction for FM, leptin showed a significant negative correlation with LBM in men (R = 0.240, P = 0.039), but not in women (R = 0.214, P = 0.132). The positive relationship observed between leptin, insulin and LS persisted after adjustment of leptin and insulin for body composition only in men (R = 0.415, P < 0.001 and R = 0.339, P = 0.003 respectively for leptin and insulin vs LS). Adjusted means (95% confidence intervals) of leptin increased significantly across categories of LS in men even when insulin was considered in the model (absent = 7.1 ng/ml (5.68.5), mild = 8.2 ng/ml (7.29.2), moderate/severe = 12.1 ng/ml (10.314 Continue reading >>

Frontiers | The Role Of Leptin In The Control Of Insulin-glucose Axis | Neuroscience

Frontiers | The Role Of Leptin In The Control Of Insulin-glucose Axis | Neuroscience

Front. Neurosci., 08 April 2013 | The role of leptin in the control of insulin-glucose axis Marie Amitani *, Akihiro Asakawa , Haruka Amitani and Akio Inui Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan Obesity and diabetes mellitus are great public health concerns throughout the world because of their increasing incidence and prevalence. Leptin, the adipocyte hormone, is well known for its role in the regulation of food intake and energy expenditure. In addition to the regulation of appetite and satiety that recently has attracted much attentions, insight has also been gained into the critical role of leptin in the control of the insulin-glucose axis, peripheral glucose and insulin responsiveness. Since the discovery of leptin, leptin has been taken for its therapeutic potential to obesity and diabetes. Recently, the therapeutic effects of central leptin gene therapy have been reported in insulin-deficient diabetes in obesity animal models such as ob/ob mise, diet-induced obese mice, and insulin-deficient type 1 diabetes mice, and also in patients with inactivating mutations in the leptin gene. Herein, we review the role of leptin in regulating feeding behavior and glucose metabolism and also the therapeutic potential of leptin in obesity and diabetes mellitus. Obesity and diabetes mellitus are important public health concerns throughout the world because of their increasing incidence and prevalence. The pooled prevalence of obesity is currently as high as 23.5%, and the general prevalence of diabetes among adults in the US is 6.3% ( Sullivan et al., 2005 ). Obese individuals have an increased risk of morbidity because of the various related disorders, including diabetes, cardiovascu Continue reading >>

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