
The Role Of Leptin/adiponectin Ratio In Metabolic Syndrome And Diabetes
The role of leptin/adiponectin ratio in metabolic syndrome and diabetes The role of leptin/adiponectin ratio in metabolic syndrome and diabetes Direccin de Investigaciones, Fundacin Oftalmolgica de Santander, FOSCAL, Floridablanca, Colombia Escuela de Medicina, Universidad de Santander, UDES, Bucaramanga, Colombia Direccin de Investigaciones, Fundacin Oftalmolgica de Santander, FOSCAL, Floridablanca, Colombia Escuela de Medicina, Universidad de Santander, UDES, Bucaramanga, Colombia Escuela de Medicina, Universidad Autonoma de Bucaramanga, UNAB, Bucaramanga, Colombia Escuela de Medicina, Universidad Autonoma de Bucaramanga, UNAB, Bucaramanga, Colombia Escuela de Medicina, Universidad Autonoma de Bucaramanga, UNAB, Bucaramanga, Colombia Escuela de Medicina, Universidad Autonoma de Bucaramanga, UNAB, Bucaramanga, Colombia Escuela de Medicina, Universidad Autonoma de Bucaramanga, UNAB, Bucaramanga, Colombia Published Online: 2013-12-13 | DOI: The metabolic syndrome comprises a cluster of cardiometabolic risk factors, with insulin resistance and adiposity as its central features. Identifying individuals with metabolic syndrome is important due to its association with an increased risk of coronary heart disease and type 2 diabetes mellitus. Attention has focused on the visceral adipose tissue production of cytokines (adipokines) in metabolic syndrome and type 2 diabetes mellitus, as the levels of the anti-inflammatory adipokine adiponectin are decreased, while proinflammatory cytokines are elevated, creating a proinflammatory state associated with insulin resistance and endothelial dysfunction. In this review, we will give special attention to the role of the leptin/adiponectin ratio. We have previously demonstrated that in individuals with severe coronary artery disease, a Continue reading >>
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Role Of Leptin Deficiency In Type 1 Diabetes
Home / Conditions / Type 1 Diabetes / Role of Leptin Deficiency in Type 1 Diabetes Role of Leptin Deficiency in Type 1 Diabetes A new study in rats shows that a lack of the hormone leptin triggers a cascade of neuroendocrine events that affects adipose tissue as well as the liver, resulting in hyperglycemia and ketoacidosis. Leptin is a hormone made by fat cells which regulates the amount of fat stored in the body. It does this by adjusting both the sensation of hunger and adjusting energy expenditures. Studies suggest that there is an inverse relationship between leptin levels and insulin secretion. It has also been suggested that the association between plasma leptin and diabetes may be a result of an underlying leptin resistance due to obesity. In leptin-deficient diabetic rats, systemic administration of leptin rapidly reversed ketoacidosis and normalized blood glucose levels by decreasing the delivery of glycerol and fatty acids to the liver. The effect of leptin occurred via decreased hypothalamic pituitary adrenal (HPA) axis activity. In other words, less ACTH was released from the pituitary gland, which results in less corticosterone (the equivalent of human cortisol) secretion from the adrenal gland and less corticosterone induced lipolysis of adipose tissue triglycerides. In addition, leptin reduces the availability of actyl-CoA, which activates pyruvate carboxylase, produced by hepatic fatty acid catabolism, which is responsible for the inhibition of conversion of pyruvate to glucose. These findings indicate that either leptin or downstream targets of leptin may have therapeutic potential for the treatment of diabetes. In contrast with the rat models used in the study, patients who have well controlled type 1 diabetes do not consistently have low plasma lept Continue reading >>

Role Of Leptin In The Pancreatic Β-cell: Effects And Signaling Pathways
Introduction A fine regulation of pancreatic β-cell function is essential for the control of plasma glucose homeostasis and nutrient metabolism. β-cell secretion and mass are dynamic features that adapt in the short and/or long term to the insulin requirements of the organism (Sachdeva & Stoffers 2009). These insulin needs depend on multiple factors, including nutritional status and metabolic, hormonal, and neural signals. This functional plasticity also occurs during physiological or pathological situations such as pregnancy or obesity respectively (Sachdeva & Stoffers 2009). The regulation of β-cell function in the short and long term allows for an adequate level of plasma insulin levels, which restores plasma glucose concentrations to normoglycemia by inducing glucose uptake and accumulation as glycogen and fatty acids, principally in muscle, liver, and adipose tissue. However, a decrease in β-cell mass or impaired β-cell function can lead to abnormal plasma insulin levels that can promote glucose intolerance and diabetes. Among the different risk factors for the development of diabetes, obesity is a major one. The progression of obese individuals to diabetes is attributed to an altered compensation in β-cell mass and function in response to insulin demand (Sachdeva & Stoffers 2009). Obesity involves an increasing accumulation of adipose tissue and enhanced release of adipokines. Among others, leptin has been revealed as an important regulator of pancreatic β-cell function at different levels including insulin gene expression, insulin secretion, apoptosis, and cell growth. Thus, in addition to its central actions for the control of glucose metabolism (Morton & Schwartz 2011), leptin can modulate glucose homeostasis owing to these different direct effects on th Continue reading >>

A Review Of The Leptin Hormone And The Association With Obesity And Diabetes Mellitus
Received Date: February 06, 2017; Accepted Date: March 01, 2017; Published Date: March 08, 2017 Citation: Facey A, Dilworth L, Irving R (2017) A Review of the Leptin Hormone and the Association with Obesity and Diabetes Mellitus. JDiabetes Metab 8:727. doi:10.4172/2155-6156.1000727 Copyright: 2017 Facey A, 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. Leptin is a protein hormone that regulates food intake. It is secreted by the adipocytes and contains 167 amino acids. The hormone signals the hypothalamus and is released to reduce the desire for food thereby controlling appetite. Research shows that diet-induced obesity results in leptin resistance, so while the level of leptin may be high, it is ineffective. Leptin is also increased in type 2 diabetes mellitus which is strongly associated with obesity and insulin resistance . While leptin may be elevated in both diabetes and obesity, it is not the cause of either disease. It has been suggested that leptin mediates insulin resistance and as such may be a possible treatment for insulin resistance. Diet induced leptin resistance can be reversed through dietary changes and its administration can be effective in combating insulin resistance. Leptin levels may also decrease with increased exercise. The pathophysiology involving leptin resistance is unclear. More leptin studies are needed as it may be an unexplored treatment for diabetes and may be able to provide a more detailed understanding of the disease. Leptin; Obesity; Diabetes; Insulin resistance Leptin which contains 167 amino acids, was discovered in 1994. It isa hormone s Continue reading >>
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Potential Role Of Leptin In Diabetes Discovered
Follow all of ScienceDaily's latest research news and top science headlines ! Potential Role Of Leptin In Diabetes Discovered Leptin, a hormone known mainly for regulating appetite control and energy metabolism, has been found to play a major role in islet cell growth and insulin secretion. This finding opens up new avenues for studying leptin and its role in islet cell biology, which may lead to new treatments for diabetes. A new Joslin-led study has shown that leptin, a hormone known mainly for regulating appetite control and energy metabolism, plays a major role in islet cell growth and insulin secretion. This finding opens up new avenues for studying leptin and its role in islet cell biology, which may lead to new treatments for diabetes. Previous in vitro studies suggested that leptin receptors, which are found in tissues throughout the body including the pancreas as well as the brain, mediate leptin-induced inhibition of insulin secretion in islet cells, also known as beta cells. "We wanted to further our understanding of leptin and its role in beta cells independent of its effects in the brain," said Rohit N. Kulkarni, M.D., Ph.D., principal investigator at Joslin Diabetes Center and Assistant Professor of Medicine at Harvard Medical School, who led this study. It is currently not known why obese individuals exhibit a high incidence of diabetes despite high levels of both insulin and leptin circulating in the bloodstream. To understand the role of leptin in the islets, researchers developed a mouse model (known as a "knock out" or KO mouse) genetically engineered not to produce leptin receptors in the pancreas, while maintaining the receptors in the brain and the rest of the body. Researchers found that the mice lacking leptin receptors in the pancreas showed im Continue reading >>

The Role Of Leptin In Diabetes: Metabolic Effects
N2 - While it is well established that the adiposity hormone leptin plays a key role in the regulation of energy homeostasis, growing evidence suggests that leptin is also critical for glycaemic control. In this review we examine the role of the brain in the glucose-lowering actions of leptin and the potential mediators responsible for driving hyperglycaemia in states of uncontrolled insulin-deficient diabetes (uDM). These considerations highlight the possibility of targeting leptin-sensitive pathways as a therapeutic option for the treatment of diabetes. This review summarises a presentation given at the Is leptin coming back? symposium at the 2015 annual meeting of the EASD. It is accompanied by two other reviews on topics from this symposium (by Christoffer Clemmensen and colleagues, DOI: 10.1007/s00125-016-3906-7, and by Gerald Shulman and colleagues, DOI: 10.1007/s00125-016-3909-4) and an overview by the Session Chair, Ulf Smith (DOI: 10.1007/s00125-016-3894-7). AB - While it is well established that the adiposity hormone leptin plays a key role in the regulation of energy homeostasis, growing evidence suggests that leptin is also critical for glycaemic control. In this review we examine the role of the brain in the glucose-lowering actions of leptin and the potential mediators responsible for driving hyperglycaemia in states of uncontrolled insulin-deficient diabetes (uDM). These considerations highlight the possibility of targeting leptin-sensitive pathways as a therapeutic option for the treatment of diabetes. This review summarises a presentation given at the Is leptin coming back? symposium at the 2015 annual meeting of the EASD. It is accompanied by two other reviews on topics from this symposium (by Christoffer Clemmensen and colleagues, DOI: 10.1007/s00125 Continue reading >>

The Glucoregulatory Actions Of Leptin - Sciencedirect
Volume 6, Issue 9 , September 2017, Pages 1052-1065 Author links open overlay panel Anna M.D'souza13 The hormone leptin is an important regulator of metabolic homeostasis, able to inhibit food intake and increase energy expenditure. Leptin can also independently lower blood glucose levels, particularly in hyperglycemic models of leptin or insulin deficiency. Despite significant efforts and relevance to diabetes, the mechanisms by which leptin acts to regulate blood glucose levels are not fully understood. Here we assess literature relevant to the glucose lowering effects of leptin. Leptin receptors are widely expressed in multiple cell types, and we describe both peripheral and central effects of leptin that may be involved in lowering blood glucose. In addition, we summarize the potential clinical application of leptin in regulating glucose homeostasis. Leptin exerts a plethora of metabolic effects on various tissues including suppressing production of glucagon and corticosterone, increasing glucose uptake, and inhibiting hepatic glucose output. A more in-depth understanding of the mechanisms of the glucose-lowering actions of leptin may reveal new strategies to treat metabolic disorders. Continue reading >>

The Potential Of Leptin For Treating Diabetes And Its Mechanism Of Action
The Potential of Leptin for Treating Diabetes and Its Mechanism of Action We are experimenting with display styles that make it easier to read articles in PMC. The ePub format uses eBook readers, which have several "ease of reading" features already built in. The ePub format is best viewed in the iBooks reader. You may notice problems with the display of certain parts of an article in other eReaders. Generating an ePub file may take a long time, please be patient. The Potential of Leptin for Treating Diabetes and Its Mechanism of Action Following the discovery of leptin in 1994, major research efforts have brought us much closer to a fuller understanding of the cellular and molecular mechanisms underlying the biological effects of the hormone. Interestingly, leptin exerts potent anti-diabetic actions that are independent of its effects on body weight and food intake. In particular, leptin can correct diabetes in animal models of either diabetes mellitus type 1 (T1DM) or type 2 (T2DM). In addition, long-term leptin-replacement therapy is well tolerated and dramatically improves glycemic control, insulin sensitivity, and plasma triglycerides in patients with severe insulin resistance due to lipodystrophy. Together, these results have spurred enthusiasm for the use of leptin therapy to treat humans suffering from diabetes mellitus. Here, we review current understandings of these glucoregulatory functions of leptin, with particular emphasis on its central mechanisms of action, lessons from clinical studies and discuss possible therapeutic applications of leptin in the treatment of T1DM and T2DM. Even with the improved anti-diabetic drugs, enhanced glycemia monitor systems, easier patient-to-physician accessibility, people who have type 2 diabetes mellitus (T2DM; an illness Continue reading >>

The Role Of Leptin In Diabetes: Metabolic Effects.
The role of leptin in diabetes: metabolic effects. Diabetes and Obesity Center of Excellence, Department of Medicine, University of Washington at South Lake Union, 850 Republican St., N335, Box 358055, Seattle, WA, 98195, USA. Diabetes and Obesity Center of Excellence, Department of Medicine, University of Washington at South Lake Union, 850 Republican St., N335, Box 358055, Seattle, WA, 98195, USA. [email protected] Diabetologia. 2016 May;59(5):928-32. doi: 10.1007/s00125-016-3898-3. Epub 2016 Mar 11. While it is well established that the adiposity hormone leptin plays a key role in the regulation of energy homeostasis, growing evidence suggests that leptin is also critical for glycaemic control. In this review we examine the role of the brain in the glucose-lowering actions of leptin and the potential mediators responsible for driving hyperglycaemia in states of uncontrolled insulin-deficient diabetes (uDM). These considerations highlight the possibility of targeting leptin-sensitive pathways as a therapeutic option for the treatment of diabetes. This review summarises a presentation given at the 'Is leptin coming back?' symposium at the 2015 annual meeting of the EASD. It is accompanied by two other reviews on topics from this symposium (by Christoffer Clemmensen and colleagues, DOI: 10.1007/s00125-016-3906-7 , and by Gerald Shulman and colleagues, DOI: 10.1007/s00125-016-3909-4 ) and an overview by the Session Chair, Ulf Smith (DOI: 10.1007/s00125-016-3894-7 ). Continue reading >>

Serum Leptin Levels In Children With Diabetes Type 1 And Its Relation With Diabetic Nephropathy And Retinopathy
Endocrine Abstracts (2017) 51 P061 | DOI: 10.1530/endoabs.51.P061 Serum leptin levels in children with diabetes type 1 and its relation with diabetic nephropathy and retinopathy Agnieszka Brandt1, Ewa Malinowska2, Katarzyna Zorena2 & Magorzata Myliwiec1 1Clinic of Pediatrics, Diabetology and Endocrinology, Gdansk, Poland; 2Medical University of Gdansk, Gdansk, Poland. Introduction: Type 1 diabetes mellitus is one of the most common chronic diseases in children. Precise knowledge of the pathogenesis of diabetes mellitus type 1 and its chronic complications is the enormous challenge in modern diabetology. In recent years, the role of leptin in the pathogenesis of microvascular diabetic complications has been highlighted. Aim: The aim of the study was to investigate serum leptin level and correlations between leptin levels and clinical and biochemical parameters in patients with diabetes mellitus. Materials and methods: The study included 110 patients with diabetes type 1, lasting 6.053.25 years, aged 14.373.13 years from Clinic of Pediatrics, Diabetology and Endocrinology, Medical University of Gdansk, Poland and 50 matched controls. Patients with type 1 diabetes mellitus were divided in two subgroups with and without late diabetic complications (albuminuria and ophtalmological changes). In all included to the study children: HbA1c, C-reactive protein, lipid profile, albuminuria and serum leptin level with enzyme immunoassay were performed. Results: Statistically significant differences in serum leptin level, among patients with long-term type 1 diabetes mellitus (7.638.41 ng/ml) and group of healthy children (9.586.61 ng/ml) were shown with the highest level in control group (P=0.04). In patients with symptoms of late diabetic complications were reported significantly h Continue reading >>
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Leptin Resistance: The Other Hormone Important For Managing Diabetes | Everyday Health
Eating a Mediterranean-style diet with lean protein, whole grains, and healthy fats can help increase leptin sensitivity. When most people think of diabetes and hormones, insulin which controls blood sugar levels by ferrying glucose to cells for energy is usually the first that springs to mind. But there are many hormones at play when it comes to blood sugar levels and weight, and anyone living with diabetes or prediabetes should consider them all when striving to better manage their symptoms. Key among these is leptin, a hormone produced by fat cells that helps the body regulate energy by telling the brain its had enough to eat, according to a review published in December 2012 in the Indian Journal of Endocrinology and Metabolism . Leptins action is to inhibit appetite, to stimulate the burning up of fatty acids, to decrease glucose, and to reduce overall body fat and weight, says VandanaSheth, RDN, CDE , a spokesperson for the Academy of Nutrition and Dietetics. The problem, Sheth explains, is, just like insulin resistance whereby cells are resistant to insulin, leading glucose to accumulate in the blood people can develop leptin resistance, an effect that can further complicate their diabetes management . When this occurs, Sheth says, People can gain weight, have increased body fat, and, even though there are adequate fat stores, their brains are getting the signal that they are hungry, so they eat more. It's a vicious cycle. Unfortunately, just adding more leptin, as people with diabetes often do with insulin injections , cant fix this problem because the issue isnt always how much leptin is in the body, but whether the body is able to process it efficiently. In fact, for people without diabetes, or for those who have been diagnosed with prediabetes, leptin resista Continue reading >>

The Leptin Receptor And Its Role In Obesity And Type 2 Diabetes
Obesity is considered as a major public health problem, which is often associated with type 2 diabetes mellitus, cardiovascular diseases and cancer. In most cases, obesity is accompanied by a decreased responsiveness for a hormone called leptin. This cytokine is primarily secreted by the white adipose tissue and targets specific receptors in the arcuate nucleus of the hypothalamus to regulate energy expenditure and food intake. Stimulation of leptin receptors (OB-R) activates several intracellular signaling pathways such as the JAK2/STAT3, MAPK, PI3K and AMPK pathways. Mutations that abolish leptin or OB-R expression result in massive obesity in mice and humans. However, the prevalence of such mutants are not very high in the human population. Most obese individuals have paradoxically high leptin levels and are unable to respond adequately to this hormone. This pathological state is termed "leptin resistance". Several hypothesis attempt to explain this leptin resistance such as impaired transport of leptin across the blood-brain-barrier, impaired OB-R signaling or altered OB-R trafficking. Our research is oriented towards three major topics aiming to understand the mechanism of OB-R function, which regulates the sensitivity to leptin: Continue reading >>

The Role Of Leptin In Diabetes: Metabolic Effects
, Volume 59, Issue5 , pp 928932 | Cite as The role of leptin in diabetes: metabolic effects While it is well established that the adiposity hormone leptin plays a key role in the regulation of energy homeostasis, growing evidence suggests that leptin is also critical for glycaemic control. In this review we examine the role of the brain in the glucose-lowering actions of leptin and the potential mediators responsible for driving hyperglycaemia in states of uncontrolled insulin-deficient diabetes (uDM). These considerations highlight the possibility of targeting leptin-sensitive pathways as a therapeutic option for the treatment of diabetes. This review summarises a presentation given at the Is leptin coming back? symposium at the 2015 annual meeting of the EASD. It is accompanied by two other reviews on topics from this symposium (by Christoffer Clemmensen and colleagues, DOI: 10.1007/s00125-016-3906-7 , and by Gerald Shulman and colleagues, DOI: 10.1007/s00125-016-3909-4 ) and an overview by the Session Chair, Ulf Smith (DOI: 10.1007/s00125-016-3894-7 ). BrainCorticosteroneDiabetesGlucagonHepatic glucose productionLeptinReview Diabetes is increasing steadily all over the world. The International Diabetes Federation estimates that more than 382 million people have diabetes globally and this number is expected to exceed 590 million by 2035 [ 1 ]. This is a serious health concern since people with diabetes are vulnerable to both short- and long-term complications, including cardiovascular and renal disease, blindness and amputation [ 2 ]. Given the continued prevalence and incidence of diabetes and its considerable health burden, a better understanding of its pathogenesis is required to facilitate the development of new strategies for its treatment. Ever since its discov Continue reading >>

Leptin
Not to be confused with Lectin or Lecithin. Leptin (from Greek λεπτός leptos, "thin"), “the hormone of energy expenditure”,[a] is a hormone predominantly made by adipose cells that helps to regulate energy balance by inhibiting hunger. Leptin is opposed by the actions of the hormone ghrelin, the "hunger hormone". Both hormones act on receptors in the arcuate nucleus of the hypothalamus to regulate appetite to achieve energy homeostasis.[6] In obesity, similar to resistance of insulin in type 2 diabetes, a decreased sensitivity to leptin occurs, resulting in an inability to detect satiety despite high energy stores.[7] Although regulation of fat stores is deemed to be the primary function of leptin, it also plays a role in other physiological processes, as evidenced by its multiple sites of synthesis other than fat cells, and the multiple cell types beside hypothalamic cells that have leptin receptors. Many of these additional functions are yet to be defined.[8][9][10][11][12][13] Identification of the gene[edit] In 1949, a non-obese mouse colony being studied at the Jackson Laboratory produced a strain of obese offspring, suggesting that a mutation had occurred in a hormone regulating hunger and energy expenditure. Mice homozygous for the so-called ob mutation (ob/ob) ate voraciously and were massively obese.[14] In the 1960s, a second mutation causing obesity and a similar phenotype was identified by Douglas Coleman, also at the Jackson Laboratory, and was named diabetes (db), as both ob/ob and db/db were obese.[15][16][17] In 1990 Rudolph Leibel and Jeffrey M. Friedman reported mapping of the db gene.[18][19][20] Consistent with Coleman’s and Leibel's hypothesis, several subsequent studies from Leibel's and Friedman’s labs and other groups confirmed that Continue reading >>

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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