Etiology for type 1 diabetes mellitus,drugs for type 2 diabetes weight loss exercises,type 2 diabetes uk statistics 2013 worldwide,free diabetes testing chicago area - You Shoud Know

Tufts OCW material is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License. We will be provided with an authorization token (please note: passwords are not shared with us) and will sync your accounts for you. The onset of Type 1 diabetes mellitus (T1DM) often occurs in childhood or adolescence and is characterized by the immune-mediated destruction of pancreatic β-cells leading to insulin deficiency. While the etiology of T1DM and T2DM are distinct, the end result is number of common co-morbidities including nephropathy, neuropathy, and cardiovascular disease.
Satellite cells from streptozotocin (STZ)-treated diabetic mice fail to activate properly, resulting in failed regeneration following chemically induced muscle injury (Jeong et al., 2013). With diabetes progression, a multitude of pro-inflammatory factors are elevated, constituting a state of chronic low-grade inflammation, or a chronic low-grade inflammatory profile (CLIP). The presence of CLIP, as found in diabetes, will undoubtedly alter skeletal muscle homeostasis. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. From The gut–renal axis: do incretin-based agents confer renoprotection in diabetes?
Haemodynamic and metabolic factors, with a central role for chronic hyperglycaemia, have pivotal roles in the pathophysiology of diabetic nephropathy.
Diabetes Centre, Department of Internal Medicine, VU University Medical Centre, De Boelelaan 1117, 1081 HV Amsterdam, Netherlands. The Mediterranean Group for the Study of Diabetes (MGSD) was set up in 1985, on the initiative of Professor Molinatti from Turin, Italy, as a specific center of excellence in diabetes, grouping together well-recognized experts from Mediterranean countries to meet the unrequited needs of all health professionals in the Mediterranean area involved in the delivery of diabetes care.
The organization of specific scientific societies throughout the world into local networks of expertise is a very important development for multidisciplinary research groups, maintaining connections among specialists and promoting the sharing of experience and funding resources.
The Mediterranean area represents a unique regional example of interplay between varying ethnic and socio-economic groups. Diabetes is no longer an epidemic that can be ignored: the disease is a widespread problem, increasing rapidly in every part of the world. We must unite to prevent diabetes, to improve diabetes care for the millions affected, and, ultimately, to find cost-effective ways of tackling one of the largest health problems we now face.
In the Mediterranean and neighboring areas, the incidence rates of type 1 diabetes in children under the age of 15 years show wide variations. The beneficial effects on health of the Mediterranean Diet have been tested in various intervention studies. It is difficult to conduct such studies since the complexity of dietary modifications makes it impossible to develop a double-blind intervention to analyze its effect on health. The effects of various important dietary components in the Mediterranean Diet in mortality in diabetic patients have not been extensively investigated. The MGSD was founded in 1985 with the aim of fostering collaboration and research in diabetes as well as providing the means of networking for health-care professionals working in different areas of the Mediterranean. The missions of the MGSD have been defined in its constitutional text (12th July, 1985) as attempting to respond to the need for information and training in diabetology on both sides of the Mediterranean. The main MGSD meeting, held every 2 years, provides an excellent forum for the discussion of original papers relating to specific issues in diabetes by means of either oral or poster presentations. The last meeting, following those held in Rome, Athens, Nice, Madrid, Tunis, Rome, Marrakech, Lisbon, Nice, and Istanbul, was held in Malta in April 2009. As years went by and experience was gained, it appeared to successive presidents that the Group’s main mission was to provide quality information to health professionals in charge of diabetic patients and training to the youngest doctors in this field. Although this was sufficient justification in itself for setting up the MGSD, the founders felt duty bound to develop their aims and working practices along similarly original lines. For this reason, and thanks to the unflagging commitment of its successive presidents—Profs Molinatti (Italy), Alivisatos (Greece), Serrano Rios (Spain), Crepaldi (Italy), Drouin (France), Kadiri (Morocco), Charbonnel (France), and Duran- Garcia (Spain)—the MGSD sought to establish training programs empowering those entering the specialty with the requisite technical skills to conduct wide-ranging national studies. The relative high prevalence of T2DM should be reflected in a similarly elevated prevalence of gestational diabetes mellitus (GDM), since pregnancy uncovers any underlying insulin resistance. All in all, with some 525 members on its books and backed by a committed board and chairman, the MGSD, which has been a member of the International Diabetes Federation since 1995, has more than fulfilled its founders’ purpose in focusing on specifically Mediterranean issues in diabetes and the delivery of diabetes care.
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This page doesn't support Internet Explorer 6, 7 and 8.Please upgrade your browser or activate Google Chrome Frame to improve your experience. While the development of each form of diabetes (Type 1 or Type 2) drastically differs, resultant pathologies often overlap. A critical component in skeletal muscle maintenance and plasticity is the presence of muscle progenitor cells. Diabetic myopathy, characterized by reduced physical capacity, strength, and muscle mass (Andersen et al., 1996, 1997, 2004, 2005), is a relatively understudied complication of diabetes mellitus, but is believed to directly influence the rate of co-morbidity development.
This extreme catabolic state has previously been shown to promote the fusion of SCs to adjacent muscle fibers in T1DM mice, as this is thought to promote the release of factors that function to sustain muscle integrity in this less than favorable metabolic condition (Brannon et al., 1989).
For instance, 3 weeks of a high fat feeding (HFF) affected SC content and functionality, with the latter classified as the quantity of regenerating fibers present following injury (Fitzpatrick et al., 2011). Dysregulation of nitric oxide (NO) production also occurs, as hyperglycemia promotes the formation of reactive nitrogen species (RNS) to further exacerbate levels of oxidative stress (Zou et al., 2002). This emerging and exciting new area of interest, though still in its infancy, presents an intriguing avenue for further therapeutic investigations. Within muscle, inhibition of PAI-1 (a critical inhibitor of the plasminogen system) was found to increase MyoD expression and accelerate muscle repair (Koh et al., 2005). Obesity and chronic hyperglycaemia alter vasoactive regulators of afferent and efferent arteriolar tone, leading to increased PGC, hyperperfusion and hyperfiltration.
The MGSD, a member of the International Diabetes Federation since 1995, is a nonprofit, nonpolitical association of diabetologists from Mediterranean countries. The region can be regarded as a single unit with a large number of common ethnic and cultural features, but it is heterogeneous in terms of socio-economic and demographic factors. In a population-based prospective study with 22 043 adult participants in Greece with a median follow-up of 44 months, better adherence to the Mediterranean Diet pattern (judged by a 2 unit increment in a scoring system on a 10-point scale) was associated with a reduction in overall mortality (hazard ratio [HR], 0.75).
In a recent publication, the tenyear all-cause mortality of 1000 diabetic patients was related independently to saturated fat and egg consumption. To promote, through congresses held every two years and by other suitable means, information and studies in the field of assistance to diabetic patients, with particular regard to self-management, prevention of complications, and social and legislative problems. To coordinate and standardize research in the epidemiology of diabetes in Mediterranean countries.
To promote studies regarding patient education, upgrading these according to the needs of each country. Members mingle, meet, and talk, applaud the winners of the Hippocrates and Averroes prizes awarded for the two best abstracts, and conduct MGSD official business, the election of the board and the appointment of the president. Thus, in addition to the 2-yearly conference, fellowships are also offered to assist the organization of postgraduate courses within teams of international repute. It soon became apparent that on top of conventional meetings that bring health professionals together and keep them abreast of the latest key developments in the specialty, there was little point, given the absence of adequate training and resources, in trying to set up topic-based study groups (eg, on the Mediterranean Diet, diabetes and migration) to produce clinical or epidemiologic studies.
Results are due in 2011 and should lead to a number of international communications and publications.

For its part too, Servier has been committed to providing financial and logistic support to the project since its inception. In each diabetic condition, a failure to maintain healthy muscle is often observed, and is termed diabetic myopathy. A complex network of intrinsic and extrinsic factors mediate changes to these progenitor cells, with such factors influenced by, and influential to, skeletal muscle health. This is based on the fact that skeletal muscle functions as the largest site for glucose uptake (DeFronzo et al., 1981), and therefore changes to skeletal muscle health can impact whole-body glucose homeostasis. While these studies are well conducted, it was not within their scope to investigate all components required for skeletal muscle growth and maintenance. These modifications were based on T2DM-induced epigenetic changes to muscle cell gene programming, modifying protein expression of factors essential to myogenesis, thereby permanently affecting muscle SCs (Broholm et al., 2012). Given the chronic elevations in IL-6 with diabetes, it is reasonable to surmise that impairments to SC functionality are occurring. Inhibition of myoblast differentiation by tumor necrosis factor alpha is mediated by c-Jun N-terminal kinase 1 and leukemia inhibitory factor.
These early renal haemodynamic changes, combined with systemic hypertension, are important in the development and progression of renal disease in T2DM.
She is also a speaker for Astra Zeneca, Bristol-Myers Squibb, Eli Lilly, Novo Nordisk and Sanofi. The specific aim of the MGSD is to act as a bridge between both sides of Mediterranean basin by promoting an exchange of information and knowledge on diabetes research and care delivery, with special emphasis on epidemiology, education, and clinical therapy. Thus, most of the Northern Mediterranean countries (European coast) share the features of other industrialized countries, while most of the Southern Mediterranean (African coast) belongs to the developing world. However, an earlier peak incidence in children aged 5-9 years is a common feature of insular Italian areas, but not of Northern Italy.
There is no association between egg intake and mortality in the nondiabetic population, as has been shown in a special analysis of the above-mentioned Health Professionals Followup Study (HPFS).
The Maltese population has repeatedly been shown to have a marked increased prevalence of insulin resistance, which exhibits itself via an overall higher prevalence of diabetes mellitus and impaired glucose tolerance (IGT), mainly of the non–insulin-dependent variety.
Incidence of insulin-dependent diabetes mellitus among Sardinian-heritage children born in Lazio region, Italy. Combined effects of routine blood pressure lowering and intensive glucose control on macrovascular and microvascular outcomes in patients with type 2 diabetes.
A prospective study of egg consumption and risk of cardiovascular disease in men and women. Diet and physical activity in relation to overall mortality amongst adult diabetics in a general population cohort.
The clinical significance of gestational impaired glucose tolerance in the Maltese population.
This significant, but often overlooked, complication is believed to contribute to the progression of additional diabetic complications due to the vital importance of skeletal muscle for our physical and metabolic well-being.
Indeed, SCs are indispensable for such events (Zammit and Relaix, 2012), and thus a more complete understanding of the impact of the diabetic environment on SC function is needed. The paucity of data available from human diabetic muscle exposed to insulin treatment merits further consideration. Satellite cells are critical to muscle health, and are affected by diabetes mellitus at varying stages of adult myogenesis.
While examination of each of these factors on SC function is beyond the breadth of this review, it is important to highlight a select few.
Consistent with this hypothesis, obese diabetic individuals displayed significant impairments in IL-6 signaling within their skeletal muscle that persisted within the satellite cells even upon removal from the diabetic environment (Nielsen et al., 2012). Excessive ECM levels are likely the result of altered protein expression (Lecker et al., 2004), especially in regards to matrix metalloproteinases (Hopps and Caimi, 2012). Based on the limited number of studies to date, it is evident that various stages of the myogenic process are affected by diabetes mellitus and impairments to SC function are occurring. Slower conduction velocity and motor unit discharge frequency are associated with muscle fatigue during isometric exercise in Type 1 diabetes mellitus.
Additionally, chronic hyperglycaemia and dyslipidaemia induce mitochondrial superoxide overproduction, which activates several well-defined pathways leading to the development and progression of diabetic nephropathy. While the countries involved share a common geographical basin, they have very different ethnic origins, languages, and dietary habits, offering a unique opportunity for comparison in the field of diabetes worldwide. The Mediterranean Group for the Study of Diabetes (MGSD) was set up to bring the medical community face to face with these issues and challenges. The Mediterranean islands and Eastern Mediterranean countries (Asian coast) share a mixture of these features. This higher prevalence of insulin resistance is reflected by a relatively high prevalence of GDM.
While studies have investigated the link between changes to skeletal muscle metabolic health following diabetes mellitus onset (particularly Type 2 diabetes mellitus), few have examined the negative impact of diabetes mellitus on the growth and reparative capacities of skeletal muscle that often coincides with disease development. As such, these cells (or a sub-population therein) function as a primary therapeutic target to attenuate deficits in muscle health with disease progression. Adverse health behaviors, particularly sedentary lifestyles and increased adiposity, have lead to a high incidence of insulin resistance and impaired fasting glucose (American Diabetes Association, 2006). As such, changes to SC functionality with diabetes mellitus would impact skeletal muscle health. Collectively, these studies highlight the negative impact T1DM is having on skeletal muscle and its potential for growth, maintenance, and repair. In vitro studies have also shown that SCs incubated in high glucose medium have an increased propensity to differentiate into adipocytes (Aguiari et al., 2008), suggesting that SC myogenic capacity may be impacted by uncontrolled diabetes. In the absence of insulin, or poorly managed diabetic states, there may be a myriad of factors and processes stemming from the diabetic environment that have the potential to influence SC activity.
As outlined in this review, and schematized here, chronic low grade inflammation (also known as CLIP, or chronic low-grade inflammatory profile), oxidative stress, and impaired extracellular matrix remodeling are proposed to be common denominators for mechanisms underlying impairments to muscle health and decreased satellite cell functionality in diabetes mellitus.
In vitro work has found that acute treatment of human muscle SCs with the ROS-inducing agent hydrogen peroxide (H2O2) led to reduced cell viability, shortened lifespan, and decreased proliferative capacity (Renault et al., 2002). The improper turnover of ECM proteins may also hinder growth factor signaling, further impeding myogenesis (Gopinath and Rando, 2008). Given the vital role of these cells in the lifelong maintenance of skeletal muscle, and the importance of a physically and metabolically healthy skeletal muscle mass in attenuating the morbidity and mortality associated with diabetes mellitus, a comprehensive understanding of SC in the diabetic environment is of fundamental significance.
Collectively, these factors in the diabetic milieu lead to glomerular damage, histologically characterized by thickening of the glomerular and tubular basement membranes, mesangial expansion and podocytopathy. Muskiet is a clinical research physician at the Diabetes Centre, VU Medical Centre (VUMC), Amsterdam, Netherlands. Since its establishment, the MGSD has grown and become an association that attracts the medical community in the field of diabetes from the north and south banks of the Mediterranean Basin.Within this domain, theMGSD facilitates the exchange of diabetic knowledge and expertise in scientific research, in practical aspects of patient care, and in patient education.
In the Mediterranean Basin, epidemiologic evidence shows increases in both the incidence of diabetes and its complications.
Probably differences in environmental factors (diet, toxins, and viral infections), genetic susceptibility, or both are important for such a wide variation.
Moreover, several studies have found significantly higher prevalence rates in urban environments than in rural ones, within the same country.

The effects of the Mediterranean Diet in diabetics warrant further research.12,13 The beneficial effects on health of the Mediterranean Diet have been tested in various intervention studies.
Epidemiological studies15 have shown that the prevalence of GDM in the pregnant Maltese population is approximately 5.9%. Importantly, evidence is accumulating that the muscle progenitor cell population (particularly the muscle satellite cell population) is also negatively affected by the diabetic environment, and as such, likely contributes to the declining skeletal muscle health observed in diabetes mellitus.
Without therapeutic intervention, the insulin-resistant state often precipitates to pancreatic β-cell death and progression to insulin-dependent T2DM. Here we review the current state of knowledge on the relationship between skeletal muscle health and diabetes mellitus, with a particular focus on the fate and function of skeletal muscle progenitor cell populations.
The impaired regeneration with diabetes was attributed to an elevation in plasma PAI-1 resulting from attenuated extracellular matrix (ECM) turnover. A more severe T2DM phenotype, as is found in genetic models of T2DM, results in impairments to the early stages of myogenesis (proliferation, activation), while the HFF models will alter the differentiation potential of the SCs. After a review of many of these mechanisms, a select few are evident in both T1DM and T2DM.
While the aforementioned studies identify that aspects of muscle health are clearly subject to modification with diabetes mellitus, one must also account for diabetic-induced changes to the environment in which the muscle SCs reside. Identifying the proponents that attenuate normal SC function in diabetes mellitus will lead to the development of therapies that restore SC activity in order to sustain muscle health, and subsequently attenuate other diabetic complications. He received his MD degree cum laude in 2012 from the VU University in Amsterdam, Netherlands. Thus, the disease, especially type 2 diabetes mellitus (T2DM), is evolving as a major health problem in this area. As in other areas of the world, variation in incidence appears to be related to ethnicity, demonstrating the importance of the differential genetic susceptibility in different populations. Comparisons of migrant populations living in rural and urban settings in the same country also show an excess of diabetes in urban communities.
In this review, we summarize the current knowledge surrounding the influence of diabetes mellitus on skeletal muscle growth and repair, with a particular emphasis on the impact of diabetes mellitus on skeletal muscle progenitor cell populations. Finally, long-term exposure to T2DM may promote detrimental epigenetic changes to SCs that will inevitably affect their functionality, and ultimately, overall skeletal muscle health.
The precise modifications to skeletal muscle following diabetes onset is depicted along with the predicted mechanisms of action (Figure 1). The adverse remodeling of the ECM in diabetic muscle, as evidenced by increased collagen presence, will inevitably affect SC functionality and its capacity to migrate within regenerating muscle (Krause et al., 2013). He has been involved in diabetes-related research since 2006 at the Diabetes Centre, VUMC, Amsterdam, collaborating on ongoing projects in the fields of hepatic steatosis, inflammation and cardiovascular disease, as well as the effects of pharmacological interventions on human β-cell function. Indeed Sardinians, who together with Finns have the highest incidence of type 1 diabetes in the world, have a high frequency of HLA haplotypes implicated in type 1 diabetes susceptibility and paucity of protective alleles when compared with other white populations.2 Moreover, the interactions between different genes and environmental factors may be important, as suggested by some studies performed in Israel. This aspect is actually not only very interesting, but highly relevant since we are witnessing an important migratory flow from developing countries to Europe.
Interestingly, despite systemic increases in PAI-1, the impaired regeneration occurred in a muscle-specific pattern (Krause et al., 2013), indicating that muscles are intrinsically resistant to the T1DM environment. These include, but are not limited to: oxidative stress, chronic low-grade inflammation, and impaired ECM remodeling.
Since 2013, he has been working on his PhD thesis, under the supervision of Professor Michaela Diamant, investigating renoprotective mechanisms of human diabetic kidney disease, with special emphasis on incretin-based therapies.Contact Marcel H.
In contrast, studies in Sardinian migrants showed that the high incidence of type 1 diabetes is more a consequence of their genetic background than of environmental influences.5 This does not mean that environmental factors are not relevant in the etiology of type 1 diabetes, but rather that environmental triggers may have a major impact on genetically predisposed subjects.
Since both the prevalence of T2DM and the mean age of patients are increasing in most European countries, there has been a consequent increase in the prevalence of cardiovascular and microvascular complications.
It is becoming increasingly clear that alterations to muscle protein turnover cannot, by itself, account for diabetic myopathy.
Specifically, impaired SC proliferation and activation were observed and were reflected in measurable impairments of muscle regeneration (Nguyen et al., 2011). Though the impact of metabolic diseases on the changing metabolic needs of the muscle satellite cells as they move from quiescence through to differentiation is certainly of note, it is beyond the scope of this mini-review.
It is interesting to note that oxidative stress has been implicated in the adipogenic conversion of muscle SCs (Vettor et al., 2009). Thus, potential therapies to attenuate negative alterations to SC behavior with diabetes onset may also function to mitigate sarcopenia.
Worldwide a female excess is found in low-incidence populations, while the reverse is true in several high-incidence populations. Although studies investigating SCs in T1DM remains limited, evidence indicates that functionality is affected. A critical, but as of yet unanswered, question is the role of altered leptin signaling in mediating changes to SCs in these animal models. Now whether this occurs within diabetic muscle has yet to be defined, however, given that the demonstrated impairments in myogenesis with diabetes appear to be linked to oxidative stress, it is clear that this area requires further investigation. Interestingly, these authors found no difference in SC function or regenerative capacity in HFF mice (Nguyen et al., 2011). Thus, understanding alterations to the SC population in T1DM is essential for the development of therapeutic strategies to maximize muscle health during this vulnerable time. Smits is a clinical research physician and received his MD degree cum laude in 2012 from the VU University in Amsterdam, Netherlands. He has been working in human research since 2008 starting at the Department of Gastroenterology (VUMC) Amsterdam, where he participated in projects focusing on hepatic and pancreatic steatosis and pancreatitis. In 2011, as part of a research internship, he participated in epidemiological studies at the University of Washington, Seattle, WA, USA, under the supervision of Professor Steven Kahn. Morsink received her MD degree cum laude in 2010 from the VU University in Amsterdam, Netherlands. She started her research activities in 2006 at the Department of Gastroenterology, VUMC, Amsterdam, assisting in studies on fatty liver in type 2 diabetes mellitus. After obtaining an MD degree (1987, cum laude; Leiden University, Leiden) and a PhD degree in Neuroscience (1991, Utrecht University, Utrecht, both in the Netherlands) she trained in internal medicine, nephrology and endocrinology.
In 2000, she joined the Diabetes Centre, Department of Endocrinology VUMC, Amsterdam, headed by Prof. She works as a clinical diabetologist and supervises multiple research projects, focusing on the pathogenesis, mechanisms and treatment of type 2 diabetes mellitus and its complications.
She has co-authored 270 original research papers, reviews, chapters and patents (H-index 44). She has served on many national and international scientific committees, writing groups and faculties (European Association for the Study of Diabetes, European Foundation for the Study of Diabetes, European Medicines Agency, American Diabetes Association, Endocrine Society) and editorial boards (Diabetologia, Journal of Clinical Endocrinology & Metabolism, Cardiovascular Diabetology).

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