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        <title>Diabetology &amp; Metabolic Syndrome - Most accessed articles</title>
        <link>http://www.dmsjournal.com</link>
        <description>The most accessed research articles published by Diabetology &amp; Metabolic Syndrome</description>
        <dc:date>2012-01-19T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.dmsjournal.com/content/3/1/26" />
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        <title>Effect of Carnitine and herbal mixture extract on obesity induced by high fat diet in rats</title>
        <description>Background:
Obesity-associated type 2 diabetes is rapidly increasing throughout the world. It is generally recognized that natural products with a long history of safety can modulate obesity.AimTo investigate the development of obesity in response to a high fat diet (HFD) and to estimate the effect of L-carnitine and an Egyptian Herbal mixture formulation (HMF) (consisting of T. chebula, Senae, rhubarb, black cumin, aniseed, fennel and licorice) on bodyweight, food intake, lipid profiles, renal, hepatic, cardiac function markers, lipid Peroxidation, and the glucose and insulin levels in blood and liver tissue in rats.MethodWhite male albino rats weighing 80-90 gm, 60 days old. 10 rats were fed a normal basal diet (Cr), 30 rats fed a high-fat diet (HFD) for 14 weeks during the entire study. Rats of the HFD group were equally divided into 3 subgroups each one include 10 rats. The first group received HFD with no supplement (HFD), the 2nd group HFD+L-carnitine and the third group received HFD+HMF. Carnitine and HMF were administered at 10th week (start time for treatments) for 4 weeks.Body weight, lipid profile &amp; renal function (urea, uric acid creatinine) ALT &amp; AST activities, cardiac markers, (LDH, C.K-NAC and MB) the oxidative stress marker reduced glutathione (GSH), and Malondialdehyde (MDA) catalase activity, in addition to glucose, insulin, and insulin resistance in serum &amp; tissues were analyzed.
Results:
Data showed that feeding HFD diet significantly increased final body weight, triglycerides (TG), total cholesterol, &amp; LDL concentration compared with controls, while significantly decreasing HDL; meanwhile treatment with L-carnitine, or HMF significantly normalized the lipid profile.Serum ALT, urea, uric acid, creatinine, LDH, CK-NAC, CK-MB were significantly higher in the high fat group compared with normal controls; and administration of L-carnitine or herbal extract significantly lessened the effect of the HFD. Hyperglycemia, hyperinsulinemia, and high insulin resistance (IR) significantly increased in HFD in comparison with the control group. The treatment with L-carnitine or HMF improved the condition. HFD elevated hepatic MDA and lipid peroxidation associated with reduction in hepatic GSH and catalase activity; whereas administration of L-carnitine or herbal extract significantly ameliorated these hepatic alterations.
Conclusion:
HFD induced obesity associated with a disturbed lipid profile, defective antioxidant stability, and high values of IR parameters; this may have implications for the progress of obesity related problems. Treatment with L-carnitine, or HMF extract improved obesity and its associated metabolic problems in different degrees. Also HMF has antioxidant, hypolipidaemic insulin sensitizing effects. Moreover HMF might be a safe combination on the organs whose functions were examined, as a way to surmount the obesity state; and it has a distinct anti-obesity effect.</description>
        <link>http://www.dmsjournal.com/content/1/1/17</link>
                <dc:creator>Kamal Amin</dc:creator>
                <dc:creator>Mohamed Nagy</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2009, null:17</dc:source>
        <dc:date>2009-10-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-1-17</dc:identifier>
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        <title>Ten-week lifestyle changing program reduces several indicators for metabolic syndrome in overweight adults</title>
        <description>We aim to investigate the effectiveness of a 10-week lifestyle intervention focusing on physical activity and high fiber intake for reducing indicators for metabolic syndrome in overweight-obese individuals. A prospective study of 50 overweight (OW) adults (22 in the general educational group - G1; 28 in the high fiber nutrition group - G2) was performed.  Both groups were offered dietary counseling and supervised exercise. Clinical, anthropometric, dietary and plasma biochemical tests were performed at baseline - time 0 (T0) and after 10 weeks - time 1 (T1). Both groups improved their dietary quality, but only G2 presented higher intake of fruit and vegetables (servings/day), higher plasma beta-carotene levels and a 24% reduction of MetS incidence. Additionally G2 showed greater reductions in body fat (4%), and waist circumference (7%), obesity class III (2%) and obesity class II (14%) rate. Lifestyle intervention, including a high dietary fiber intake, improved healthy eating index and decreased body fat composition and plasma lipid concentrations leading to MetS incidence reduction.</description>
        <link>http://www.dmsjournal.com/content/4/1/1</link>
                <dc:creator>Marita Mecca</dc:creator>
                <dc:creator>Fernando Moreto</dc:creator>
                <dc:creator>Franz Burini</dc:creator>
                <dc:creator>Reinaldo Dalanesi</dc:creator>
                <dc:creator>Katia McLellan</dc:creator>
                <dc:creator>Roberto Burini</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2012, null:1</dc:source>
        <dc:date>2012-01-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-4-1</dc:identifier>
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        <title>Diabetic nephropathy</title>
        <description>Diabetic nephropathy is the leading cause of chronic renal disease and a major cause of cardiovascular mortality. Diabetic nephropathy has been categorized into stages: microalbuminuria and macroalbuminuria. The cut-off values of micro- and macroalbuminuria are arbitrary and their values have been questioned. Subjects in the upper-normal range of albuminuria seem to be at high risk of progression to micro- or macroalbuminuria and they also had a higher blood pressure than normoalbuminuric subjects in the lower normoalbuminuria range. Diabetic nephropathy screening is made by measuring albumin in spot urine. If abnormal, it should be confirmed in two out three samples collected in a three to six-months interval. Additionally, it is recommended that glomerular filtration rate be routinely estimated for appropriate screening of nephropathy, because some patients present a decreased glomerular filtration rate when urine albumin values are in the normal range. The two main risk factors for diabetic nephropathy are hyperglycemia and arterial hypertension, but the genetic susceptibility in both type 1 and type 2 diabetes is of great importance. Other risk factors are smoking, dyslipidemia, proteinuria, glomerular hyperfiltration and dietary factors. Nephropathy is pathologically characterized in individuals with type 1 diabetes by thickening of glomerular and tubular basal membranes, with progressive mesangial expansion (diffuse or nodular) leading to progressive reduction of glomerular filtration surface. Concurrent interstitial morphological alterations and hyalinization of afferent and efferent glomerular arterioles also occur. Podocytes abnormalities also appear to be involved in the glomerulosclerosis process. In patients with type 2 diabetes, renal lesions are heterogeneous and more complex than in individuals with type 1 diabetes. Treatment of diabetic nephropathy is based on a multiple risk factor approach, and the goal is retarding the development or progression of the disease and to decrease the subject&apos;s increased risk of cardiovascular disease. Achieving the best metabolic control, treating hypertension (&lt;130/80 mmHg) and dyslipidemia (LDL cholesterol &lt;100 mg/dl), using drugs that block the renin-angiotensin-aldosterone system, are effective strategies for preventing the development of microalbuminuria, delaying the progression to more advanced stages of nephropathy and reducing cardiovascular mortality in patients with diabetes.</description>
        <link>http://www.dmsjournal.com/content/1/1/10</link>
                <dc:creator>Themis Zelmanovitz</dc:creator>
                <dc:creator>Fernando Gerchman</dc:creator>
                <dc:creator>Amely Balthazar</dc:creator>
                <dc:creator>Fulvio Thomazelli</dc:creator>
                <dc:creator>Jorge Matos</dc:creator>
                <dc:creator>Luis Canani</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2009, null:10</dc:source>
        <dc:date>2009-09-21T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-1-10</dc:identifier>
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        <title>Stem cell therapy for type 1 diabetes mellitus: a review of recent clinical trials 

</title>
        <description>Stem cell therapy is one of the most promising treatments for the near future. It is expected that this kind of therapy can ameliorate or even reverse some diseases. With regard to type 1 diabetes, studies analyzing the therapeutic effects of stem cells in humans began in 2003 in the Hospital das Cl&#237;nicas of the Faculty of Medicine of Ribeir&#227;o Preto - SP USP, Brazil, and since then other centers in different countries started to randomize patients in their clinical trials. Herein we summarize recent data about beta cell regeneration, different ways of immune intervention and what is being employed in type 1 diabetic patients with regard to stem cell repertoire to promote regeneration and/or preservation of beta cell mass.The Diabetes Control and Complications Trial (DCCT) was a 7-year longitudinal study that demonstrated the importance of the intensive insulin therapy when compared to conventional treatment in the development of chronic complications in patients with type 1 diabetes mellitus (T1DM). This study also demonstrated another important issue: there is a reverse relationship between C-peptide levels (endogenous indicator of insulin secretion) chronic complications - that is, the higher the C-peptide levels, the lower the incidence of nephropathy, retinopathy and hypoglycemia. From such data, beta cell preservation has become an additional target in the management of T1DM 1.</description>
        <link>http://www.dmsjournal.com/content/1/1/19</link>
                <dc:creator>Carlos Eduardo Barra Couri</dc:creator>
                <dc:creator>Julio Cesar Voltarelli</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2009, null:19</dc:source>
        <dc:date>2009-10-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-1-19</dc:identifier>
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        <prism:startingPage>19</prism:startingPage>
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        <item rdf:about="http://www.dmsjournal.com/content/2/1/55">
        <title>Metabolic syndrome, dyslipidemia, hypertension and type 2 diabetes in youth: from diagnosis to treatment</title>
        <description>Overweight and obesity in youth is a worldwide public health problem. Overweight and obesity in childhood and adolescents have a substantial effect upon many systems, resulting in clinical conditions such as metabolic syndrome, early atherosclerosis, dyslipidemia, hypertension and type 2 diabetes (T2D). Obesity and the type of body fat distribution are still the core aspects of insulin resistance and seem to be the physiopathologic links common to metabolic syndrome, cardiovascular disease and T2D. The earlier the appearance of the clustering of risk factors and the higher the time of exposure, the greater will be the chance of developing coronary disease with a more severe endpoint. The age when the event may occur seems to be related to the presence and aggregation of risk factors throughout life.The treatment in this age-group is non pharmacological and aims at promoting changes in lifestyle. However, pharmacological treatments are indicated in special situations.The major goals in dietary treatments are not only limited to weight loss, but also to an improvement in the quality of life. Modification of risk factors associated to comorbidities, personal satisfaction of the child or adolescent and trying to establish healthy life habits from an early age are also important. There is a continuous debate on the best possible exercise to do, for children or adolescents, in order to lose weight. The prescription of physical activity to children and adolescents requires extensive integrated work among multidisciplinary teams, patients and their families, in order to reach therapeutic success.The most important conclusion drawn from this symposium was that if the growing prevalence of overweight and obesity continues at this pace, the result will be a population of children and adolescents with metabolic syndrome. This would lead to high mortality rates in young adults, changing the current increasing trend of worldwide longevity. Government actions and a better understanding of the causes of this problem must be implemented worldwide, by aiming at the prevention of obesity in children and adolescents.</description>
        <link>http://www.dmsjournal.com/content/2/1/55</link>
                <dc:creator>Alfredo Halpern</dc:creator>
                <dc:creator>Marcio Mancini</dc:creator>
                <dc:creator>Maria Eliane Magalhaes</dc:creator>
                <dc:creator>Mauro Fisberg</dc:creator>
                <dc:creator>Rosana Radominski</dc:creator>
                <dc:creator>Marcelo Bertolami</dc:creator>
                <dc:creator>Adriana Bertolami</dc:creator>
                <dc:creator>Maria Edna de Melo</dc:creator>
                <dc:creator>Maria Teresa Zanella</dc:creator>
                <dc:creator>Marcia Queiroz</dc:creator>
                <dc:creator>Marcia Nery</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2010, null:55</dc:source>
        <dc:date>2010-08-18T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-2-55</dc:identifier>
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        <item rdf:about="http://www.dmsjournal.com/content/2/1/44">
        <title>Combination therapy in hypertension: an update</title>
        <description>Meticulous control of blood pressure is required in patients with hypertension to produce the maximum reduction in clinical cardiovascular end points, especially in patients with comorbidities like diabetes mellitus where more aggressive blood pressure lowering might be beneficial. Recent clinical trials suggest that the approach of using monotherapy for the control of hypertension is not likely to be successful in most patients. Combination therapy may be theoretically favored by the fact that multiple factors contribute to hypertension, and achieving control of blood pressure with single agent acting through one particular mechanism may not be possible. Regimens can either be fixed dose combinations or drugs added sequentially one after other. Combining the drugs makes them available in a convenient dosing format, lower the dose of individual component, thus, reducing the side effects and improving compliance. Classes of antihypertensive agents which have been commonly used are angiotensin receptor blockers, thiazide diuretics, beta and alpha blockers, calcium antagonists and angiotensin-converting enzyme inhibitors. Thiazide diuretics and calcium channel blockers are effective, as well as combinations that include renin-angiotensin-aldosterone system blockers, in reducing BP. The majority of currently available fixed-dose combinations are diuretic-based. Combinations may be individualized according to the presence of comorbidities like diabetes mellitus, chronic renal failure, heart failure, thyroid disorders and for special population groups like elderly and pregnant females.</description>
        <link>http://www.dmsjournal.com/content/2/1/44</link>
                <dc:creator>Sanjay Kalra</dc:creator>
                <dc:creator>Bharti Kalra</dc:creator>
                <dc:creator>Navneet Agrawal</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2010, null:44</dc:source>
        <dc:date>2010-06-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-2-44</dc:identifier>
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        <item rdf:about="http://www.dmsjournal.com/content/3/1/35">
        <title>Different exercise protocols improve metabolic syndrome markers, tissue triglycerides content and antioxidant status in rats.</title>
        <description>Background:
An increase in the prevalence of obesity entails great expenditure for governments. Physical exercise is a powerful tool in the combat against obesity and obesity-associated diseases. This study sought to determine the effect of three different exercise protocols on metabolic syndrome and lipid peroxidation markers and the activity of antioxidant enzymes in adult Wistar rats (120 days old).Methods: Animals were randomly divided into four groups: the control (C) group was kept sedentary throughout the study; the aerobic group (A) swam1 h per day, 5days per week, at 80% lactate threshold intensity; the strength group (S) performed strength training with four series of 10jumps, 5 days per week; and the Concurrent group (AS) was trained using the aerobic protocol three days per week and the strength protocol two days per week. Results Groups A and S exhibited a reduction in body weight compared to group C. All exercised animals showed a reduction in triglyceride concentrations in fatty tissues and the liver. Exercised animals also exhibited a reduction in lipid peroxidation markers (TBARS) and an increase in serum superoxide dismutase activity. Animals in group A had increased levels of liver catalase and superoxide dismutase activities. Conclusions We concluded that all physical activity protocols improved the antioxidant systems of the animals and decreased the storage of triglycerides in the investigated tissues.</description>
        <link>http://www.dmsjournal.com/content/3/1/35</link>
                <dc:creator>Jose Botezelli</dc:creator>
                <dc:creator>Lucieli Cambri</dc:creator>
                <dc:creator>Ana Ghezzi</dc:creator>
                <dc:creator>Rodrigo Dalia</dc:creator>
                <dc:creator>Pedro Scariot</dc:creator>
                <dc:creator>Carla Ribeiro</dc:creator>
                <dc:creator>Fabricio Voltarelli</dc:creator>
                <dc:creator>Maria Mello</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2011, null:35</dc:source>
        <dc:date>2011-12-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-3-35</dc:identifier>
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        <item rdf:about="http://www.dmsjournal.com/content/3/1/26">
        <title>Depression, glycemic control and type 2 diabetes</title>
        <description>Background:
Comorbid depression in diabetes has been suggested as one of the possible causes of an inadequate glycemic control. The purpose of this study was to investigate the association between major depression and the glycemic control of type 2 diabetes mellitus (T2DM).
Methods:
Seventy T2DM patients were evaluated. They underwent a psychiatric examination using the following instruments: Structured Clinical Interview for DSM-IV and Beck Depression Inventory. The diabetes status was assessed in the short-term (glycemia, glycated hemoglobin) clinical control.
Results:
The presence of current depression was observed in 18.6% (13/70). In addition, type 2 diabetes patients who displayed depression evidenced higher levels of glycated hemoglobin (8.6 &#177; 2.0 vs. 7.5 &#177; 1.8; p = 0.05) when compared to those who did not exhibit a mood disorder.
Conclusions:
In our sample, the presence of depression seems to impact on the short-term control of T2DM. The authors discuss the clinical utility of these findings in the usual treatment of diabetes.</description>
        <link>http://www.dmsjournal.com/content/3/1/26</link>
                <dc:creator>Marcelo Papelbaum</dc:creator>
                <dc:creator>Rodrigo Moreira</dc:creator>
                <dc:creator>Walmir Coutinho</dc:creator>
                <dc:creator>Rosane Kupfer</dc:creator>
                <dc:creator>Leao Zagury</dc:creator>
                <dc:creator>Silvia Freitas</dc:creator>
                <dc:creator>Jose Appolinario</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2011, null:26</dc:source>
        <dc:date>2011-10-07T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-3-26</dc:identifier>
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        <item rdf:about="http://www.dmsjournal.com/content/3/1/34">
        <title>Nature of Fatty Acids in High Fat Diets Differentially Delineates Obesity-Linked Metabolic Syndrome Components in Male and Female C57BL/6J Mice.</title>
        <description>Background:
Adverse effects of high-fat diets (HFD) on metabolic homeostasis are linked to adipose tissue dysfunction. The goal of this study was to examine the effect of the HFD nature on adipose tissue activity, metabolic disturbances and glucose homeostasis alterations in male mice compared with female mice.
Methods:
C57BL/6J mice were fed either a chow diet or HFD including vegetal (VD) or animal (AD) fat. Body weight, plasmatic parameters and adipose tissue mRNA expression levels of key genes were evaluated after 20 weeks of HFD feeding.
Results:
HFD-fed mice were significantly heavier than control at the end of the protocol. Greater abdominal visceral fat accumulation was observed in mice fed with AD compared to those fed a chow diet or VD. Correlated with weight gain, leptin levels in systemic circulation were increased in HFD-fed mice in both sexes with a significant higher level in AD group compared to VD group. Circulating adiponectin levels as well as adipose tissue mRNA expression levels were significantly decreased in HFD-fed male mice. Although its plasma levels remained unchanged in females, adiponectin mRNA levels were significantly reduced in adipose tissue of both HFD-fed groups with a more marked decrease in AD group compared to VD group. Only HFD-fed male mice were diabetic with increased fasting glycaemia. On the other hand, insulin levels were only increased in AD-fed group in both sexes associated with increased resistin levels. VD did not induce any apparent metabolic alteration in females despite the increased weight gain. Peroxisome Proliferator-Activated Receptors gamma-2 (PPARgamma2) and estrogen receptor alpha (ERalpha) mRNA expression levels in adipose tissue were decreased up to 70% in HFD-fed mice but were more markedly reduced in male mice as compared with female mice.
Conclusions:
The nature of dietary fat determines the extent of metabolic alterations reflected in adipocytes through modifications in the pattern of adipokines secretion and modulation of key genes mRNA expression. Compared with males, female mice demonstrate higher capacity in controlling glucose homeostasis in response to 20 weeks HFD feeding. Our data suggest gender specific interactions between the diet&apos;s fatty acid source, the adipocyte-secreted proteins and metabolic disorders.</description>
        <link>http://www.dmsjournal.com/content/3/1/34</link>
                <dc:creator>Souhad El Akoum</dc:creator>
                <dc:creator>Vikie Lamontagne</dc:creator>
                <dc:creator>Isabelle Cloutier</dc:creator>
                <dc:creator>Jean-Francois Tanguay</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2011, null:34</dc:source>
        <dc:date>2011-12-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-3-34</dc:identifier>
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                <prism:publicationName>Diabetology &amp; Metabolic Syndrome</prism:publicationName>
        <prism:issn>1758-5996</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>34</prism:startingPage>
        <prism:publicationDate>2011-12-14T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.dmsjournal.com/content/3/1/12">
        <title>Visceral adiposity, insulin resistance and cancer risk</title>
        <description>Background:
There is a well established link between obesity and cancer. Emerging research is characterising this relationship further and delineating the specific role of excess visceral adiposity, as opposed to simple obesity, in promoting tumorigenesis. This review summarises the evidence from an epidemiological and pathophysiological perspective.
Methods:
Relevant medical literature was identified from searches of PubMed and references cited in appropriate articles identified. Selection of articles was based on peer review, journal and relevance.
Results:
Numerous epidemiological studies consistently identify increased risk of developing carcinoma in the obese. Adipose tissue, particularly viscerally located fat, is metabolically active and exerts systemic endocrine effects. Putative pathophysiological mechanisms linking obesity and carcinogenesis include the paracrine effects of adipose tissue and systemic alterations associated with obesity. Systemic changes in the obese state include chronic inflammation and alterations in adipokines and sex steroids. Insulin and the insulin-like growth factor axis influence tumorigenesis and also have a complex relationship with adiposity. There is evidence to suggest that insulin and the IGF axis play an important role in mediating obesity associated malignancy.
Conclusions:
There is much evidence to support a role for obesity in cancer progression, however further research is warranted to determine the specific effect of excess visceral adipose tissue on tumorigenesis. Investigation of the potential mechanisms underpinning the association, including the role of insulin and the IGF axis, will improve understanding of the obesity and cancer link and may uncover targets for intervention.</description>
        <link>http://www.dmsjournal.com/content/3/1/12</link>
                <dc:creator>Claire Donohoe</dc:creator>
                <dc:creator>Suzanne Doyle</dc:creator>
                <dc:creator>John Reynolds</dc:creator>
                <dc:source>Diabetology &amp; Metabolic Syndrome 2011, null:12</dc:source>
        <dc:date>2011-06-22T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1758-5996-3-12</dc:identifier>
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                <prism:publicationName>Diabetology &amp; Metabolic Syndrome</prism:publicationName>
        <prism:issn>1758-5996</prism:issn>
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        <prism:startingPage>12</prism:startingPage>
        <prism:publicationDate>2011-06-22T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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