Experimental Diabetes Research最新文献

{"title":"A protocol for measurement of noncoding RNA in human serum.","authors":"Caroline J Taylor,&nbsp;Sarang N Satoor,&nbsp;Amaresh K Ranjan,&nbsp;Maria V Pereira e Cotta,&nbsp;Mugdha V Joglekar","doi":"10.1155/2012/168368","DOIUrl":"https://doi.org/10.1155/2012/168368","url":null,"abstract":"<p><p>MicroRNAs (miRNAs) are small noncoding RNAs that act as regulators of gene expression by targeting mature messenger RNAs. Following the initial report of the presence of miRNAs in serum and plasma a number of studies have successfully demonstrated the use of these miRNAs as biomarkers of disease. Currently, there are many methods of isolating total RNA from liquid samples. Here, we describe a simple, cost effective method for extraction of RNA from human serum as well as subsequent real time PCR analysis of miRNA levels.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"168368"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/168368","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30773934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blockade of renin angiotensin system increased resistance to STZ-induced diabetes in rats with long-term high-fat diet.","authors":"Xin Li,&nbsp;Li Yuan,&nbsp;Jin Li,&nbsp;Hailing Li,&nbsp;Suosuo Cheng","doi":"10.1155/2012/618923","DOIUrl":"https://doi.org/10.1155/2012/618923","url":null,"abstract":"<p><p>This study aimed to investigate whether rennin-angiotensin system (RAS) blockade through telmisartan would increase the resistance to streptozotocin- (STZ-) induced diabetes in insulin resistance rats. There were sixty Wistar rats that were divided into four groups: normal control (NC), high-fat diet (HF), high-fat diet plus STZ injection (HF+S), and high-fat diet plus STZ injection and telmisartan intervention (HF+S+T). Five rats were chosen randomly and respectively from groups NC and HF to undergo a hyperinsulinemic euglycemic clamp. Another five rats were selected randomly from the four groups, respectively, for intravenous injection insulin releasing test (IVIRT), and the other five rats for pancreas specimens used in islet cell immunohistochemistry staining (stained for insulin, NF-κB, and caspase-3), islet cell apoptosis staining, and reverse transcription PCR (AT1R and IL-1 beta). There was a significant difference of overt diabetes incidence between groups HF+S+T and HF+S (P < 0.05). Furthermore, inflammatory markers and islet cell apoptosis were found to be significantly reduced in group HF+S+T compared with group HF+S (all P < 0.01 or P < 0.05). Overall, telmisartan-treated rats were found to have reduced RAS activity, increased resistance to STZ-induced diabetes, reduced inflammatory markers, and improvement of islet cell function and morphology.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"618923"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/618923","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31084260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increased oxidative stress and imbalance in antioxidant enzymes in the brains of alloxan-induced diabetic rats.","authors":"Luciane B Ceretta,&nbsp;Gislaine Z Réus,&nbsp;Helena M Abelaira,&nbsp;Karine F Ribeiro,&nbsp;Giovanni Zappellini,&nbsp;Francine F Felisbino,&nbsp;Amanda V Steckert,&nbsp;Felipe Dal-Pizzol,&nbsp;João Quevedo","doi":"10.1155/2012/302682","DOIUrl":"https://doi.org/10.1155/2012/302682","url":null,"abstract":"<p><p>Diabetes Mellitus (DM) is associated with pathological changes in the central nervous system (SNC) as well as alterations in oxidative stress. Thus, the main objective of this study was to evaluate the effects of the animal model of diabetes induced by alloxan on memory and oxidative stress. Diabetes was induced in Wistar rats by using a single injection of alloxan (150 mg/kg), and fifteen days after induction, the rats memory was evaluated through the use of the object recognition task. The oxidative stress parameters and the activity of antioxidant enzymes, superoxide dismutase (SOD), and catalase (CAT) were measured in the rat brain. The results showed that diabetic rats did not have alterations in their recognition memory. However, the results did show that diabetic rats had increases in the levels of superoxide in the prefrontal cortex, and in thiobarbituric acid reactive species (TBARS) production in the prefrontal cortex and in the amygdala in submitochondrial particles. Also, there was an increase in protein oxidation in the hippocampus and striatum, and in TBARS oxidation in the striatum and amygdala. The SOD activity was decreased in diabetic rats in the striatum and amygdala. However, the CAT activity was increased in the hippocampus taken from diabetic rats. In conclusion, our findings illustrate that the animal model of diabetes induced by alloxan did not cause alterations in the animals' recognition memory, but it produced oxidants and an imbalance between SOD and CAT activities, which could contribute to the pathophysiology of diabetes.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"302682"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/302682","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30653179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficient differentiation of mouse embryonic stem cells into insulin-producing cells.","authors":"Szu-Hsiu Liu,&nbsp;Lain-Tze Lee","doi":"10.1155/2012/201295","DOIUrl":"https://doi.org/10.1155/2012/201295","url":null,"abstract":"<p><p>Embryonic stem (ES) cells are a potential source of a variety of differentiated cells for cell therapy, drug discovery, and toxicology screening. Here, we present an efficacy strategy for the differentiation of mouse ES cells into insulin-producing cells (IPCs) by a two-step differentiation protocol comprising of (i) the formation of definitive endoderm in monolayer culture by activin A, and (ii) this monolayer endoderm being induced to differentiate into IPCs by nicotinamide, insulin, and laminin. Differentiated cells can be obtained within approximately 7 days. The differentiation IPCs combined application of RT-PCR, ELISA, and immunofluorescence to characterize phenotypic and functional properties. In our study, we demonstrated that IPCs produced pancreatic transcription factors, endocrine progenitor marker, definitive endoderm, pancreatic β-cell markers, and Langerhans α and δ cells. The IPCs released insulin in a manner that was dose dependent upon the amount of glucose added. These techniques may be able to be applied to human ES cells, which would have very important ramifications for treating human disease.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"201295"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/201295","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30857348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antioxidant sol-gel improves cutaneous wound healing in streptozotocin-induced diabetic rats.","authors":"Yen-Hsien Lee,&nbsp;Jung-Jhih Chang,&nbsp;Chiang-Ting Chien,&nbsp;Ming-Chien Yang,&nbsp;Hsiung-Fei Chien","doi":"10.1155/2012/504693","DOIUrl":"https://doi.org/10.1155/2012/504693","url":null,"abstract":"<p><p>We examined the effects of vitamin C in Pluronic F127 on diabetic wound healing. Full-thickness excision skin wounds were made in normal and diabetic Wistar rats to evaluate the effect of saline, saline plus vitamin C (antioxidant sol), Pluronic F127, or Pluronic F127 plus vitamin C (antioxidant sol-gel). The rate of wound contraction, the levels of epidermal and dermal maturation, collagen synthesis, and apoptosis production in the wound tissue were determined. In vitro data showed that after 6 hours of air exposure, the order of the scavenging abilities for HOCl, H(2)O(2), and O(2) (-) was antioxidant sol-gel > antioxidant saline > Pluronic F127 = saline. After 7 and 14 days of wound injury, the antioxidant sol-gel improved wound healing significantly by accelerated epidermal and dermal maturation, an increase in collagen content, and a decrease in apoptosis formation. However, the wounds of all treatments healed mostly at 3 weeks. Vitamin C in Pluronic F127 hastened cutaneous wound healing by its antioxidant and antiapoptotic mechanisms through a good drug delivery system. This study showed that Pluronic F127 plus vitamin C could potentially be employed as a novel wound-healing enhancer.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"504693"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/504693","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30857349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlation between blood activin levels and clinical parameters of type 2 diabetes.","authors":"Hui Wu,&nbsp;Michael Wu,&nbsp;Yi Chen,&nbsp;Carolyn A Allan,&nbsp;David J Phillips,&nbsp;Mark P Hedger","doi":"10.1155/2012/410579","DOIUrl":"https://doi.org/10.1155/2012/410579","url":null,"abstract":"<p><strong>Aims: </strong>Activins A and B, and their binding protein, follistatin, regulate glucose metabolism and inflammation. Consequently, their role in type 2 diabetes (T2D) was examined.</p><p><strong>Methods: </strong>Blood was taken from fasted participants (34 males; 58 females; 50-75 years) with diabetes or during an oral glucose tolerance test (OGTT). Clinical parameters were assessed, and blood assayed for activins, follistatin, and C-reactive protein.</p><p><strong>Results: </strong>Serum levels of activin A (93.3 ± 27.0 pg/mL, mean ± SD), B (81.8 ± 30.8 pg/mL), or follistatin (6.52 ± 3.15 ng/mL) were not different (P > 0.05) between subjects with normal OGTT (n = 39), impaired glucose tolerance and/or fasting glucose (n = 17), or T2D (n = 36). However, activin A and/or activin B were positively correlated with parameters of insulin resistance and T2D, including fasting glucose (P < 0.001), fasting insulin (P = 0.02), glycated hemoglobin (P = 0.003), and homeostasis model assessment of insulin resistance (HOMA-IR; P < 0.001). Follistatin was positively correlated with HOMA-IR alone (P = 0.01).</p><p><strong>Conclusions: </strong>These data indicate that serum measurements of activin A, B, or follistatin cannot discriminate risk for T2D in individual patients, but the activins display a positive relationship with clinical parameters of the disease.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"410579"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/410579","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31147458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation and oxidative stress in obesity, metabolic syndrome, and diabetes.","authors":"Pietro Galassetti","doi":"10.1155/2012/943706","DOIUrl":"https://doi.org/10.1155/2012/943706","url":null,"abstract":"I do not think anybody even remotely connected with the field of diabetes, either as a researcher or as a health care provider, would have any serious objection to the concept that some degree of altered inflammatory activity or oxidative stress plays a serious role in multiple aspects of diabetes. Just to mention two of the best-known processes, a violent, acute inflammatory event leads to the destruction of beta cells at the onset of type 1 diabetes, and a chronic, subclinical proinflammatory state is at the base of the slow development of micro- and macrovascular complications accounting for the larger part of morbidity and mortality related to all forms of diabetes. This connection has led to a remarkable increase in research activity in this field in recent years. Running a PubMed search with “inflammation and diabetes” as search terms, for instance, returns 14,059 articles; “Oxidative stress and diabetes” 8850 articles; “inflammation and atherosclerosis” 11209 articles; and “inflammation and cardiovascular disease” 49245 articles. To a smaller extent, the very content of this special issue is a clear example of the variety and complexity of issues in the prevention, diagnosis, management, and therapy of diabetes, in which one or more inflammatory or oxidative stress component plays a critical role. \u0000 \u0000Inflammation and oxidative stress, however, are two extremely broad and comprehensive terms. This wealth of studies and results certainly clarified a large number of pathways, mediators and regulatory mechanisms, genes and posttranscriptional regulators of gene expression related to inflammation and oxidative stress. However, given the very large, and constantly growing, number of cell types and molecules involved, it often feels as though the rate at which new questions accumulate far exceeds the rate at which prior questions are definitively answered. We have now identified hundreds of cytokines and chemokines, whose full physiological function remains in many cases nebulous. Terms such as “pro” or “anti-inflammatory,” earlier closely associated with individual inflammatory mediators (such as the classically defined proinflammatory interleukin-6), are now used more reluctantly, as the same molecules often display less clear-cut activity, or even shift from one end of the spectrum to the other, depending on the surrounding metabolic or cell-signaling milieu. More importantly, often only some components of the complex inflammatory network are altered in a specific pathological condition. Identifying what these components are, and using them as biomarkers of onset, progression or response to treatment of a given condition has become one the main focuses of inflammatory research. Again, however, the immense diversity of these biomarkers renders the task extremely difficult. Let us hypothesize, for the sake of discussion, that a group of cytokines, or certain leukocyte surface markers of activation, are definitively demonstrated to increase signi","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"943706"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/943706","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31161737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of autonomic dysfunction associated with aging and type 2 diabetes on daily life activities.","authors":"Jerrold Petrofsky,&nbsp;Lee Berk,&nbsp;Hani Al-Nakhli","doi":"10.1155/2012/657103","DOIUrl":"https://doi.org/10.1155/2012/657103","url":null,"abstract":"<p><p>Type 2 diabetes (T2D) and ageing have well documented effects on every organ in the body. In T2D the autonomic nervous system is impaired due to damage to neurons, sensory receptors, synapses and the blood vessels. This paper will concentrate on how autonomic impairment alters normal daily activities. Impairments include the response of the blood vessels to heat, sweating, heat transfer, whole body heating, orthostatic intolerance, balance, and gait. Because diabetes is more prevalent in older individuals, the effects of ageing will be examined. Beginning with endothelial dysfunction, blood vessels have impairment in their ability to vasodilate. With this and synaptic damage, the autonomic nervous system cannot compensate for effectors such as pressure on and heating of the skin. This and reduced ability of the heart to respond to stress, reduces autonomic orthostatic compensation. Diminished sweating causes the skin and core temperature to be high during whole body heating. Impaired orthostatic tolerance, impaired vision and vestibular sensing, causes poor balance and impaired gait. Overall, people with T2D must be made aware and counseled relative to the potential consequence of these impairments.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"657103"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/657103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30601587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal podocyte injury in a rat model of type 2 diabetes is prevented by metformin.","authors":"Junghyun Kim,&nbsp;Eunjin Shon,&nbsp;Chan-Sik Kim,&nbsp;Jin Sook Kim","doi":"10.1155/2012/210821","DOIUrl":"https://doi.org/10.1155/2012/210821","url":null,"abstract":"<p><p>Hyperglycemia promotes oxidative stress and hence generation of reactive oxygen species (ROS), which is known to play a crucial role in the pathogenesis of diabetic nephropathy. Metformin, an oral hypoglycemic drug, possesses antioxidant effects. The aim of this paper is to investigate the protective effects of metformin on the injury of renal podocytes in spontaneously diabetic Torii (SDT) rats, a new model for nonobese type 2 diabetes. Metformin (350 mg/kg/day) was given to SDT rats for 17 weeks. Blood glucose, glycated haemoglobin (HbA1c), and albuminuria were examined. Kidney histopathology, renal 8-hydroxydeoxyguanosine (8-OHdG) levels and apoptosis were examined. In 43-week-old SDT rats, severe hyperglycemia was developed, and albuminuria was markedly increased. Diabetes induced significant alterations in renal glomerular structure. In addition, urinary and renal 8-OHdG levels were highly increased, and podocyte loss was shown through application of the TUNEL and synaptopodin staining. However, treatment of SDT rats with metformin restored all these renal changes. Our data suggested that diabetes-induced podocyte loss in diabetic nephropathy could be suppressed by the antidiabetes drug, metformin, through the repression of oxidative injury.</p>","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"210821"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/210821","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30969109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diabetes and cancer: epidemiological, clinical, and experimental perspectives.","authors":"Chin-Hsiao Tseng,&nbsp;Chien-Jen Chen,&nbsp;Joseph R Landolph","doi":"10.1155/2012/101802","DOIUrl":"https://doi.org/10.1155/2012/101802","url":null,"abstract":"Diabetes is a major cause of death in many countries due to its increasing incidence, high prevalence, and clinical manifestation of a variety of micro- and macrovascular complications if it is not appropriately treated [1, 2]. Recent studies have shown that diabetic patients may also have a higher risk of cancer [2], the number one killer that threatens the lives of billions of people.","PeriodicalId":12109,"journal":{"name":"Experimental Diabetes Research","volume":"2012 ","pages":"101802"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/101802","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30990353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}