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| 1 | 脓毒症高血糖与胰岛素强化治疗策略显示文摘 | 姚咏明 孟海东 | 2006 | 中国危重病急救医学2006，18，2： | 84 |
| 2 | Oxidative stress,insulin resistance,dyslipidemia and type 2 diabetes mellitus显示文摘Oxidative stress is increased in metabolic syndrome and type 2 diabetes mellitus(T2DM) and this appears to underlie the development of cardiovascular disease,T2 DM and diabetic complications.Increased oxidative stress appears to be a deleterious factor leading toinsulin resistance,dyslipidemia,β-cell dysfunction,impaired glucose tolerance and ultimately leading to T2 DM.Chronic oxidative stress,hyperglycemia and dyslipidemia are particularly dangerous for β-cells from lowest levels of antioxidant,have high oxidative energy requirements,decrease the gene expression of key β-cell genes and induce cell death.If β-cell functioning is impaired,it results in an under production of insulin,impairs glucose stimulated insulin secretion,fasting hyperglycemia and eventually the development of T2 DM. | Surapon Tangvarasittichai | 2015 | World Journal of Diabetes2015，6，3： | 95 |
| 3 | Osteoporosis in diabetes mellitus: Possible cellular and molecular mechanisms显示文摘Osteoporosis,a global age-related health problem in both male and female elderly,insidiously deteriorates the microstructure of bone,particularly at trabecular sites,such as vertebrae,ribs and hips,culminating in fragility fractures,pain and disability.Although osteoporosis is normally associated with senescence and estrogen deficiency,diabetes mellitus(DM),especially type 1 DM,also contributes to and/or aggravates bone loss in osteoporotic patients.This topic highlight article focuses on DM-induced osteoporosis and DM/ osteoporosis comorbidity,covering alterations in bone metabolism as well as factors regulating bone growth under diabetic conditions including,insulin,insulin-like growth factor-1 and angiogenesis.Cellular and molecular mechanisms of DM-related bone loss are also discussed.This information provides a foundation for the better understanding of diabetic complications and for development of early screening and prevention of osteoporosis in diabetic patients. | Kannikar Wongdee Narattaphol Charoenphandhu | 2011 | World Journal of Diabetes2011，2，3： | 51 |
| 4 | Non-alcoholic fatty liver disease and obesity: Biochemical, metabolic and clinical presentations显示文摘Non-alcoholic fatty liver disease(NAFLD)is the most common liver disease in the world.Presentation of the disease ranges from simple steatosis to non-alcoholic steatohepatitis(NASH).NAFLD is a hepatic manifestation of metabolic syndrome that includes central abdominal obesity along with other components.Up to80%of patients with NAFLD are obese,defined as a body mass index(BMI)>30 kg/m2.However,the distribution of fat tissue plays a greater role in insulin resistance than the BMI.The large amount of visceral adipose tissue(VAT)in morbidly obese(BMI>40 kg/m2)individuals contributes to a high prevalence of NAFLD.Free fatty acids derived from VAT tissue,as well as from dietary sources and de novo lipogenesis,are released to the portal venous system.Excess free fatty acids and chronic low-grade inflammation from VAT are considered to be two of the most important factors contributing to liver injury progression in NAFLD.In addition,secretion of adipokines from VAT as well as lipid accumulation in the liver further promotes inflammation through nuclear factor kappa B signaling pathways,which are also activated by free fatty acids,and contribute to insulin resistance.Most NAFLD patients are asymptomatic on clinical presentation,even though some may present with fatigue,dyspepsia,dull pain in the liver and hepatosplenomegaly.Treatment for NAFLD and NASH involves weight reduction through lifestyle modifications,anti-obesity medication and bariatric surgery.This article reviews the available information on the biochemical and metabolic phenotypes associated with obesity and fatty liver disease.The relative contribution of visceral and liver fat to insulin resistance is discussed,and recommendations for clinical evaluation of affected individuals is provided. | Sandra Milic Davorka Lulic Davor Stimac | 2014 | World Journal of Gastroenterology2014，20，28： | 52 |
| 5 | Biomolecular basis of the role of diabetes mellitus in osteoporosis and bone fractures显示文摘Osteoporosis has become a serious health problem throughout the world which is associated with an increased risk of bone fractures and mortality among the people of middle to old ages.Diabetes is also a major health problem among the people of all age ranges and the sufferers due to this abnormality increasing day by day.The aim of this review is to summarize the possible mechanisms through which diabetes may induce osteoporosis.Diabetes mellitus generally exerts its effect on different parts of the body including bone cells specially the osteoblast and osteoclast,muscles,retina of the eyes,adipose tissue,endocrine system specially parathyroid hormone(PTH) and estrogen,cytokines,nervous system and digestive system.Diabetes negatively regulates osteoblast differentiation and function while positively regulates osteoclast differentiation and function through the regulation of different intermediate factors and thereby decreases bone formation while increases bone resorption.Some factors such as diabetic neuropathy,reactive oxygen species,Vitamin D,PTH have their effects on muscle cells.Diabetes decreases the muscle strength through regulating these factors in various ways and ultimately increases the risk of fall that may cause bone fractures. | Bipradas Roy | 2013 | World Journal of Diabetes2013，4，4： | 41 |
| 6 | Metabolic syndrome and non-alcoholic fatty liver disease:Asian definitions and Asian studies显示文摘BACKGROUND: Non-alcoholic fatty liver disease (NAFLD), as conventionally recognized, is a metabolic disorder largely confined to residents of affluent industrialized Western countries. However, obesity and insulin resistance are not restricted to the West, as witnessed by their increasingly universal distribution. In particular, there has been an upsurge in metabolic syndrome in the Asia-Pacific region, although there are critical differences in the extent of adiposity between Eastern and Western populations. DATA SOURCES: An English-language literature search using PubMed (1999-2007) on obesity, metabolic syndrome and NAFLD, focusing on Asian definitions and Asian studies. RESULTS: NAFLD appears to be of long-standing insulin resistance and likely represents the hepatic manifestation of the metabolic syndrome. With insulin resistance as a common factor, the disease is associated with atherosclerosis and cardiovascular risk. All features of the metabolic syndrome and related events are assessed for practical management of NAFLD, although the criteria for the diagnosis of obesity and central obesity differ across racial groups. CONCLUSIONS: The increasing prevalence of obesity, coupled with diabetes, dyslipidemia, hypertension and ultimately metabolic syndrome, puts a very large population at risk of developing NAFLD in the coming decades. The simultaneous identification and appropriate treatment of the components of metabolic syndrome are crucial to reduce hepatic as well as cardiovascular morbidity and mortality. | Fan, Jian-Gao Peng, Yong-De | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，6： | 42 |
| 7 | Targeting inflammation in diabetes: Newer therapeutic options显示文摘Inflammation has been recognised to both decrease beta cell insulin secretion and increase insulin resis-tance. Circulating cytokines can affect beta cell function directly leading to secretory dysfunction and increased apoptosis. These cytokines can also indirectly affect beta cell function by increasing adipocyte inflamma-tion.The resulting glucotoxicity and lipotoxicity further enhance the inflammatory process resulting in a vicious cycle. Weight reduction and drugs such as metformin have been shown to decrease the levels of C-Reactive Protein by 31% and 13%, respectively. Pioglitazone, insulin and statins have anti-inflammatory effects. In-terleukin 1 and tumor necrosis factor-α antagonists are in trials and NSAIDs such as salsalate have shown an improvement in insulin sensitivity. Inhibition of 12-lipo-oxygenase, histone de-acetylases, and activation of sirtuin-1 are upcoming molecular targets to reduce in-flammation. These therapies have also been shown to decrease the conversion of pre-diabetes state to diabe-tes. Drugs like glicazide, troglitazone, N-acetylcysteine and selective COX-2 inhibitors have shown benefit in diabetic neuropathy by decreasing inflammatory mark-ers. Retinopathy drugs are used to target vascular en-dothelial growth factor, angiopoietin-2, various protein-ases and chemokines. Drugs targeting the proteinases and various chemokines are pentoxifylline, inhibitors of nuclear factor-kappa B and mammalian target of rapa-mycin and are in clinical trials for diabetic nephropathy. Commonly used drugs such as insulin, metformin, per-oxisome proliferator-activated receptors, glucagon like peptide-1 agonists and dipeptidyl peptidase-4 inhibitors also decrease inflammation. Anti-inflammatory thera-pies represent a potential approach for the therapy of diabetes and its complications. | Neeraj Kumar Agrawal Saket Kant | 2014 | World Journal of Diabetes2014，5，5： | 41 |
| 8 | 新诊断2型糖尿病患者的短期胰岛素强化治疗意义显示文摘 | 祝群 | 2005 | 中国实用内科杂志2005，25，6： | 48 |
| 9 | WJD 5^(th) Anniversary Special Issues(2): Type 2 diabetes Type 2 diabetes and cardiovascular disease: Have all risk factors the same strength?显示文摘Diabetes mellitus is a chronic condition that occurs when the body cannot produce enough or effectively use of insulin.Compared with individuals without diabetes,patients with type 2 diabetes mellitus have a considerably higher risk of cardiovascular morbidity and mortality,and are disproportionately affected by cardiovascular disease.Most of this excess risk is it associated with an augmented prevalence of well-known risk factors such as hypertension,dyslipidaemia and obesity in these patients.However the improved cardiovascular disease in type 2 diabetes mellitus patients can not be attributed solely to the higher prevalence of traditional risk factors.Therefore other non-traditional risk factors may be important in people with type 2 diabetes mellitus.Cardiovascular disease is increased in type 2 diabetes mellitus subjects due to a complex combination of various traditional and non-traditional risk factors that have an important role to play in the beginning and the evolution of atherosclerosis over its long natural history from endothelial function to clinical events.Many of these risk factors could be common history for both di-abetes mellitus and cardiovascular disease,reinforcing the postulate that both disorders come independently from'common soil'.The objective of this review is to highlight the weight of traditional and non-traditional risk factors for cardiovascular disease in the setting of type 2 diabetes mellitus and discuss their position in the pathogenesis of the excess cardiovascular disease mortality and morbidity in these patients. | Iciar Martín-Timón Cristina Sevillano-Collantes Amparo Segura-Galindo Francisco Javier del Caizo-Gómez | 2014 | World Journal of Diabetes2014，5，4： | 32 |
| 10 | Changing trends in management of gestational diabetes mellitus显示文摘Gestational diabetes mellitus(GDM)is on the rise globally.In view of the increasing prevalence of GDM and fetal and neonatal complications associated with it,there is a splurge of research in this field and management of GDM is undergoing a sea change.Trends are changing in prevention,screening,diagnosis,treatment and future follow up.There is emerging evidence regarding use of moderate exercise,probiotics and vitamin D in the prevention of GDM.Regarding treatment,newer insulin analogs like aspart,lispro and detemir are associated with better glycemic control than older insulins.Continuous glucose monitoring systems and continuous subcutaneous insulin systems may play a role in those who require higher doses of insulin for sugar control.Evidence exists that favors metformin as a safer alternative to insulin in view of good glycemic control and better perinatal outcomes.As the risk of developing GDM in subsequent pregnancies and also the risk of overt diabetes in later life is high,regular assessment of these women is required in future.Lifestyle interventions or metformin should be offered to women with a history of GDM who develop pre-diabetes.Further studies are required in the field of prevention of GDM for optimizing obstetric outcome. | Gunasekaran Kala Poomalar | 2015 | World Journal of Diabetes2015，6，2： | 32 |
| 11 | Nonalcoholic fatty liver disease as a multi-systemic disease显示文摘Nonalcoholic fatty liver disease(NAFLD) is the most common cause of chronic liver disease. NAFLD includes a wide spectrum of liver conditions ranging from simple steatosis to nonalcoholic steatohepatitis and advanced hepatic fibrosis. NAFLD has been recognized as a hepatic manifestation of metabolic syndrome linked with insulin resistance. NAFLD should be considered not only a liver specific disease but also an early mediator of systemic diseases. Therefore, NAFLD is usually associated with cardiovascular disease, chronic kidney disease, type 2 diabetes, obesity, and dyslipidemia. NAFLD is highly prevalent in the general population and is associated with increased cardiovascular morbidity and mortality. The underlying mechanisms and pathogenesis of NAFLD with regard to other medical disorders are not yet fully understood. This review focuses on pathogenesis of NAFLD and its relation with other systemic diseases. | Hakan Fotbolcu Elcin Zorlu | 2016 | World Journal of Gastroenterology2016，22，16： | 29 |
| 12 | Effects of probiotics on nonalcoholic fatty liver disease:A meta-analysis显示文摘AIM:To investigate the relationship between the gutliver axis and nonalcoholic fatty liver disease(NAFLD),we performed a meta-analysis to evaluate the effects of probiotic therapy in NAFLD.METHODS:We searched PubMed,Medline,Embase,Web of Science,the Cochrane Library and Chinese Biomedicine Database for all relevant randomized controlled trials on probiotics in patients with NAFLD/nonalcoholic steatohepatitis(NASH).A statistical analysis was performed using RevMan 5.0 software.RESULTS:Four randomized trials involving 134 NAFLD/NASH patients were included.The results showed that probiotic therapy signifcantly decreased alanine aminotransferase(ALT),aspartate transaminase(AST),total-cholesterol(T-chol),high density lipoprotein(HDL),tumor necrosis factor(TNF)-αand homeostasis model assessment of insulin resistance(HOMAIR)[ALT:weighted mean difference(WMD)-23.71,95%CI:-33.46--13.95,P<0.00001;AST:WMD-19.77,95%CI:-32.55--7.00,P=0.002;T-chol:WMD-0.28,95%CI:-0.55--0.01,P=0.04;HDL:WMD-0.09,95%CI:-0.16-0.01,P=0.03;TNF-α:WMD-0.32,95%CI:-0.48--0.17,P<0.0001;HOMA-IR:WMD-0.46,95%CI:-0.73--0.19,P=0.0008].However,the use of probiotics was not associated with changes in body mass index(BMI),glucose(GLU)and low density lipoprotein(LDL)(BMI:WMD 0.05,95%CI:-0.18-0.29,P=0.64;GLU:WMD 0.05,95%CI:-0.25-0.35,P=0.76;LDL:WMD-0.38,95%CI:-0.78-0.02,P=0.06).CONCLUSION:Probiotic therapies can reduce liver aminotransferases,total-cholesterol,TNF-αand improve insulin resistance in NAFLD patients.Modulation of the gut microbiota represents a new treatment for NAFLD. | Yan-Yan Ma Lin Li Chao-Hui Yu Zhe Shen Li-Hua Chen You-Ming Li | 2013 | World Journal of Gastroenterology2013，19，40： | 28 |
| 13 | Helicobacter pylori infection and diabetes:Is it a myth or fact?显示文摘Helicobacter pylori(H.pylori)is one of the most common human bacterial pathogens,and infection causes a wide array of gastric disorders,including simple gastritis,peptic ulcers and gastric malignancies.Gastrointestinal inflammation caused by H.pylori can influence the absorption of glucose and lipids,which are also abnormal in diabetes mellitus.Type 2 diabetes mellitus(T2DM),formerly known as non-insulin-dependent diabetes mellitus or adult-onset diabetes,is a metabolic disorder that is characterized by high levels of blood glucose resulting from insulin resistance and relative insulin deficiency.It is an emerging pandemic and is rapidly becoming a serious threat to public health.Emerging data now indicate a strong relationship between H.pylori infection and the incidence of T2DM.The mechanisms underlying the pathogenesis of diabetes are complex,involving insulin resistance,chronic inflammation,insulin secretion deficiency as a result of pancreasβ-cell dysfunction,glucotoxicity,and lipotoxicity.H.pylori infection is known to be involved in the pathogenesis of insulin resistance,and the growing awareness of its role in diabetes is important for the early detection of glucose dysregulation and prevention of T2DM in high-risk communities.This review probes the possible relationship between H.pylori and diabetes according to epidemiological surveys and discusses putative mechanisms underlying this correlation. | Cong He Zhen Yang Nong-Hua Lu | 2014 | World Journal of Gastroenterology2014，20，16： | 28 |
| 14 | Coronary microvascular dysfunction in diabetes mellitus:A review显示文摘The exploration of coronary microcirculatory dysfunction in diabetes has accelerated in recent years.Cardiac function is compromised in diabetes.Diabetic patients manifest accelerated atherosclerosis in coronary arteries.These data are confirmed in diabetic animal mod-els,where lesions of small coronary arteries have been described.These concepts are epitomized in the classic microvascular complications of diabetes,i.e.blindness,kidney failure and distal dry gangrene.Most importantly,accumulating data indicate that insights gained from the link between inflammation and diabetes can yield predictive and prognostic information of considerable clinical utility.This review summarizes the evidence for the predisposing factors and the mechanisms involved in diabetes,and assesses the current state of knowledge regarding the triggers for inflammation in this disease.We evaluate the roles of hyperglycemia,oxidative stress,polyol pathway,protein kinase C,advanced glycation end products,insulin resistance,peroxisome proliferator-activated receptor-γ,inflammation,and diabetic cardiomyopathy as a 'stem cell disease'.Furthermore,we discuss the mechanisms responsible for impaired coronary arteriole function.Finally,we consider how new insights in diabetes may provide innovative therapeutic strategies. | Andrea Picchi Stefano Capobianco Marta Focardi | 2010 | World Journal of Cardiology2010，2，11： | 24 |
| 15 | Molecular mechanisms of insulin resistance in type 2 diabetes mellitus显示文摘Free fatty acids are known to play a key role in promoting loss of insulin sensitivity in type 2 diabetes mellitus but the underlying mechanism is still unclear.It has been postulated that an increase in the intracellular concentration of fatty acid metabolites activates a serine kinase cascade,which leads to defects in insu-lin signaling downstream to the insulin receptor.In addition,the complex network of adipokines released from adipose tissue modulates the response of tissues to insulin.Among the many molecules involved in the intracellular processing of the signal provided by insulin,the insulin receptor substrate-2,the protein kinase B and the forkhead transcription factor Foxo 1a are of particular interest,as recent data has provided strong evidence that dysfunction of these proteins results in insulin resistance in vivo.Recently,studies have revealed that phosphoinositidedependent kinase 1-independent phosphorylation of protein kinase Cε causes a reduction in insulin receptor gene expression.Additionally,it has been suggested that mitochondrial dysfunction triggers activation of several serine kinases,and weakens insulin signal transduction.Thus,in this review,the current developments in understanding the pathophysiological processes of insulin resistance in type 2 diabetes have been summarized.In addition,this study provides potential new targets for the treatment and prevention of type 2 diabetes. | Vandana Saini | 2010 | World Journal of Diabetes2010，1，3： | 23 |
| 16 | Dipeptidyl peptidase-4: A key player in chronic liver disease显示文摘Dipeptidyl peptidase-4 (DPP-4) is a membrane-associated peptidase, also known as CD26. DPP-4 has widespread organ distribution throughout the body and exerts pleiotropic effects via its peptidase activity. A representative target peptide is glucagon-like peptide-1, and inactivation of glucagon-like peptide-1 results in the development of glucose intolerance/diabetes mellitus and hepatic steatosis. In addition to its peptidase activity, DPP-4 is known to be associated with immune stimulation, binding to and degradation of extracellular matrix, resistance to anti-cancer agents, and lipid accumulation. The liver expresses DPP-4 to a high degree, and recent accumulating data suggest that DPP-4 is involved in the development of various chronic liver diseases such as hepatitis C virus infection, non-alcoholic fatty liver disease, and hepatocellular carcinoma. Furthermore, DPP-4 occurs in hepatic stem cells and plays a crucial role in hepatic regeneration. In this review, we described the tissue distribution and various biological effects of DPP-4. Then, we discussed the impact of DPP-4 in chronic liver disease and the possible therapeutic effects of a DPP-4 inhibitor. | Minoru Itou Takumi Kawaguchi Eitaro Taniguchi Michio Sata | 2013 | World Journal of Gastroenterology2013，19，15： | 22 |
| 17 | Diabetes mellitus and cognitive impairments显示文摘There is strong evidence that diabetes mellitus increases the risk of cognitive impairment and dementia. Insulin signaling dysregulation and small vessel disease in the base of diabetes may be important contributing factors in Alzheimer's disease and vascular dementia pathogenesis, respectively. Optimal glycemic control in type 1 diabetes and identification of diabetic risk factors and prophylactic approach in type 2 diabetes are very important in the prevention of cognitive complications. In addition, hypoglycemic attacks in children and elderly should be avoided. Anti-diabetic medications especially Insulin may have a role in the management of cognitive dysfunction and dementia but further investigation is needed to validate these findings. | Elham Saedi Mohammad Reza Gheini Firoozeh Faiz Mohammad Ali Arami | 2016 | World Journal of Diabetes2016，7，17： | 23 |
| 18 | Enhanced recovery program is safe and improves postoperative insulin resistance in gastrectomy显示文摘AIM: To assess the safety of enhanced recovery after surgery(ERAS) program in gastrectomy and influences on nutrition state and insulin-resistance. METHODS: Our ERAS program involved shortening the fasting periods and preoperative carbohydrate loading. Eighty gastrectomy patients were randomly assigned to either the conventional group(CG) or ERAS group(EG). We assessed the clinical characteristics and postoperative outcomes prospectively. The primary endpoint was noninferiority in timely discharge from the hospital within 12 d. Secondary endpoints were the incidence of aspiration at anesthesia induction, incidence of postoperative complications, health related quality of life(HRQOL) using the SF8 Health Survey questionnaire, nutrition state [e.g., albumin, transthyretin(TTR), retinal-binding protein(RBP), and transferrin(Tf)], the homeostasis model assessment-insulin resistance(HOMA-R) index, postoperative urine volume,postoperative weight change, and postoperative oral intake.RESULTS: The ERAS program was noninferior to the conventional program in achieving discharge from the hospital within 12 d(95.0% vs 92.5% respectively; 95%CI:-10.0%-16.0%). There was no significant difference in postoperative morbidity between the two groups. Adverse events such as vomiting and aspiration associated with the induction of general anesthesia were not observed. There were no significant differences with respect to postoperative urine volume, weight change, and oral intake between the two groups. EG patients with preoperative HOMA-R scores above 2.5 experienced significant attenuation of their HOMA-R scores on postoperative day 1 compared to CG patients(P = 0.014). There were no significant differences with respect to rapid turnover proteins(TTR, RBP and Tf) or HRQOL scores using the SF8 method.CONCLUSION: Applying the ERAS program to patients who undergo gastrectomy is safe, and improves insulin resistance with no deterioration in QOL. | Nobuaki Fujikuni Kazuaki Tanabe Noriaki Tokumoto Takahisa Suzuki Minoru Hattori Toshihiro Misumi Hideki Ohdan | 2016 | World Journal of Gastrointestinal Surgery2016，8，5： | 23 |
| 19 | Expression of insulin-like growth factor Ⅱ and its receptor in liver cells of chronic liver diseases显示文摘ExpressionofinsulinlikegrowthfactorⅡanditsreceptorinlivercelsofchronicliverdiseasesYANGDongHua1,XIUChong1,YANGBo1,GUJianR... | YANG Dong Hua 1, XIU Chong 1, YANG Bo 1, GU Jian Ren 2, QIAN Lian Fang 2 and QU Shu Ming 2 | 1997 | World Journal of Gastroenterology1997，3，2： | 21 |
| 20 | 葛根素对胰岛素抵抗高血压模型大鼠血压和肾素血管紧张素系统的影响显示文摘目的:观察葛根素对胰岛素抵抗高血压模型大鼠血压(BP)以及胰岛素敏感性的影响,并探讨其降压作用与肾素血管紧张素系统之间的关系。方法:采用高脂、高糖和高盐饲料喂养大鼠,饲养8周时,肌肉注射葛根素,每天1次,连续4周。于造模前、造模8周后和给药4周末测定大鼠血压,并于给药4周末测量大鼠血浆肾素(Renin)和血管紧张素Ⅱ(AngⅡ)水平,测定空腹血清血糖(fastingserumglucose ,FSG)和胰岛素(fastinginsulin ,FINS)水平,并计算胰岛素敏感指数(in sulinsensitivityindex ,IAI)。结果:葛根素高、中剂量均能明显降低胰岛素抵抗高血压模型大鼠的BP和血浆AngⅡ的水平。结论:葛根素对胰岛素抵抗高血压模型大鼠具有降低血压的作用,其降压机制可能与其影响RAS系统有关。 | 玉从容 吕俊华 | 2005 | 四川中医2005，23，4： | 20 |
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