Trials clinici fondamentali Intensive blood-glucose control with sulphonlureas or insulin compared with conventional treatment and risk of complications in patients with type 2 diabetes (UKPDS 33). Iperglicemia a digiuno Fisiopatologia diabete Fisiopatologia diabete Legata soprattutto ad aumento produzione epatica di glucosio glucosio insulina Iperglicemia postprandiale glucosio Legata ad alterata soppressione Insulino-mediata) della produzione Epatica glucosio+ ridotta utilizzazione (insulinostimolata) del glucosio da Parte del muscolo. Diabete mellito di tipo 2: fase precoce della secrezione insulinica nel soggetto sano e nel paziente diabetico Ward WK, et al. GLINIDI Farmaci di seconda linea in aggiunta alla metformina quando non si raggiunge lobiettivo di HbA1c Prevalente iperglicemia postprand.
Trials clinici fondamentali Trials clinici fondamentali Effect of intensive blood-glucose control with metformin on complication in overweight patients with type 2 diabetes (UKPDS 34). Willkommen zur Diabetesassistentinnen-Ausbildung CEB Fortbildungswerk, Merzig-Hilbringen Fruhjahr 2007 Pathophysiologie – Metabolisches Syndrom Dr.
Prasentation zum Thema: "Willkommen zur Diabetesassistentinnen-Ausbildung CEB Fortbildungswerk, Merzig-Hilbringen Fruhjahr 2007 Pathophysiologie – Metabolisches Syndrom Dr. Globale Hochrechnungen fur die Diabetesepidemie: 2003 – 2025 (in Millionen) Sicree R, et alSicree R, et al. Geschatzte Pravalenz des Diabetes in der globalen Erwachsenenpopulation, 1995-2025 Weltweit IndustrielanderSchwellenlander King H, et alKing H, et al. Gestorte Insulinproduktion und -sekretion Die zugrunde liegenden Schadigungen: Insulinresistenz und Betazellfunktionsstorung Saltiel AR, et alSaltiel AR, et al. Normale Blutglukose Normales Insulin 4–7 Jahre Naturlicher Verlauf des Typ 2 Diabetes: Insulinresistenz und Betazellfunktionsstorung Diabetes Nuchternblutglukose Postprandiale Blutglukose Gestorte Glukosetoleranz Diagnosestellung des Diabetes Insulinsekretion Modifiziert nach Ramlo-Halsted BA, et al. Insulin und Glukagon steuern die normale postprandiale Blutglukoseregulation Unger RHUnger RH. Die postprandiale Hyperglykamie geht einher mit einer gestorten Insulinsekretion und Glukagonsuppression Mitrakou A, et alMitrakou A, et al. Zeit (min) Gestorte erste Phase der Insulinsekretion bei Typ 2 Diabetes iv-Glukose -40-30-20-100102030 0 20 40 60 80 100 Porte DPorte D.
Der Typ 2 Diabetes ist eine fortschreitende Erkrankung: 6-Jahresdaten der UKPDS 6,2% HbA 1c Obergrenze des Normalbereichs Konventionell Chlorpropamid Glibenclamid Insulin Metformin Zeit ab der Randomisierung (Jahre) HbA 1c (Median %) UKPDSUKPDS. Jahre ab der Diagnose Betazellfunktion (%) Die Betazellfunktion nimmt bei Patienten mit Typ 2 Diabetes im Zeitverlauf ab Holman RRHolman RR.
Korrelation zwischen Betazellfunktion und Insulinsensibilitat Normale Glukosetoleranz Diabetes Gestorte Glukosetoleranz Das hyperbolische Gesetz der Blutglukose Stumvoll MStumvoll M.
Die Hyperglykamie entsteht, wenn die Betazellarbeitslast zunimmt und die Betazellreaktion abnimmt Seely B, et alSeely B, et al.
Die Betazellfunktion sinkt im Zeitverlauf unter Monotherapie oder unter alleiniger Diat Sulfonylharnstoffe Diat Metformin UKPDSUKPDS. Die Inkretinhormone sind ein weiterer wesentlicher Bestandteil der normalen Blutglukoseregulation Als Reaktion auf die Nahrungsaufnahme setzt der Darm Peptidhormone in den Blutkreislauf frei, die auf das Pankreas wirken Diese Hormone werden als Inkretine bezeichnet GLP-1 GIP Inkretinhormone tragen zur Blutglukoseregulation bei durch: Verstarkung der glukoseabhangigen Insulinsekretion Unterdruckung der Glukagonsekretion Regulation der Magenentleerung Regulation der Nahrungsaufnahme Meier JJ, et alMeier JJ, et al. Inkretinwirkung: Intestinale Faktoren beeinflussen die Insulinsekretion Probanden ohne Diabetes Patienten mit Diabetes Orale Glukose Intravenose Glukose Mean (SEM) Modifiziert nach Perley MJ, et al.
Das therapeutische Potenzial von GLP-1 wird durch seine schnelle Inaktivierung begrenzt Schnelle Inaktivierung (DPP-IV), Kurze Eliminationshalbwertszeit (ca.


Acknowledgments: The authors thank the patients and many National Health Service (NHS) and non-NHS staff at the centers for their cooperation. Requests for Reprints: United Kingdom Prospective Diabetes Study Group, Diabetes Research Laboratories, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, United Kingdom. Trials clinici fondamentali Intensive blood-glucose control with sulphonlureas or insulin compared with conventional treatment. Um die Prasentation herunterzuladen, empfehlen Sie diese Ihren Freunden uber beliebiges soziales Netzwerk. Beeinflussen die Insulinproduktion (Pankreas) Insulinsekretagoga: Sulfonylharnstoffe und Glinide 2. 1–2 min) GLP-1 muss kontinuierlich verabreicht werden (Infusion) Unpraktisch fur die Behandlung einer chronischen Krankheit wie dem Typ 2 Diabetes Drucker DJ, et alDrucker DJ, et al. United Kingdom Prospective Diabetes Study 17: A 9-Year Update of a Randomized, Controlled Trial on the Effect of Improved Metabolic Control on Complications in Non-Insulin-dependent Diabetes Mellitus. Turner, Cull, and Holman: United Kingdom Prospective Diabetes Study Group, Diabetes Research Laboratories, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, United Kingdom. Obese patients assigned to conventional therapy are compared with those assigned to metformin therapy (marked by an asterisk). Ersetzen Insulin (Leber, Muskeln und Fettgewebe) Insulin, Insulinmischungen und Insulinanaloga 3. Additionally, patients assigned to sulfonylurea are compared with those assigned to insulin and patients assigned to the first-generation sulfonylurea chlorpropamide are compared with those assigned to second-generation glyburide or glipizide. The right-hand panels shows the median fasting plasma glucose level (C) and hemoglobin A level (D) in obese patients assigned to conventional therapy 0 and those assigned to intensive therapy with metformin (+) and with sulfonylurea or insulin (open diamond). Reprinted from Lancet, 352, UKPDS, Effect of intensive blood-glucose control with metformin on complications in overweight patients with type 2 diabetes (UKPDS 34), 854-865. Beeinflussen die Insulinwirkung Hemmen die hepatische Glukose-Freisetzung (Leber) Biguanide Insulinresistenz (Leber, Muskeln und Fettgewebe) - Thiazolidinedione und Biguanide 4.
Sue Manley, David Matthews, Andrew Neil, and Jonathan Levy for their collaboration and advice and Ms.
Regardless of the assigned therapy, however, the fasting plasma glucose and hemoglobin A1c levels increased, and maintaining near-normal glycemia was, in general, not feasible. Verlangsamen die Kohlenhydratresorption (Darm) Alphaglucosidase-Inhibitoren Moller DEMoller DE. Even insulin therapy did not achieve the therapeutic goal of near-normal glycemia because of the difficulty in treating marked hyperglycemia and the risk for hypoglycemic episodes.
Sensitivity and subgroup analyses evaluated the robustness and explained the heterogeneity of the results. Results were represented as "standard mean difference or odds ratio [95% confidence internals] P value".ResultsFifteen RCTs with 1681 adult T2DM patients were included for meta-analysis. Metformin was not better than glimepiride in overall efficacy in controlling the levels of HbA1c, postprandial blood sugar (PPBS), fasting plasma insulin (FINS), systolic and diastolic blood pressures (SBP and DBP), and high density lipoprotein (HDL). The UK Prospective Diabetes Study (UKPDS) found metformin more effective than chlorpropamide, glibenclamide and insulin[3a€“5].


The American Diabetes Association (ADA) recommended metformin as the first drug of choice for treating T2DM patients, especially those who are overweight[2]. The UK National Institute for Health and Clinical Excellence (NICE) recommended metformin if the patients are at danger under hypoglycaemia[1]. The latest recommendations of ADA[2] and NICE[1] were updated with the results of UKPDS[6, 7], post-trial monitoring of UKPDS[8], and systematic reviews of comparing metformin with placebo, sulfonylureas and other anti-diabetic drugs[7, 9], as well as the randomized controlled trials (RCTs) comparing metformin monotherapy with pioglitazone[10], metformin plus nateglinide[11], metformin plus rosiglitazone[12] and other non-metformin treatments[13].
A meta-analysis of RCTs on the efficacy of metformin in treating T2DM[14] found metformin lacking clear evidence for efficacy over the conventional or placebo treatment. A recent literature review suggested that metformin, albeit old, remained the best treatment for T2DM[15] but the review was not a systematic review or meta-analysis. It did not include the latest RCTs comparing metformin and glimepiride in monotherapy of T2DM.Glimepiride is of the latest generation sulfonylureas for treating T2DM[16]. Recent RCTs found it comparable to metformin in treating T2DM patients[20, 21] including those who are not responding well to non-glimepiride sulfonylureas[22, 23]. Probably due to the late launch of glimepiride[24, 25] and lack of head-to-head comparative RCTs, early UKPDS, ADA and NICEa€™s recommendations did not include the results of RCTs comparing metformin with glimepiride in monotherapy but they did include the findings that sulfonlyureas had increased risks in hypoglycemia, weight gain and cardiovascular issues. Recent cohort studies confirmed the increased cardiovascular risks of glimepiride[26] but did no cardiovascular harm to the patients with diagnosed coronary artery disease[27]. Basically, the articles with the terms "glimepiride" and "metformin" in titles, abstracts, and keywords were retriered. Disagreements were resolved by group discussion.Data extraction and quality assessmentTwo reviewers (HZ, XZ) independently extracted data of study characteristics and outcome measures from the selected RCTs.
The extracted data were cross-checked before quality assessment according to the Cochranea€™s risks of bias tool[29]. Numeric outcome measures were represented in standardized mean differences (SMD) or odds ratios (OR) and their 95% confidence intervals (CI).
A total of 1023 records were identified in accordance with the search strategies from specific bibliographical databases, i.e. PubMed (na€‰=a€‰208), Cochrance Library (na€‰=a€‰89), Science Direct (na€‰=a€‰48), Chinese National Knowledge Infrastructure (na€‰=a€‰267), WangFang (na€‰=a€‰206) and Google (na€‰=a€‰205).
Among the 440 records after removal of duplicates, 27 records met the eligibility criteria. After full-text assessment, 12 of 27 studies were excluded for the reasons stated in FigureA 1. The SMD, 95% CI and P values for outcomes between metformin and glimepiride are shown in TableA 2.
TableA 5 shows that only the effect of metformin on BMI became statistically significant after excluding the studies with participants who were non-responders to other sulfonyureas.



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Comments

  1. 23.04.2014 at 20:44:27


    Exercise will cause the release of glucose make to reach your blood sugar goals mothers who had.

    Author: King
  2. 23.04.2014 at 13:27:34


    Another aspect of this phenomenon occurs in type I glycogenosis.

    Author: Sevimli_oglan