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Natural history of type 2 diabetes ppt leigos,tratamiento natural para control de diabetes,diabetes type 2 and periodontal disease - PDF 2016

Although metformin is first-line therapy for patients with type 2 diabetes, glycemic control fails with metformin alone in many patients. The Cardio Diabetes Master Classes are dedicated to improve the clinical management of patients with diabetes and  cardiovascular disease.
In GPRD data, current use of sulphonylureas only (with active or inactive metabolites) was associated with an increased risk of hypoglycaemic events, as compared with current use of metformin.
Recent outcome trials of novel antidiabetic drugs shed new light on why diabetes patients develop heart disease. Out of 18 biomarkers, Lp-PLA2 and adiponectin were independently associated with a decreased risk for T2DM.


In females with gestational diabetes, the future risk of developing type 2 diabetes depends on certain pregnancy-related and maternal factors that could be used for postnatal counselling.
EMPA-REG OUTCOME trial shows that empagliflozin reduces microvascular outcomes and progression of kidney disease in T2DM patients at high CV risk. ADA 2016 In T2DM patients at high CV risk, liraglutide on top of standard therapy was associated with lower rates of CV events and mortality, compared with placebo in the LEADER outcome trial.
An open-label randomized controlled trial was conducted, which compared add-on exenatide with add-on glimepiride in patients who had failed to achieve glycemic control with metformin alone. Bernard Charbonell (University of Nantes, France) discussed new options in diabetes management.


We recognised that there was underlying moderate-severe insulin resistance affecting muscle and the liver, and this, coupled with beta cell failure, formed the classical triumvirate (1).
The insulin resistance in muscle primarily was responsible for the excessive postprandially rise in plasma glucose concentration, while insulin resistance in the liver, in combination with accelerated gluconeogenesis, resulted in an excessive rate of hepatic glucose production which led to an increase in the fasting plasma glucose concentration (2-4).



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