摘要：
Major goals of therapy include achieving glycaemic targets (glycated haemoglobin [HbA1c] ≤7%) to minimise the development and progression of microvascular and, to a lesser extent, macrovascular complications, while avoiding hypoglycaemia.1 Obesity is a key risk factor of type 2 diabetes—hence, the terminology diabesity.2 Weight loss, even when modest, might improve not only glycaemic control and cardiovascular risk but also hepatic steatosis—the non-alcoholic fatty liver disease that is now the most common cause of chronic liver disease globally.3 The success of bariatric surgery, particularly Roux-en-Y gastric bypass, in induction of weight loss and amelioration of type 2 diabetes attests to the central role of the gastrointestinal tract in the regulation of glycaemia and bodyweight.4 The rate of gastric emptying determines the availability of carbohydrates for absorption, while the interaction of nutrients with the gut leads to the release of peptides that modulate glycaemia and energy balance, including glucagon-like peptide 1 (GLP-1) and *** magnitude of HbA1c reduction induced by GLP-1RAs is at least equivalent to that by basal insulin, but because insulin stimulation is glucose dependent, risk of hypoglycaemia is minimal.[...]at least some GLP-1RAs (liraglutide and semaglutide) reduce cardiovascular events in high-risk patients.5 GLP-1RAs also induce modest weight loss, and liraglutide is approved by the US Food and Drug Administration and European Medicines Agency for the treatment of obesity.6 Current guidelines for the use of GLP-1RAs assume that they are essentially all the same,1 and interpretation of trials relating to their comparative efficacy is compromised by open-label *** finding that postprandial glucose concentration was reduced without a change in insulin concentration strongly suggests that MEDI0382 slows gastric emptying, which was not measured.
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