利拉鲁肽降低内脏脂肪降糖之外,更多获益.pptVIP

利拉鲁肽降低内脏脂肪降糖之外,更多获益.ppt

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利拉鲁肽降低内脏脂肪降糖之外,更多获益

* 这张图中列出了目前常用的糖尿病治疗药物在降糖、减轻体重和减少内脏脂肪方面的作用情况。从图中可见,与二甲双胍、磺脲、TZD类药物及DPP-4抑制剂相比,GLP-1受体激动剂在这三方面具有非常明显的优势。 * 利拉鲁肽作为人GLP-1类似物,目前已知它可以通过延缓胃排空、抑制胃酸分泌以及刺激中枢中枢神经系统而增加饱食感进而减少能量的摄入,实现减轻体重的作用。 The effect of GLP-1 on weight: GLP-1 affects the gastrointestinal system and delays absorption of food. This is caused by several means, including decreased gastric emptying and acid secretion. For example, the infusion of GLP-1 to generate plasma levels similar to those normally observed following meals delays gastric emptying (Wettergren et al. 1993). Combined, these gastrointestinal effects reduce the meal-related increase in glucose. Prolonged presence of food in the stomach through delayed gastric emptying may also reduce energy intake by inducing satiety. Additionally, GLP-1 receptors are present in several areas in the brain. The receptors in the brainstem (area postrema and subfornical organ) are believed to be involved in inducing satiety, regardless of the presence of food in the gastric system. This action therefore provides another means for decreasing energy intake. * Background Aims: Glucagon-like peptide-1 (GLP-1), a gutderived peptide degraded by dipeptidyl peptidase-4 (DPP4), stimulates insulin secretion in response to nutrients, yet its direct effect on the liver is controversial. We investigated the effects of GLP-1 on hepatic fat and glucose metabolism and elucidated its mechanism of action. Methods: Hepatic fat metabolism, including lipogenic enzymes and signal transduction regulators, was assessed in livers of DPP4-deficient rats (DPP4-) with chronically elevated GLP-1 and in GLP-1-treated primary hepatocytes. The effect of chronic elevated GLP-1 on insulin sensitivity was measured using the hyperinsulinemic–euglycemic clamp. Results: Normal and high fat diet fed DPP4-rats displayed reduced hepatic triglycerides, accompanied by down-regulation of lipogenesis enzymes and parallel up-regulation of carnitine palmitoyltransferase-1, a key enzyme in fatty acid b-ox

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