Glucose-dependent insulinotropic polypeptide has impaired effect on abdominal, subcutaneous adipose tissue metabolism in obese subjects
Glucose-dependent insulinotropic polypeptide has impaired effect on abdominal, subcutaneous adipose tissue metabolism in obese subjects
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DOI：
10.1038/ijo.2013.73
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发表时间：
2014-02-01
影响因子：
4.9
通讯作者：
Bulow, J.
中科院分区：
文献类型：
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作者：
Asmar, M.;Simonsen, L.;Bulow, J.
目的：葡萄糖依赖性促胰岛素多肽（GIP）似乎在脂质代谢中发挥作用。最近，我们发现 GIP 与高胰岛素血症和高血糖相结合会增加瘦人腹部、皮下脂肪组织中甘油三酯的摄取。有人提出，肥胖时GIP分泌增加会促进脂肪组织中的脂质沉积。鉴于目前使用GIP拮抗剂治疗和预防人类肥胖的尝试，进行本实验是为了阐明在糖耐量正常(NGT)或糖耐量受损(IGT)的肥胖受试者中，在GIP、高胰岛素和高血糖(HI-HG)钳夹期间，脂肪组织脂质代谢是否会增强或减弱。 设计：16名肥胖受试者(BMI>30 kg m(-2))被分为两组根据他们对口服葡萄糖挑战的血浆葡萄糖反应，分组：(i) NGT 和 (ii) IGT。通过结合 HI-HG 钳在 GIP（1.5 pmol kg(-1) min(-1)）期间测量动静脉代谢物浓度和区域脂肪组织血流量 (ATBF)，研究腹部、皮下脂肪组织脂质代谢。 结果：在两组中，ATBF 反应均显着低于我们之前在健康瘦受试者中发现的结果 (P
OBJECTIVE: Glucose-dependent insulinotropic polypeptide (GIP) appears to have a role in lipid metabolism. Recently, we showed that GIP in combination with hyperinsulinemia and hyperglycemia increases triglyceride uptake in abdominal, subcutaneous adipose tissue in lean humans. It has been suggested that increased GIP secretion in obesity will promote lipid deposition in adipose tissue. In light of the current attempts to employ GIP antagonists in the treatment and prevention of human obesity, the present experiments were performed in order to elucidate whether the adipose tissue lipid metabolism would be enhanced or blunted during a GIP, hyperinsulinemic and hyperglycemic (HI-HG) clamp in obese subjects with either normal glucose tolerance (NGT) or impaired glucose tolerance (IGT).DESIGN: Sixteen obese (BMI>30 kg m(-2)) subjects were divided into two groups, based on their plasma glucose response to an oral glucose challenge: (i) NGT and (ii) IGT. Abdominal, subcutaneous adipose tissue lipid metabolism was studied by conducting measurements of arteriovenous concentrations of metabolites and regional adipose tissue blood flow (ATBF) during GIP (1.5 pmol kg(-1) min(-1)) in combination with a HI-HG clamp.RESULTS: In both groups, ATBF responses were significantly lower than what we have found previously in healthy, lean subjects (P