California State University, Long Beach, CA, United States; Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, Torrance, CA, United States.
Los Angeles Biomedical Research Institute at Harbor UCLA Medical Center, Torrance, CA, United States.
Diabetes Res Clin Pract. 2018 Jan;135:185-191. doi: 10.1016/j.diabres.2017.11.010. Epub 2017 Nov 16.
Glucagon-like peptide-1 (GLP-1) contributes to insulin secretion after meals. Though Hispanics have increased risk for type 2 diabetes mellitus, it is unknown if impaired GLP-1 secretion contributes to this risk. We therefore studied plasma GLP-1 secretion and action in Hispanic adults.
Hispanic (H; n = 31) and non-Hispanic (nH; n = 15) participants underwent an oral glucose tolerance test (OGTT). All participants were categorized by glucose tolerance into four groups: normal glucose tolerant non-Hispanic (NGT-nH; n = 15), normal glucose tolerant Hispanic (NGT-H; n = 12), impaired glucose tolerant Hispanic (IGT-H; n = 11), or newly diagnosed type 2 diabetes mellitus, Hispanic (T2D-H; n = 8).
Glucose-induced increments in plasma GLP-1 (Δ-GLP-1) were not different in NGT-H and NGT-nH (p = .38), nor amongst Hispanic subgroups with varying degrees of glucose homeostasis (p = .6). In contrast, the insulinogenic index in T2D-H group was lower than the other groups (p = .016). Subjects with abnormal glucose homeostasis (AGH), i.e., T2D-H plus IGT-H, had a diminished glucagon suppression index compared to patients with normal glucose homeostasis (NGT-H plus NGT-nH) (p = .035).
GLP-1 responses to glucose were similar in Hispanic and Non-Hispanic NGT. Despite similar glucose-induced Δ-GLP-1, insulin and glucagon responses were abnormal in T2D-H and AGH, respectively. Thus, impaired GLP-1 secretion is unlikely to play a role in islet dysfunction in T2D. Although GLP-1 therapeutics enhance insulin secretion and glucagon suppression, it is likely due to pharmacological amplification of the GLP-1 pathways rather than treatment of hormonal deficiency.
胰高血糖素样肽-1（GLP-1）有助于餐后胰岛素分泌。尽管西班牙裔人群患 2 型糖尿病的风险增加，但尚不清楚 GLP-1 分泌受损是否会导致这种风险。因此，我们研究了西班牙裔成年人的血浆 GLP-1 分泌和作用。
西班牙裔（H；n=31）和非西班牙裔（nH；n=15）参与者接受了口服葡萄糖耐量试验（OGTT）。根据葡萄糖耐量将所有参与者分为四组：非西班牙裔正常糖耐量（NGT-nH；n=15）、西班牙裔正常糖耐量（NGT-H；n=12）、西班牙裔糖耐量受损（IGT-H；n=11）或新诊断的 2 型糖尿病，西班牙裔（T2D-H；n=8）。
NGT-H 和 NGT-nH 之间（p=0.38）以及不同血糖稳态的西班牙裔亚组之间（p=0.6），葡萄糖诱导的血浆 GLP-1 增加（Δ-GLP-1）没有差异。相反，T2D-H 组的胰岛素原指数低于其他组（p=0.016）。葡萄糖稳态异常（AGH）患者，即 T2D-H 加 IGT-H，与葡萄糖稳态正常（NGT-H 加 NGT-nH）患者相比，胰高血糖素抑制指数降低（p=0.035）。
在西班牙裔和非西班牙裔 NGT 中，GLP-1 对葡萄糖的反应相似。尽管葡萄糖诱导的 Δ-GLP-1 相似，但 T2D-H 和 AGH 分别存在胰岛素和胰高血糖素反应异常。因此，GLP-1 分泌受损不太可能在 T2D 中导致胰岛功能障碍。尽管 GLP-1 治疗可增强胰岛素分泌和胰高血糖素抑制，但这可能是由于 GLP-1 途径的药理学放大，而不是治疗激素缺乏。
