INSULIN-SECRETION, INSULIN ACTION, AND HEPATIC GLUCOSE-PRODUCTION IN IDENTICAL-TWINS DISCORDANT FOR NON-INSULIN-DEPENDENT DIABETES-MELLITUS
INSULIN-SECRETION, INSULIN ACTION, AND HEPATIC GLUCOSE-PRODUCTION IN IDENTICAL-TWINS DISCORDANT FOR NON-INSULIN-DEPENDENT DIABETES-MELLITUS
复制标题
DOI：
10.1172/jci117715
复制
发表时间：
1995-02-01
影响因子：
15.9
通讯作者：
BECKNIELSEN, H
中科院分区：
文献类型：
--
作者：
VAAG, A;HENRIKSEN, JE;BECKNIELSEN, H
研究了12对非胰岛素依赖型糖尿病（NIDDM）的同卵双生子对的胰岛素敏感性（正常血糖胰岛素钳夹，40 mU/m2/min）、肝葡萄糖生成（HGP，[3-H-3]葡萄糖输注）和胰岛素分泌（口服葡萄糖耐量试验和高血糖[12 mM]钳夹，包括胰高血糖素给药）。五个非糖尿病双胞胎正常，七个糖耐量受损。纳入13名无糖尿病家族史的匹配健康受试者作为对照受试者。与非糖尿病双胞胎相比，NIDDM双胞胎更肥胖。与对照组相比，非糖尿病双胞胎有胰岛素抵抗，在口服葡萄糖耐量试验中胰岛素和C肽反应延迟。此外，在高血糖钳夹和静脉注射胰高血糖素期间，非糖尿病双胞胎的第一时相胰岛素反应降低，最大胰岛素分泌能力降低。非糖尿病双胞胎和对照组的HGP发生率相似。与非糖尿病双胞胎和对照组相比，NIDDM双胞胎的HGP基础率升高，胰岛素敏感性进一步降低，胰岛素分泌模式进一步受损。总之，体内胰岛素分泌和胰岛素作用的缺陷存在于非糖尿病和可能的前驱糖尿病双胞胎谁拥有必要的NIDDM易感基因。然而，所有的缺陷，胰岛素分泌和葡萄糖代谢的定量表达更严重的同卵双胞胎与显性NIDDM。
12 identical twin pairs discordant for non-insulin-dependent diabetes mellitus (NIDDM) were studied for insulin sensitivity (euglycemic insulin clamp, 40 mU/m(2) per min), hepatic glucose production (HGP, [3-H-3]glucose infusion), and insulin secretion (oral glucose tolerance test and hyperglycemic [12 mM] clamp, including glucagon administration). Five of the nondiabetic twins had normal and seven had impaired glucose tolerance. 13 matched, healthy subjects without a family history of diabetes were included as control subjects. The NIDDM twins were more obese compared with their non-diabetic co-twins. The nondiabetic twins were insulin resistant and had a delayed insulin and C-peptide response during oral glucose tolerance tests compared with controls. Furthermore, the nondiabetic twins had a decreased first-phase insulin response and a decreased maximal insulin secretion capacity during hyperglycemic clamping and intravenous glucagon administration. Nondiabetic twins and controls had similar rates of HGP. Compared with both nondiabetic twins and controls, the NIDDM twins had an elevated basal rate of HGP, a further decreased insulin sensitivity, and a further impaired insulin secretion pattern as determined by all tests. In conclusion, defects of both in vivo insulin secretion and insulin action are present in non- and possibly prediabetic twins who possess the necessary NIDDM susceptibility genes. However, all defects of both insulin secretion and glucose metabolism are expressed quantitatively more severely in their identical co-twins with overt NIDDM.