Mild type II diabetes markedly increases glucose cycling in the postabsorptive state and during glucose infusion irrespective of obesity.
Mild type II diabetes markedly increases glucose cycling in the postabsorptive state and during glucose infusion irrespective of obesity.
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无论是否肥胖，轻度 II 型糖尿病都会显着增加吸收后状态和葡萄糖输注期间的葡萄糖循环。
DOI：
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发表时间：
1988
影响因子：
15.9
通讯作者：
Mladen Vranic
中科院分区：
文献类型：
--
作者：
Suad Efendić;S. Karlander;Mladen Vranic
葡萄糖循环(GC；平衡G6P中的G)相当于人体吸收后葡萄糖产量的14%。我们的目的是测定6名消瘦的和6名超重的轻度II型糖尿病患者(空腹血糖：139+/-10和152+/-7 mg/dl)、吸收后状态(PA)和葡萄糖输注(2 mg/kg/min)时的葡萄糖循环。14名对照组为体重和年龄匹配的受试者。GC是催化与净流量相反的反应的酶的一种功能，是肝脏总葡萄糖产量(HTGO)(2-[~3H]葡萄糖)和肝脏葡萄糖产量(HGP)(6-[~3H]葡萄糖)之间的差值。吸收后，GC是葡糖激酶的一种功能。葡萄糖输注的流量是反向的(净葡萄糖摄取量)，而GC是葡萄糖6-磷酸酶的函数。在PA中，瘦肉型糖尿病患者和肥胖糖尿病患者的GC增加了100%(从每分钟0.25+/-0.07 mg/kg增加到0.43+/-0.08 mg/kg)和肥胖(从0.22+/-0.05增加到0.50+/-0.07)。瘦和肥胖糖尿病患者的HGP和HTGO分别增加了41%和33%。葡萄糖输注对糖尿病患者的表观磷酸酶活性和糖异生的抑制作用比对照组小得多，导致HTGO和HGP显著增强(400%)，GC仍增加100%。尽管C-肽和胰岛素的绝对反应与对照组相当，但它们不适合于高血糖。外周胰岛素抵抗与代谢葡萄糖清除(MCR)降低和葡萄糖输注过程中摄取不足有关。我们得出结论，HGP和HTGO的升高以及MCR的降低是轻度II型糖尿病的特征，在葡萄糖输注期间更为明显。肝脏的GC也有增加，这是一种权宜之计，控制着从葡萄糖产生到摄取的变化。吸收后，这限制了HGP和血糖的增加。相比之下，在葡萄糖输注过程中，增加的GC会降低肝脏对葡萄糖的摄取，从而导致高血糖。肥胖本身并不影响GC。葡萄糖循环和周转增加表明，除了外周胰岛素抵抗外，还存在肝脏胰岛素抵抗。推测在II型糖尿病的发病机制中，葡萄糖-6-磷酸酶和激酶活性增强可能起重要作用。
Glucose cycling (GC; G in equilibrium G6P) equals 14% of glucose production in postabsorptive man. Our aim was to determine glucose cycling in six lean and six overweight mild type II diabetics (fasting glycemia: 139 +/- 10 and 152 +/- 7 mg/dl), in postabsorptive state (PA) and during glucose infusion (2 mg/kg per min). 14 control subjects were weight and age matched. GC is a function of the enzyme that catalyzes the reaction opposite the net flux and is the difference between hepatic total glucose output (HTGO) (2-[3H]glucose) and hepatic glucose production (HGP) (6-[3H]-glucose). Postabsorptively, GC is a function of glucokinase. With glucose infusion the flux is reversed (net glucose uptake), and GC is a function of glucose 6-phosphatase. In PA, GC was increased by 100% in lean (from 0.25 +/- 0.07 to 0.43 +/- .08 mg/kg per min) and obese (from 0.22 +/- 0.05 to 0.50 +/- 0.07) diabetics. HGP and HTGO increased in lean and obese diabetics by 41 and 33%. Glucose infusion suppressed apparent phosphatase activity and gluconeogenesis much less in diabetics than controls, resulting in marked enhancement (400%) in HTGO and HGP, GC remained increased by 100%. Although the absolute responses of C-peptide and insulin were comparable to those of control subjects, they were inappropriate for hyperglycemia. Peripheral insulin resistance relates to decreased metabolic glucose clearance (MCR) and inadequate increase of uptake during glucose infusion. We conclude that increases in HGP and HTGO and a decrease of MCR are characteristic features of mild type II diabetes and are more pronounced during glucose infusion. There is also an increase in hepatic GC, a stopgap that controls changes from glucose production to uptake. Postabsorptively, this limits the increase of HGP and glycemia. In contrast, during glucose infusion, increased GC decreases hepatic glucose uptake and thus contributes to hyperglycemia. Obesity per se did not affect GC. An increase in glucose cycling and turnover indicate hepatic insulin resistance that is observed in addition to peripheral resistance. It is hypothesized that in pathogenesis of type II diabetes, augmented activity of glucose-6-phosphatase and kinase may be of importance.
无效循环在肝脏碳水化合物代谢调节中的作用。
DOI：
10.1002/9780470122976.ch4
发表时间：
1981
期刊：
Advances in enzymology and related areas of molecular biology
影响因子：
--
作者：
Hue,L
通讯作者：
Hue,L
影响因子：
20.3
作者：
BERGMAN, RN;FINEGOOD, DT;ADER, M
通讯作者：
ADER, M
妥拉磺酰胺和外源性胰岛素对非胰岛素依赖型糖尿病患者胰岛素作用的影响。
DOI：
10.1056/nejm198605153142003
发表时间：
1986
期刊：
The New England journal of medicine
影响因子：
--
作者：
Firth,RG;Bell,PM;Rizza,RA
通讯作者：
Rizza,RA