Choukem S P, Sobngwi E, Garnier J P, Letellier S, Mauvais-Jarvis F, Calvo F, Gautier J-F
Department of Diabetes and Endocrinology, Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, University Paris-Diderot Paris-7, 75010 Paris, France; Clinical Investigation Centre, Inserm-CIC9504, Saint-Louis University Hospital, Assistance Publique-Hôpitaux de Paris, University Paris-Diderot Paris-7, 75010 Paris, France; Department of Internal Medicine and Paediatrics, Faculty of Health Sciences, University of Buea, Buea, Cameroon.
Department of Diabetes and Endocrinology, Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, University Paris-Diderot Paris-7, 75010 Paris, France; Clinical Investigation Centre, Inserm-CIC9504, Saint-Louis University Hospital, Assistance Publique-Hôpitaux de Paris, University Paris-Diderot Paris-7, 75010 Paris, France; Institute of Health and Society, Newcastle University, Newcastle upon Tyne, UK.
Diabetes Metab. 2015 Sep;41(4):326-330. doi: 10.1016/j.diabet.2014.07.002. Epub 2015 Sep 1.
Previously, we described patients with ketosis-prone type 2 diabetes (KPD) and glucose-6-phosphate dehydrogenase (G6PD) deficiency, but no mutation of the G6PD gene. Our present study used two complementary approaches to test whether hyperglycaemia might inhibit G6PD activity: (1) effect of acute hyperglycaemia induced by glucose ramping; and (2) effect of chronic hyperglycaemia using correlation between G6PD activity and HbA1c levels.
In the first substudy, 16 KPD patients were compared with 11 healthy, non-diabetic control subjects of the same geographical background. Erythrocyte G6PD activity and plasma glucose were assessed at baseline and every 40 min during intravenous glucose ramping that allowed maintaining hyperglycaemia for more than 3h. In the second substudy, erythrocyte G6PD activity and HbA1c levels were evaluated in 108 consecutive African patients with either type 2 diabetes or KPD, and a potential correlation sought between the two variables.
The maximum plasma glucose level after 200 min of glucose perfusion was 20.9±3.7 mmol/L for patients and 10.7±2.3mmol/L for controls. There was no difference between baseline and repeated G6PD activity levels during acute hyperglycaemia in either KPD patients (P=0.94) or controls (P=0.57), nor was there any significant correlation between residual erythrocyte G6PD activity and HbA1c levels (r=-0.085, P=0.38).
Neither acute nor chronic hyperglycaemia affects erythrocyte G6PD activity. Thus, hyperglycaemia alone does not explain cases of G6PD deficiency in the absence of gene mutation as described earlier.
此前，我们描述了酮症倾向2型糖尿病（KPD）合并葡萄糖-6-磷酸脱氢酶（G6PD）缺乏但G6PD基因无突变的患者。我们目前的研究采用了两种互补方法来测试高血糖是否可能抑制G6PD活性：（1）葡萄糖递增诱导的急性高血糖的影响；（2）利用G6PD活性与糖化血红蛋白（HbA1c）水平之间的相关性研究慢性高血糖的影响。
在第一项子研究中，将16例KPD患者与11名具有相同地理背景的健康非糖尿病对照者进行比较。在静脉输注葡萄糖递增过程中，于基线时以及每40分钟评估一次红细胞G6PD活性和血浆葡萄糖水平，该过程可使高血糖状态维持超过3小时。在第二项子研究中，对108例连续的患有2型糖尿病或KPD的非洲患者评估红细胞G6PD活性和HbA1c水平，并探寻这两个变量之间的潜在相关性。
葡萄糖灌注200分钟后，患者的最高血浆葡萄糖水平为20.9±3.7 mmol/L，对照者为10.7±2.3 mmol/L。在急性高血糖期间，KPD患者（P=0.94）或对照者（P=0.57）的基线和重复测量的G6PD活性水平之间均无差异，残余红细胞G6PD活性与HbA1c水平之间也无显著相关性（r=-0.085，P=0.38）。
急性和慢性高血糖均不影响红细胞G6PD活性。因此，如前所述，仅高血糖不能解释无基因突变情况下的G6PD缺乏病例。
