5 12 15 25 27 36 37 1 14 22 24 30 2 7 8 18 21 23 26 32 33 35 38 7 8 18 32 33 35 2 23 13 10 11 29 19 Subjects and methods 2 2 Procedure to induce hyperglycemia After a 10-hour overnight fast, the subjects were given a subcutaneous injection of a low dose (100 μg) of synthetic somatostatin (Sandostatin, Novartis, Basel, Switzerland) in order to suppress endogenous insulin secretion. Each subject underwent an oral glucose tolerance test (OGTT) (75 g glucose) 30 minutes after the somatostatin injection, and blood glucose levels were measured with a blood glucose analyzer (HemoCue Diagnostics BV, Oisterwijk, the Netherlands). Endogenous insulin levels were measured by means of immunometric assays (Luminescence, Bayer Diagnostics, Mijdrecht, the Netherlands) in the Endocrinology Laboratory at the Department of Clinical Chemistry of the VU University Medical Center. The subjects remained in fasting state during the entire procedure. Ocular measurements 6 19 4 20 28 3 31 P Results 1 Fig. 1 Graph of normalized blood glucose levels in the five subjects after the administration of somatostatin and glucose. Data are normalized by subtracting the value at baseline from the measured value in each subject. The oral glucose load (75 g) was administered at T 0. Subject 01 received an extra 75 g oral glucose load at T 30  2 p 3 3 3 Fig. 2 * p  Fig. 3 a b c dark grey area  Discussion Blurred vision is a symptom that occurs frequently in patients with DM and hyperglycemia. The underlying mechanism is still unclear, and therefore the present study was carried out in an attempt to identify a possible cause of this symptom. The effect of reproducible hyperglycemia on retinal thickness and refractive error was studied in healthy young subjects who did not suffer from the systemic effects of DM. 13 2 7 8 18 21 23 26 32 33 35 38 34 8 16 17 9 In conclusion, the results of this study indicate that in healthy subjects, hyperglycemia does not cause any change in retinal thickness. Furthermore, ocular refraction in general was not affected by hyperglycemia. However, there were interindividual variations, as illustrated by subject 01, who had a hyperopic shift of refraction during hyperglycemia. Therefore, it seems that a refractive change during hyperglycemia cannot be explained by a change in retinal thickness. It could well be that other refractive components, such as the lens, are involved in causing blurred vision and refractive alterations during hyperglycemia.