Effect of glycaemic control on apoptosis in diabetic wounds

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Abstract
To study the effect of glycaemic control on apoptosis in chronic ulcers in diabetic patients and the differential roles of insulin and oral hypoglycaemic agents (OHAs). Ten non-diabetic (group I) and 20 diabetic patients (groups II and III), with a wound of more than four weeks' duration, who were attending the wound clinic at University Hospital, Varanasi, India were recruited. The 10 patients in group 11 received insulin and the 10 in group III an oral hypoglycaemic agent; all had diabetic foot ulcers. Wound biopsy and other routine investigations were performed. Both DNA fragmentation and morphological changes under light microscopy (apoptotic index) were used as determinants of apoptosis. Different variables, including fasting and post-prandial blood sugar, serum low-density lipoprotein (LDL) and markers of microangiopathy, such as proteinuria and diabetic retinopathy, were compared with apoptosis. DNA fragmentation in groups I, II and III was 40.00 +/- 2.97, 45.26 +/- 3.21 and 60.8 +/- 3.13 respectively (p < 0.01). Near linear correlation was observed with blood sugar level, particularly post-prandial blood sugar (p < 0.05) and DNA fragmentation. DNA fragmentation was significantly correlated with serum LDL and proteinuria, and it was much greater in the OHA group than in the insulin group (p < 0.05). Similarly, in the diabetic patients with background retinopathy the DNA fragmentation was 46.50 +/- 3.42 (n=3) in the insulin group and 66.70 +/- 6.48 (n=4) in the OHA group (p < 0.05). There is a significant increase in apoptosis in diabetic wounds with poorly controlled blood sugar and microangiopathy. This increase was greater in patients on OHAs than those on insulin, and it contributes to delayed wound healing. Morphological markers do not appear to be a reliable index of apoptosis in the diabetic wound.

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