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Effect of glycaemic control on apoptosis in diabetic wounds
1Department of General Medicine, Institute of Medical Sciences, Banaras Hindu University, India.
Objective:
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).
Method:
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.
Results:
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).
Conclusion:
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.
Insights
Poor glycemic control and microangiopathy increase apoptosis in diabetic wounds, delaying healing. Oral hypoglycemic agents showed higher apoptosis rates than insulin in diabetic foot ulcers.
Area of Science:
- Endocrinology
- Cell Biology
- Wound Healing Research
Background:
- Diabetic foot ulcers represent a significant clinical challenge.
- Apoptosis, or programmed cell death, plays a role in wound healing.
- The impact of glycemic control and specific treatments on apoptosis in diabetic wounds requires further elucidation.
Purpose of the Study:
- To investigate the effect of glycemic control on apoptosis in chronic diabetic ulcers.
- To compare the differential roles of insulin and oral hypoglycemic agents (OHAs) in modulating apoptosis.
- To correlate apoptosis markers with glycemic control and microangiopathy in diabetic patients.
Main Methods:
- Recruited non-diabetic and diabetic patients with chronic foot ulcers.
- Assessed apoptosis using DNA fragmentation and morphological changes (apoptotic index).
- Compared apoptosis with fasting/post-prandial blood sugar, serum LDL, proteinuria, and retinopathy.
Main Results:
- Significantly increased DNA fragmentation (apoptosis) in diabetic wounds compared to non-diabetic controls.
- DNA fragmentation showed a positive correlation with blood sugar levels, serum LDL, and proteinuria.
- Apoptosis was significantly higher in patients treated with OHAs compared to those on insulin, particularly in those with retinopathy.
Conclusions:
- Poor glycemic control and microangiopathy significantly enhance apoptosis in diabetic wounds.
- Treatment with OHAs resulted in greater apoptosis than insulin therapy.
- Increased apoptosis contributes to delayed wound healing in diabetic patients.
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Diabetic Foot Ulcer
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Diabetic Retinopathy
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