The onset of type 2 diabetes mellitus (T2DM) in prepubertal age is not uncommon nowadays. Here we are reporting on a young boy who was diagnosed with diabetes at the age of eight years. Diagnosis of diabetes was made based on symptoms of hyperglycemia (new onset bed wetting, also polyphagia and polydipsia) and laboratory evidence of high plasma glucose. The patient was obese (body mass index, BMI > 95th percentile) and had acanthosis nigricans during presentation. The type of diabetes was not confirmed at the time of diagnosis based on the supporting laboratory investigations. His initial high blood glucose was managed with a basal bolus insulin regimen with symptomatic improvement. Due to poor follow-up and inadequate adherence to a complex insulin regimen, his blood glucose was not well controlled. Sometimes the patient stopped insulin for several weeks without evidence of hyperglycemic crisis. We excluded type 1 diabetes by checking fasting C-peptide and islet autoantibodies. He had a strong family history of diabetes at a very young age of onset, affecting all generations. Both parents had diabetes, and he was exposed to high maternal blood glucose during gestation. He was delivered by cesarean section at 37 completed weeks of gestation, his birth weight was 3.5 kg, and he did not experience post-delivery hypoglycemia, according to the statement of his guardian. Mother was treated with insulin during gestation, but blood glucose control was not satisfactory. All these conditions are considered risk factors of T2DM. However, maturity-onset diabetes of the young (MODY) could be a possible differential diagnosis, considering a strong family history. So, we checked 14 MODY-related genes (GCK, HNF1A, HNF4A, HNF1B, INS, NEUROD1, PDX1, PAX4, ABCC8, KCNJ11, KLF11, CEL, BLK, and APPL1) and found no pathogenic variant. Finally, we confirmed him as a case of type 2 DM. We changed his treatment from a complex basal bolus insulin regimen to twice-daily premixed insulin with continuation of metformin (500 mg, twice daily), which was already prescribed by another physician. On follow-up, his glycated hemoglobin reduced significantly (from 11.1% to 8.0%). As his obesity was an important issue, we initiated semaglutide at a dose of 0.25 mg later on. Metformin was stopped due to dyspepsia. On the last follow-up, the patient lost significant weight with better control of diabetes (ranging from 5.0 to 5.7 mmol/L in a fasting state and post-meal capillary glucose <8.2 mmol/L using a glucometer at home) without any evidence of hypoglycemia after the initiation of semaglutide, and the dose of insulin was reduced significantly. We planned to stop insulin and maintain an ideal body weight while ensuring good compliance with lifestyle advice. We checked diabetes-related macro- and microvascular complications, which were negative, except in one episode, trace albumin was present in urine, which was negative on subsequent investigations.
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