ESPE2024 Poster Category 2 Fat, Metabolism and Obesity (39 abstracts)
1University of Health Sciences, Izmir Faculty of Medicine, Department of Pediatrics, Division of Pediatric Endocrinology, Izmir, Turkey. 2Izmir City Hospital, Department of Internal Medicine, Izmir, Turkey. 3Family Health Center, Number 1. Menemen, İzmir, Turkey. 4Dokuz Eylul University, Izmir, Turkey
Background: Vitamin D deficiency has been shown to increase fatty liver disease (FLD) incidence in patients with obesity (4,5). This study aim ed to determine the effects of a single dose of 300,000 IU cholecalciferol on insulin resistance and fatty liver disease (FLD) in children with obesity with vitamin D deficiency.
Methods: In this clinical study, 128 patients aged 8-18 years with obesity and vitamin D deficiency were included. Exclusion criteria included participants on vitamin D supplements and any medication primary liver disease, obesity secondary to endocrine disorder, intake of calcium/vitamin D preparation in the preceding six months, hepatic, intestinal or renal disorders, active malignancy, diabetes mellitus, or use of sunscreen creams. At the initial clinic visit, anthropometric measurements, baseline biochemical parameters and ultrasonographic signs of FLD were recorded. The homeostasis model assessment of insulin resistance (HOMA-IR) score was calculated with the equation FBS (mmol/L) × fasting insulin (mIU/mL)/22.5. After 6 months, the serum biochemical and hormone levels and ultrasonographic signs of FLD were evaluated. The effects of vitamin D therapy on insulin resistance and FLD in children with obesity were assessed.
Results: The study cohort consisted of 128 patients, 88 (68.1%) females and 40 (31.9%) males. Serum 25(OH) vitamin D levels were negatively correlated with BMI (P =0.02, r =-0,03), BMI SDS (P =0.08, r = -0,071), insulin (P =0.06 r = -0,029), HOMA-IR (P =0.47, r = -0,048), triglycerides (P =0.02, r = -0.013), cholesterol (P = 0.03, r = -0,037), LDL cholesterol (P = 0.02, r = -0,031), systolic BP (P =0.41, r = 0.44), diastolic BP (P =0.46, r = 0.62) and hepatosteatosis (P =0.52, r = 0.503). There was no significant difference between the pre- and posttreatment grades of fasting insulin resistance or FLD (1(1) vs. 1.5(1), P = 0.27), but the posttreatment 25OHD levels were significantly greater than the pretreatment levels (4.4 (3.52) vs. 34 (11.35) ng/ml, P < 0.001). Moreover, the posttreatment HOMA-IR values were significantly lower than the pretreatment values (pretreatment HOMA-IR: 5.2 (3.5) vs. posttreatment HOMA-IR: 4.4 (3.7), P < 0.01).
Conclusion: Our study revealed that the majority of children with obesity with FLD failed to respond to cholecalciferol supplementation, although their serum 25(OH)D levels were within the normal range. In individuals with obesity, vitamin D supplementation cannot correct progressing FLD through epigenetic effects. Few other studies have explored this relationship in children. Prospective, longer-term studies are needed to confirm our results and elucidate causal relationships.