ESPE2024 Free Communications Fat, Metabolism and Obesity 1 (6 abstracts)
Corneal Nerve Loss and regeneration after GLP-1 Therapy in Children with Simple and Monogenic Obesity
Hoda Gad 1 , Hajar Dauleh 2 , Shiga Chirayath 2 , Rasha Amin 2 , Ghassan Mohamadsalih 2 , Maheen Pasha 2 , Idris Mohammed 2,3 , Tara Al-Barazenji 2 , Amel Khalifa 2 , Goran Petrovski 2 , Elwaseila Hamdoun 2 , Khalid Al Bureshad 2 , Marwa Ibrahim 2 , Rayaz A. Malik 1,4 & Khalid Hussain 2
1Weill Cornell Medicine-Qatar (WCM-Q), Doha, Qatar. 2Sidra Medicine, Doha, Qatar. 3Hamad Bin Khalifa University, Doha, Qatar. 4University of Manchester, Manchester, United Kingdom
Background: Obesity is highly prevalent in the MENA region, especially in children and it has been associated with neurodegeneration. We have undertaken corneal confocal microscopy (CCM) to assess for evidence of neurodegeneration in children with simple obesity and monogenic obesity (MC4R gene mutation) and further assessed the effect of glucagon-like peptide 1 agonist (GLP-1) therapy on corneal nerve regeneration.
Methods: Participants with obesity and healthy controls (HC) without symptoms of neuropathy, underwent CCM. Corneal nerve fiber density (CNFD), branch density (CNBD), and fiber length (CNFL) were quantified using ACCMetrics software.
Results: 104 children and adolescents with obesity (normoglycemic n = 50, prediabetes n = 14, T2DM n = 20) (age 14 (13.8-15) years, BMI 31.9 (29.9-34.7) kg/m2) and 20 HC underwent CCM and neuropathy assessments. CNFD was comparable in obese children without diabetes (28.9±8.3, P = 0.99), showed a trend for being lower in obese children with prediabetes (25.7±6.15, P = 0.99) and T2DM (25.6±6.99, P = 0.99) compared to HC (27.8±7.11). CNBD was significantly lower in obese children without diabetes (37.5 (33.3 – 41.6), P = 0.005), prediabetes (29.2 (21.8-35.4), P <0.001) and T2DM (33.8 (25-43.7), P = 0.011) compared to HC (48.9 (43.8-66.2)). CNFL was significantly lower in obese children without diabetes (17.5±3.5, P = 0.035), prediabetes (15.8±2.8, P = 0.006) and T2DM (15.7±3.9, P = 0.001) compared to healthy controls (20.5±4.5). Of this cohort, 5 children aged 13.8±2.05 years, weight 101.8±7.8 kg with normal HbA1c, and lipids were treated with once daily subcutaneous (S.C.). liraglutide. After 3 months of treatment, weight did not change, but CNFD (P = 0.02) and CNFL (P = 0.046) increased significantly with no change in CNBD. Another 7 children, aged 16.0±1.9 years, weight 130.1±34.1 kg with normal HbA1c, and lipids were treated with once weekly 1 mg S.C. semaglutide. After 3 months of treatment, weight did not change, but CNFD (P = 0.03) and CNFL (P = 0.03) increased significantly with no change in CNBD. Two siblings carrying a heterozygous missense variant c.508A>G, p.Ille170Val in the MC4R gene showed evidence of corneal nerve fibre degeneration. Treatment with once weekly 1 mg S.C. Semaglutide for 6 months was associated with no change in weight. However, there was evidence of nerve regeneration with an increase in CNFD (child A (13.9%), child B (14.7%)), CNBD (child A (110.2%), child B (58.7%)) and CNFL (child A (21.5%), child B (44.0%)).
Conclusion: CCM identified early corneal nerve degeneration in children with both simple and monogenic obesity and treatment with liraglutide and Semaglutide was associated with nerve regeneration.
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