MON-030 Effective Use of Low-dose Glucagon-like Peptide-1 Receptor Agonist for Hypothalamic Obesity in a Patient with Type 1 Diabetes Mellitus

Abstract J. Aurora: None. E. Tirthani: None. R.M. Lechan: None. R.D. Siegel: None. Background: Hypothalamic obesity (HO) can occur after damage to the hypothalamus, typically due to suprasellar tumor infiltration, cranial radiation, or craniotomy. As the hypothalamus plays an important role in metabolic and appetite regulation, hypothalamic damage can result in hyperphagia, weight gain, hyperinsulinemia, and leptin dysregulation. Currently, there are no medications approved to treat HO, but glucagon-like peptide-1 (GLP-1) receptor agonists have been evaluated given their central and peripheral satiety effects, but there have been mixed results even at higher dosing. We present a case of a patient with HO and T1DM who responded well to low-dose liraglutide. Clinical Case: A 52-year-old male with T1DM, obesity, CKD, HTN, and a silent corticotroph macroadenoma (2 x 2.2 x 2.8 cm) with multiple transsphenoidal surgeries and craniotomies resulting in panhypopituitarism was seen for diabetes management. His T1DM was poorly controlled with an A1c of 13.5% on once daily insulin degludec and insulin aspart before meals. Since his last craniotomy, after which MRI demonstrated foci of restricted diffusion in the hypothalamus concerning for acute infarcts, his BG and weight were difficult to control given his reported hyperphagia. His weight increased 16% after the craniotomies. Although HO is characterized by hyperinsulinemia, his C-peptide remained undetectable corresponding to his T1DM. Due to his cognitive and memory deficits, he was also forgetting that he had eaten previously and was snacking in between meals without insulin coverage, making his diabetes management challenging. The patient lives in a semi-independent group home, and the staff were hesitant to withhold food from the patient with the concern for behavioral outbursts. The patient’s hyperphagia, neurologic deficits, and living arrangements made adherence to the recommended insulin protocol difficult. A trial of subcutaneous semaglutide 0.25 mg weekly was initiated to reduce his hyperphagia; however, he did not tolerate it. Liraglutide 0.6 mg daily was trialed resulting in remarkable improvement in BG with GMI down to 6.8% and TIR 61% after 1 month of treatment. He reports his appetite decreased significantly. Due to significant hypoglycemia (14%), insulin aspart was discontinued and insulin degludec dose was reduced. 1 month later, his BG remained well-controlled on low-dose liraglutide and insulin degludec: GMI 7.3%, TIR 54%, and TBR 3%. His weight decreased by 8% during this time. Conclusion: Patients with HO and T1DM can be especially challenging to manage given the wide range in patient outcomes. Our patient had a dramatic response over 2 months to low-dose liraglutide, with regards to decrease in BG, weight, and total daily dose of insulin. GLP-1 receptor agonists have a strong effect on satiety in HO, especially in patients with insulin deficiency where BG can be controlled without prandial insulin. Monday, June 3, 2024