# Effect of Tirzepatide in an Adolescent With Early-Onset Obesity, Hyperphagia, and Type 2 Diabetes

## TL;DR

A 19-year-old with severe obesity and type 2 diabetes showed significant improvement with tirzepatide, suggesting it may help adolescents with similar conditions.

## Contribution

Demonstrates the potential of tirzepatide in treating severe early-onset obesity and hyperphagia in adolescents without known genetic or hypothalamic causes.

## Key findings

- The patient showed a clinically significant response to tirzepatide after failing conventional treatments.
- Tirzepatide may be effective for adolescents with severe obesity and hyperphagia, even without identifiable genetic or hypothalamic pathology.

## Abstract

Early-onset severe obesity is rare and largely treatment-resistant to standard measures. Etiologies include syndromic disorders (Prader-Willi, Bardet-Biedl and Alström syndromes), monogenic defects of appetite-regulating pathways - most significantly melanocortin-4-receptor (MC4R) deficiency, but also leptin receptor (LEPR), pro-opiomelanocortin (POMC), and secondary hypothalamic injury, most commonly craniopharyngiomas. Most childhood obesity, however, is polygenic, arising from interactions of environmental and genetic factors. In many patients, no clear etiology is identified. Treatment remains challenging, particularly if hyperphagia and reduced satiety are predominant presenting features.

We describe the case of a 19-year-old male with a history of autism spectrum disorder, attention-deficit hyperactivity disorder (ADHD), type 2 diabetes mellitus (T2DM) and morbid obesity, who showed a clinically significant response to tirzepatide therapy following failed conventional interventions.

This case highlights the potential role of dual incretin therapy in adolescents with severe early-onset obesity and hyperphagia, even in the absence (based on present knowledge) of identifiable hypothalamic or genetic pathology.