Acquired hypothalamic obesity: A clinical overview and update

Roth, Christian L.; McCormack, Shana E.

doi:10.1111/dom.15530

Cited by 42Regulation of Appetite and ObesityHypothalamic control of reproductive hormonesPituitary Gland Disorders and Treatments

Acquired hypothalamic obesity: A clinical overview and update

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Roth, Christian L., McCormack, Shana E.·2024·Diabetes, Obesity and Metabolism

DOI 10.1111/dom.15530PMC PMC13372222

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Abstract

Hypothalamic obesity (HO) is a rare and complex disorder that confers substantial morbidity and excess mortality. HO is a unique subtype of obesity characterized by impairment in the key brain pathways that regulate energy intake and expenditure, autonomic nervous system function, and peripheral hormonal signalling. HO often occurs in the context of hypothalamic syndrome, a constellation of symptoms that follow from disruption of hypothalamic functions, for example, temperature regulation, sleep–wake circadian control, and energy balance. Genetic forms of HO, including the monogenic obesity syndromes, often impact central leptin–melanocortin pathways. Acquired forms of HO occur as a result of tumours impacting the hypothalamus, such as craniopharyngioma, surgery or radiation to treat those tumours, or other forms of hypothalamic damage, such as brain injury impacting the region. Risk for severe obesity following hypothalamic injury is increased with larger extent of hypothalamic damage or lesions that contain the medial and posterior hypothalamic nuclei that support melanocortin signalling pathways. Structural damage in these hypothalamic nuclei often leads to hyperphagia, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue, the collective effect of which is rapid weight gain. Individuals with hyperphagia are perpetually hungry. They do not experience fullness at the end of a meal, nor do they feel satiated after meals, leading them to consume larger and more frequent meals. To date, most efforts to treat HO have been disappointing and met with limited, if any, long‐term success. However, new treatments based on the distinct pathophysiology of disturbed energy homeostasis in acquired HO may hold promise for the future.

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Healthful nutrition and physical activity, as well as other aspects of lifestyle modification, are critical aspects of treatment, especially to prevent or mitigate obesity-related health problems.
“Healthful nutrition and physical activity, as well as other aspects of lifestyle modification, are critical aspects of treatment, especially to prevent or mitigate obesity-related health problems”
From Approach to the patient with acquired hypothalamic syndrome (2026) · cites this paper as [36]
Healthful nutrition and physical activity are rarely sufficient to address weight gain in hypothalamic obesity.
“but are rarely sufficient to address weight gain”
From Approach to the patient with acquired hypothalamic syndrome (2026) · cites this paper as [36]
Pharmacotherapy is playing an increasing role in the treatment of hypothalamic obesity.
“as a result, pharmacotherapy is playing an increasing role (36, 37)”
From Approach to the patient with acquired hypothalamic syndrome (2026) · cites this paper as [36]

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Peripheral Effect of α-Melanocyte-stimulating Hormone on Fatty Acid Oxidation in Skeletal Muscle
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α-Melanocyte stimulating hormone promotes muscle glucose uptake via melanocortin 5 receptors
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Randomized controlled trial of Tesomet for weight loss in hypothalamic obesity
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The novel triple monoamine reuptake inhibitor tesofensine induces sustained weight loss and improves glycemic control in the diet-induced obese rat: Comparison to sibutramine and rimonabant
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Hypothalamic Obesity: 4 Years of the International Registry of Hypothalamic Obesity Disorders
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A Novel Rodent Model That Mimics the Metabolic Sequelae of Obese Craniopharyngioma Patients
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A Pilot Randomized Clinical Trial of Intranasal Oxytocin to Promote Weight Loss in Individuals With Hypothalamic Obesity
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A randomized, placebo‐controlled trial of beloranib for the treatment of hypothalamic injury‐associated obesity
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Effects of T3 treatment on brown adipose tissue and energy expenditure in a patient with craniopharyngioma and hypothalamic obesity
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Bariatric Surgery for Hypothalamic Obesity in Craniopharyngioma Patients: A Retrospective, Matched Case-Control Study
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Hyperleptinaemia rather than fasting hyperinsulinaemia is associated with obesity following hypothalamic damage in children
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<scp>MRI</scp> measures of hypothalamic injury are associated with glucagon‐like peptide‐1 receptor agonist treatment response in people with hypothalamic obesity
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Hypothalamic obesity in patients with craniopharyngioma: treatment approaches and the emerging role of gastric bypass surgery
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Serum Leptin and Leptin Binding Activity in Children and Adolescents with Hypothalamic Dysfunction
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Methylphenidate improves weight control in childhood brain tumor survivors with hypothalamic obesity
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Nonalcoholic fatty liver disease in long-term survivors of childhood-onset craniopharyngioma
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Peripheral effect of alpha-melanocyte-stimulating hormone on fatty acid oxidation in skeletal muscle
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Five-Year Changes in Weight and Diabetes Status After Bariatric Surgery for Craniopharyngioma-Related Hypothalamic Obesity: a Case–Control Study
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Impact of Setmelanotide Treatment on Reducing Hyperphagia in Pediatric and Adult Patients With Hypothalamic Obesity
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Hypothalamic obesity: from basic mechanisms to clinical perspectives
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Setmelanotide for the Treatment of Acquired Hypothalamic Obesity
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Management of Acquired Hypothalamic Obesity After Childhood-Onset Craniopharyngioma—A Narrative Review
Muller, H. L. (2025) · Biomedicines · doi:10.3390/biomedicines13051016 · Cited by 9 · see citing works
From Hypothalamic Obesity to Metabolic Dysfunction-Associated Steatotic Liver Disease: Physiology Meets the Clinics via Metabolomics
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Treatment of patients with tumor/treatment-related hypothalamic obesity in the first two years following surgical treatment or radiotherapy
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Successful Treatment of Hypothalamic Obesity with Tirzepatide
Brijmohan, S., & Mullally, J. A. (2025) · AACE Endocrinology and Diabetes · doi:10.1016/j.aed.2025.03.004 · Cited by 8 · see citing works
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Authors: Roth, C. L., & McCormack, S. E.
Affiliations: University of Washington (US)
Children's Hospital of Philadelphia (US)
Corresponding author: Roth, Christian L.
ORCID: Roth, Christian L.
McCormack, Shana E.
Venue: Diabetes, Obesity and Metabolism
Publisher: Wiley
Published: 2024-03-07
Volume: 26
Issue: S2
Pages: 34-45
ISSN: 1462-8902 (ISSN-L)
1463-1326
DOI: 10.1111/dom.15530
PMC: PMC13372222
OpenAlex: W4392557945
Cited by: 42
References: 139
Citations by year: 2026: 22 · 2025: 13 · 2024: 7
FWCI: 9.05
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Diabetes Obesity and Metabolism (publishedVersion)
PubMed (publishedVersion)
PubMed Central (publishedVersion)
Funders: National Institutes of Health (R01DK135125, R01DK135211, R01DK098466, R01DK13521)
Topics: Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pituitary Gland Disorders and Treatments
Keywords: hypothalamic syndrome, hypothalamic tumors, craniopharyngioma, hypothalamic injury, hyperphagia, leptin resistance, insulin resistance, melanocortin pathway, energy homeostasis, obesity treatment, hypothalamic nuclei
MeSH terms: Craniopharyngioma, Energy Metabolism, Humans, Hyperphagia, Hypothalamic Diseases, Hypothalamus, Obesity, Pituitary Neoplasms, Leptin, Melanocortins

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Acquired hypothalamic obesity: A clinical overview and update

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