Purpose: Patients with hypothalamic pathology often develop hypothalamic obesity, causing severe metabolic alterations resulting in increased morbidity and mortality. Treatments for hypothalamic obesity have not proven very effective, although the glucagon-like peptide-1 receptor agonist semaglutide has been shown to have positive effects. We examined semaglutide's effect on weight loss in a sample of patients with hypothalamic obesity.

Methods: Four female patients with hypothalamic obesity resulting from treatment of craniopharyngiomas were treated with semaglutide for six months. Whole Body Dual-energy x-ray absorptiometry scans were performed, and blood samples drawn at baseline and after six months. Semaglutide dosages were increased monthly along with tracking of body weight and eating behavior (Three Factor Eating Questionnaire, TFEQ-R18).

Results: BMI was reduced in all cases, with an average of 7.9 BMI (range: 6.7 to 10.1) corresponding to a weight loss of 17.0% (range: 11.3-22.4%) or 20.2 kg (range 16.2 kg to 23.4 kg). We found a comparable reduction in total fat mass (17.2%, p = 0.006) and lean mass (16.0%, p = 0.05), whereas bone mass was unchanged (2.6%, p = 0.12). All cases reported an increase in energy levels, improved mobility and physical activity. Unfavorable eating behaviors were reduced after 1 month of treatment (emotional eating - 41 points, p = 0.02, uncontrolled eating - 23 points, p = 0.11). HbA1c and total cholesterol were significantly reduced (p = 0.014 for both).

Conclusion: Semaglutide is a promising and safe treatment option for HO, that improves eating behavior, reduces weight, and improves metabolic markers.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11513775PMC
http://dx.doi.org/10.1007/s11102-024-01426-8DOI Listing

Publication Analysis

Top Keywords

hypothalamic obesity
16
patients hypothalamic
12
semaglutide promising
8
weight loss
8
eating behavior
8
hypothalamic
6
eating
6
semaglutide
5
treatment
4
promising treatment
4

Similar Publications

SF1-specific deletion of the energy sensor AMPKγ2 induces obesity.

Mol Metab

December 2024

Department of Physiology, CiMUS, University of Santiago de Compostela, Santiago de Compostela, 15782, Spain; CIBER Fisiopatología de la Obesidad y Nutrición (CIBEROBN), Santiago de Compostela, 15706, Spain. Electronic address:

Objective: AMP-activated protein kinase (AMPK) is a heterotrimer complex consisting of a catalytic α subunit (α1, α2) with a serine/threonine kinase domain, and two regulatory subunits, β (β1, β2) and γ (γ1, γ2, γ3), encoded by different genes. In the hypothalamus, AMPK plays a crucial role in regulating energy balance, including feeding, energy expenditure, peripheral glucose and lipid metabolism. However, most research on hypothalamic AMPK has concentrated on the catalytic subunits AMPKα1 and AMPKα2, with little focus on the regulatory subunits.

View Article and Find Full Text PDF
Article Synopsis
  • Non-neoplastic hypercortisolaemia, or pseudo-Cushing's syndrome (PCS), can occur due to various health conditions like depression, obesity, and diabetes, linked to overactivity of the hypothalamic-pituitary-adrenal axis.
  • A 66-year-old woman exhibited symptoms such as weakness, weight loss, and poorly controlled hypertension, which led to the discovery of pheochromocytoma, a tumor that causes hormone overproduction, upon further testing.
  • After undergoing surgery to remove the tumor and receiving supportive treatment, her symptoms improved significantly, confirming the diagnosis of PCS rather than traditional Cushing's syndrome.
View Article and Find Full Text PDF

Aims: Hypothalamic endoplasmic reticulum stress (ERS) and mitochondrial dysfunction are two important mechanisms involved in the pathophysiology of obesity, which can be reversed by aerobic exercise to improve organ function. Mitofusion 2 (Mfn2), a mitochondrial membrane protein, affects both mitochondrial dynamics and ER morphology. This study explored the contribution of hypothalamic Mfn2 to exercise-induced improvements in energy homeostasis and peripheral metabolism and the underlying mechanisms involved.

View Article and Find Full Text PDF

High-fat diet (HFD) -induced microglial activation contributes to hypothalamic inflammation and obesity, but the mechanisms linking microglia to structural changes remain unclear. This study explored the role of microglia in impairing hypothalamic synaptic plasticity in diet-induced obesity (DIO) mice and evaluated the therapeutic potential of semaglutide (Sema) and minocycline (MI). Six-week-old C57BL/6J mice were divided into low-fat diet (LFD) and HFD groups.

View Article and Find Full Text PDF

Objectives: To present cases of rapid onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) and discuss management insights.

Methods: Case records of patients fulfilling the criteria for ROHHAD and presenting to the Pediatric Endocrinology Division of All India Institute of Medical Sciences, New Delhi, between July 2019 and June 2024 were reviewed for clinical features, treatments, and outcomes.

Results: Five patients (4 boys, 1 girl) presented at a median age of 4 y (range 3.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!