Purpose Of Review: Hypothalamic alterations, pathological or treatment induced, have major impact on prognosis in craniopharyngioma patients mainly because of consequent hypothalamic obesity. Recent insight in molecular genetics, treatment strategies, risk factors and outcomes associated with hypothalamic obesity provide novel therapeutic perspectives. This review includes relevant publications since 2013.
Recent Findings: Recent findings confirm that alterations in posterior hypothalamic areas because of tumour location and/or treatment-related injuries are associated with severe hypothalamic obesity, reduced overall survival and impaired quality of life in long-term survivors of childhood-onset craniopharyngioma. However, eating disorders are observed because of hypothalamic obesity without clear disease-specific patterns. Treatment options for hypothalamic obesity are very limited. Treatment with invasive, nonreversible bariatric methods such as Roux-en-Y gastric bypass is most efficient in weight reduction, but controversial in the paediatric population because of medical, ethical, and legal considerations. Accordingly, treatment in craniopharyngioma should focus on prevention of (further) hypothalamic injury. Presurgical imaging for grading of hypothalamic involvement should be the basis for hypothalamus-sparing strategies conducted by experienced multidisciplinary teams.
Summary: Until a nonsurgical therapeutic option for hypothalamic obesity for paediatric patients is found, prevention of hypothalamic injury should be the preferred treatment strategy, conducted exclusively by experienced multidisciplinary teams.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4700877 | PMC |
| http://dx.doi.org/10.1097/MED.0000000000000214 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Hunting for heroes: Brain neurons mediating GLP-1R agonists in obesity treatment.
Obes Med
December 2024
The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, The University of Texas Health Science Center at Houston, MD Anderson Cancer Center & UTHealth Houston Graduate School for Biomedical Sciences, University of Texas Health Science at Houston, Texas, 77030, USA.
Glucagon-like peptide 1 (GLP-1) receptor agonists (GLP-1RAs) have proven to be highly effective in reducing obesity across species and ages, gaining unmet popularity in clinical treatments against obesity. Although extensive research efforts have been made to explore how the brain regulates body weight homeostasis including the effect brought up by GLP-1 and its synthetic analogs GLP-1RAs, the identity of neurons and neural pathways that are responsible for the observed anti-obesity effect of GLP-1RAs remain largely elusive. Excitingly, three recent high-profile studies presented compelling evidence that each argues for the importance of GLP-1Rs in the dorsomedial hypothalamus, hindbrain, or lateral septum, respectively, in mediating the anti-obesity effect of GLP-1RAs.
View Article and Find Full Text PDFNeurobiological mechanisms of nicotine's effects on feeding and body weight.
Neurosci Biobehav Rev
January 2025
Department of Nutrition and Health, Beijing Advanced Innovation Center for Food Nutrition and Human Health, China Agricultural University, Beijing, China; Beijing Life Science Academy, Beijing, China. Electronic address:
Nicotine, a neuroactive substance in tobacco products, has been widely studied for its effects on feeding and body weight, mostly focusing on the involvement of nervous system, metabolism, hormones, and gut microbiota. To elucidate the action mechanism of nicotine on feeding and body weight, especially the underlying neurobiological mechanisms, we reviewed the studies on nicotine's effects on feeding and body weight by the regulation of various nerve systems, energy expenditure, peripheral hormones, gut microbiota, etc. The role of neuronal signaling molecules such as AMP-activated protein kinase (AMPK) and kappa opioid receptor (κOR) were specialized in the nicotine-regulating energy expenditure.
View Article and Find Full Text PDFPollution, stress response, and obesity: A systematic review.
Obes Rev
January 2025
Inserm UMR 1256 Nutrition-Genetics-Environmental Risk Exposure (N-G-ERE), University of Lorraine, Nancy, France.
Limited literature addresses the association between pollution, stress, and obesity, and knowledge synthesis on the associations between these three topics has yet to be made. Two reviewers independently conducted a systematic review of MEDLINE, Embase, and Web of Science Core Collection databases to identify studies dealing with the effects of semi-volatile organic compounds, pesticides, conservatives, and heavy metals on the psychosocial stress response and adiposity in humans, animals, and cells. The quality of papers and risk assessment were evaluated with ToxRTool, BEES-C instrument score, SYRCLE's risk of bias tool, and CAMARADES checklist.
View Article and Find Full Text PDFEnhanced thermogenesis in PAS Kinase-deficient male mice.
Biochem Pharmacol
January 2025
Department of Cell Biology, Faculty of Medicine, Complutense University of Madrid, Spain; Institute of Medical Research at the San Carlos Clinic Hospital (IdISSC), Madrid, Spain.
PAS domain-containing serine/threonine-protein kinase (PASK) is a nutrient and energy sensor regulated by fasting/refeeding conditions in hypothalamic areas involved in controlling energy balance. In this sense, PASK plays a role in coordinating the activation/inactivation of AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR) in response to fasting. PASK deficiency protects against the development of diet-induced obesity.
View Article and Find Full Text PDFThe central control of energy metabolism; hypothalamic obesity is not one disease.
Horm Res Paediatr
January 2025
Background The hypothalamus, a neuro-endocrine gland located centrally in the brain, weighs only on average 4 grams but is the captain on the ship of our energy balance. In the hypothalamus, signals of the satiety and hunger hormones are integrated and individuals with a dysfunctional hypothalamus develop obesity. The hypothalamus, however, integrates much more than the satiety and hunger hormones and hypothalamic obesity may be the result of a combination of factors.
View Article and Find Full Text PDFWant 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!