Results 91 to 100 of about 26,081 (268)

Effects of MetAP2 inhibition on hyperphagia and body weight in Prader-Willi syndrome: a randomized, double-blind, placebo-controlled trial

open access: yesDiabetes, obesity and metabolism, 2017
There are no treatments for the extreme hyperphagia and obesity in Prader–Willi syndrome (PWS). The bestPWS clinical trial assessed the efficacy, safety and tolerability of the methionine aminopeptidase 2 (MetAP2) inhibitor, beloranib.
S. McCandless   +23 more
semanticscholar   +1 more source

Management of ring chromosome 20 syndrome: Narrative review and consensus recommendations

open access: yesEpilepsia, EarlyView.
Abstract Ring chromosome 20 (ring 20) is a rare genetic condition usually presenting as developmental and epileptic encephalopathy. The disease is caused by fusion of the long and short arms of chromosome 20. Patients are symptomatic even if there is no loss of genetic material.
Asma Khamis   +8 more
wiley   +1 more source

Biopsychosocial determinants of hyperphagia [PDF]

open access: yes, 2013
Nadmierne łaknienie jest zaburzeniem charakteryzującym się gwałtownym pochłanianiem bardzo dużych ilości pożywienia oraz równoczesną niemożnością przerwania napadu żarłoczności. Wbrew obiegowym opiniom hiperfagia nie jest tożsama z bulimia nervosa.
Kryska, S., Grajek, M.
core  

Functional constipation in children and young adults with Prader–Willi syndrome

open access: yesJPGN Reports, EarlyView.
Abstract Objectives Prader–Willi Syndrome (PWS) is characterized by hyperphagia, endocrinopathies, and gastrointestinal abnormalities. Clinical concerns about constipation and fecal incontinence (FI) are common, but no studies to date have clear data on functional defecation disorders in children with PWS.
Melinda J. Pierce   +3 more
wiley   +1 more source

A questionnaire-based survey on hyperphagia in individuals with Prader–Willi syndrome in Japan

open access: yesEndocrine Journal
Prader–Willi syndrome (PWS) is associated with increased mortality, primarily due to complications from hyperphagia-associated obesity. Clinical trials investigating anti-hyperphagic medications are currently underway.
Makiko Tachibana   +9 more
doaj   +1 more source

Effectiveness and Safety of Setmelanotide in a Patient With a Heterozygous PCSK1 Deficiency

open access: yesObesity, EarlyView.
ABSTRACT Setmelanotide, a melanocortin 4 receptor (MC4R) agonist, is a promising pharmacological treatment option for people with rare monogenic obesity conditions affecting the leptin‐melanocortin signaling pathway, including proprotein convertase subtilisin/kexin type 1 (PCSK1) gene mutations.
Ellina Lytvyak   +2 more
wiley   +1 more source

Obesity and Hyperphagia With Increased Defective ACTH: A Novel POMC Variant [PDF]

open access: yes, 2022
Context: Patients with pro-opiomelanocortin (POMC) defects generally present with early-onset obesity, hyperphagia, hypopigmentation and adrenocorticotropic hormone (ACTH) deficiency.
Delhanty, Patric J D   +33 more
core   +2 more sources

Perinatal programming effects on feeding behavior

open access: yesJournal of Behavior and Feeding
To address the growing prevalence of obesity and its associated metabolic consequences, it is essential to understand the evolutionary origins of health and disease.
Ana Patricia Zepeda Salvador   +9 more
doaj   +1 more source

Short-term feeding at the wrong time is sufficient to desynchronize peripheral clocks and induce obesity with hyperphagia, physical inactivity and metabolic disorders in mice.

open access: yesMetabolism: Clinical and Experimental, 2016
BACKGROUND The circadian clock regulates various physiological and behavioral rhythms such as feeding and locomotor activity. Feeding at unusual times of the day (inactive phase) is thought to be associated with obesity and metabolic disorders in ...
Yuki Yasumoto   +11 more
semanticscholar   +1 more source

Monogenic and syndromic obesity in children: Clinical recognition, genetics, and precision management

open access: yesPediatric Investigation, EarlyView.
Monogenic and syndromic obesity in children often arises from defects in the leptin–melanocortin pathway. Understanding these rare genetic causes not only clarifies mechanisms of appetite regulation but also enables precision therapies, offering hope beyond lifestyle interventions.
Hadel Khalil   +2 more
wiley   +1 more source

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