hyperphagia การใช้

• In each pair, one rat became obese and exhibited hyperphagia.
• These eight mutations all cause extreme obesity in infancy, with hyperphagia.
• Before 2005, hyperphagia and hypersexuality were thought to occur in all cases.
• CART hypoactivity in the hypothalamus of depressed animals is associated with hyperphagia and weight gain.
• Lesions subsequently made in the hypothalamus of two paired rats resulted in hyperphagia and obesity.
• Genetic variability may influence hedonic hyperphagia.
• Coleman and researchers further identified a gene on chromosome 4 that led to hyperphagia and obesity in mice.
• The obesity and hyperphagia may be mediated by impaired melanocortin activation of PVN neurons and oxytocin deficiency in these mice.
• In preparation for winter, bears can gain approximately, during a period of hyperphagia, before going into hibernation.
• Overexpression of SIM1 protects against diet induced obesity and rescues the hyperphagia of agouti yellow mice, who have disrupted melanocortin signaling.
• These steroid hormones increase appetite and, unlike CRH, remain in the bloodstream for a prolonged period of time, often resulting in hyperphagia.
• Additionally, studies in mice have shown that haploinsufficieny of Sim1 causes obesity that is due to hyperphagia and do not respond properly to increased dietary fat.
• It has been demonstrated that modulating Sim1 levels postnatally also leads to hyperphagia and obesity, suggesting a physiological role for Sim1 separate from its role in development.
• People with Prader Willi syndrome have high ghrelin levels, which are thought to directly contribute to the increased appetite, hyperphagia, and obesity seen in this syndrome.
• Feeding behaviors in children with ONH often include hyperphagia ( overeating ), resulting in obesity; or hypophagia ( reduced food intake ) with or without weight loss.
• In animals it produces effects including hyperphagia, hyperactivity, and anxiolysis, of which are all likely mediated predominantly or fully by blockade of the 5-HT 2C receptor.
• More aspects seen in a clinical overview include hypotonia and abnormal neurologic function, hypogonadism, developmental and cognitive delays, hyperphagia and obesity, short stature, and behavioral and psychiatric disturbances.
• Case # 1 : A 30-year-old, right-handed man was admitted to the department of neurology for irritability, inappropriate behavior, and morbid hyperphagia with obesity.
• PWS is frequently found to be the reason for secondary obesity due to early onset hyperphagia-the abnormal increase in appetite for consumption of food . There are known three molecular causes of Prader Willi syndrome development.
• These two types of cells are neuropeptide Y ( NPY )-expressing cells, which cause hyperphagia and energy conservation, and cells that pro-opiomelanocortin ( POMC ), which are related to hypophagia and increased energy expenditure.