• Journal of Nutrition and Health
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• 제21권3호
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• pp.182-187
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• 1988

Ovariectomy induced hyperphagia was reported in various animal models. It was postulated that hyperphagia resulted in interstinal hypertrophy and hyperplasia. Therefore, this study was performed to compare the food intake and intestinal changes between ovariectomized rats(OVX) and sham operated rats(Sham). Results of this study showed that the food intake and body weight of OVX animal was significantly higher than those of Sham animal. This results confirmed the effect of ovarian hormone on the food intake regulation. Hyperphagia induced by ovariectomy influence the intestinal cell growth and showed hyperplasia determined by protein/DNA ratio. Maltase and alkaline phosphatase activity suggested that the intestinal cell was fully matured in body groups. There were no difference in weight of other organs, such as liver, heart and kindney between two groups.

• 대한한의학회지
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• 제34권1호
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• pp.179-191
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• 2013

Kleine-Levin syndrome is a rare disorder characterized by recurrent episodes of hypersomnia, hyperphagia, hypersexuality and delusion and hallucination with spontaneous recovery. A 17-year-old female suddenly showed hypersomnia, severe fatigue, and compulsive hyperphagia. She was diagnosed with suspected Kleine-Levin Syndrome. The precipitating factor was an upper respiratory tract infection that the patient had undergone 2 weeks prior. Past psychiatric history included somnambulism and ADHD; her symptoms of ADHD included attention deficit, impulsiveness, hyperactivity, and irritability. This was her third episode. Her hypersomnia was longer in duration but lower in frequency compared with usual KLS. Her low LF/HF ratio in heart rate variability measurement showed high parasympathetic nerve activity. A MMPI report showed some psychological problem. The patient was diagnosed of gastric fever by pattern identification. Her hypersomnia episode improved 6 weeks after onset. This is the first reported case of suspected Kleine-Levin Syndrome in the field of Oriental Medicine in Korea.

• 한국수산과학회지
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• 제41권2호
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• pp.125-133
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• 2008

To investigate the effect of repeated food deprivation and refeeding on the hyperphagia, compensatory growth, feed efficiency, body composition, hepatosomatic index (HSI), and survival rate of the juvenile olive flounder Paralichthys olivaceus, an experiment was conducted for 90 days. Feeding treatments consisted of the following five regimes for 90 days from August to October, 2005: C: daily satiation feeding (control), S1: 1-day satiation feeding after 1-day food deprivation, S2: 1-day satiation feeding after 2-day food deprivation, S3: 1-day satiation feeding after 3-day food deprivation and S4: 1-day satiation feeding after 4-day food deprivation, respectively. Although the monthly feed intake (MFI) of the control was significantly higher than that of all of the starved groups, the daily feed intake (DFI) was more higher in S1, S2, and S3 than that in the control as a result of hyperphagia after starvation. While the feed efficiency in the summer (to day 30) decreased in all of the starved groups with prolongation of the starvation period, the feed efficiency in the autumn (to day 90) was increased with prolongation of the starvation period. The whole body proximate composition and HSI were also affected by starvation. The crude protein, lipid, and HSI decreased with prolongation of the starvation period, whereas the crude ash and moisture increased. The growth rate and condition factor also decreased in proportion to the starvation period. The survival rate was highest in the control and was the lowest in S4. In this study, although hyperphagia occurred in the deprived groups, we knew that the compensatory growth did not always occur.

• Journal of mucopolysaccharidosis and rare diseases
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• 제5권1호
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• pp.39-41
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• 2021

Prader-Willi syndrome (PWS) is a rare genetic neurodevelopmental disorder of hyperphagia leading to severe obesity, intellectual deficits, compulsivity, and other behavioral problems. PWS is caused by the inactivation of contiguous genes on chromosome 15q11-q13, which complicates the development of targeted, effective therapeutics. Various preclinical studies have been conducted by developing mouse models that exhibit phenotypes similar to PWS. Oxytocin deficiency in PWS is associated with hyperphagia with impaired satiety and, food-seeking and behavior disorders. Here, we summarize the oxytocin study of ingestion behavior tested in the PWS mouse model and published data from clinical trials that have evaluated treatment effectiveness on ingestion behavior and social dysfunction in patients with PWS.

• Molecules and Cells
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• 제45권4호
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• pp.169-176
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• 2022

A primary cilium, a hair-like protrusion of the plasma membrane, is a pivotal organelle for sensing external environmental signals and transducing intracellular signaling. An interesting linkage between cilia and obesity has been revealed by studies of the human genetic ciliopathies Bardet-Biedl syndrome and Alström syndrome, in which obesity is a principal manifestation. Mouse models of cell type-specific cilia dysgenesis have subsequently demonstrated that ciliary defects restricted to specific hypothalamic neurons are sufficient to induce obesity and hyperphagia. A potential mechanism underlying hypothalamic neuron cilia-related obesity is impaired ciliary localization of G protein-coupled receptors involved in the regulation of appetite and energy metabolism. A well-studied example of this is melanocortin 4 receptor (MC4R), mutations in which are the most common cause of human monogenic obesity. In the paraventricular hypothalamus neurons, a blockade of ciliary trafficking of MC4R as well as its downstream ciliary signaling leads to hyperphagia and weight gain. Another potential mechanism is reduced leptin signaling in hypothalamic neurons with defective cilia. Leptin receptors traffic to the periciliary area upon leptin stimulation. Moreover, defects in cilia formation hamper leptin signaling and actions in both developing and differentiated hypothalamic neurons. The list of obesity-linked ciliary proteins is expending and this supports a tight association between cilia and obesity. This article provides a brief review on the mechanism of how ciliary defects in hypothalamic neurons facilitate obesity.

• BMB Reports
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• 제48권4호
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• pp.229-233
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• 2015

The central nervous system (CNS) controls food intake and energy expenditure via tight coordinations between multiple neuronal populations. Specifically, two distinct neuronal populations exist in the arcuate nucleus of hypothalamus (ARH): the anorexigenic (appetite-suppressing) pro-opiomelanocortin (POMC) neurons and the orexigenic (appetite-increasing) neuropeptide Y (NPY)/agouti-related peptide (AgRP) neurons. The coordinated regulation of neuronal circuit involving these neurons is essential in properly maintaining energy balance, and any disturbance therein may result in hyperphagia/obesity or hypophagia/starvation. Thus, adequate knowledge of the POMC and NPY/AgRP neuron physiology is mandatory to understand the pathophysiology of obesity and related metabolic diseases. This review will discuss the history and recent updates on the POMC and NPY/AgRP neuronal circuits, as well as the general anorexigenic and orexigenic circuits in the CNS. [BMB Reports 2015; 48(4): 229-233]

• Journal of Dental Anesthesia and Pain Medicine
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• 제15권4호
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• pp.251-255
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• 2015

Prader-Willi syndrome (PWS) is a rare genetic disorder reported rarely in dentistry. Dental practitioners should know the features of PWS because affected patients have a variety of dental symptoms. The current report describes a case of PWS. An 18-year-old male patient presented with traumatic injuries. Initial emergency treatments were performed under sedation, and further treatments were conducted under general anesthesia. After adequate healing, periodic follow-up and dietary management according to the patient's age and nutritional phase were recommended. Dental management of PWS patients consists of active preventive measures in addition to dietary consultation according to age and nutritional phase.

• 수면정신생리
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• 제3권1호
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• pp.79-84
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• 1996

Kleine-Levin syndrome is a disorder characterized by recurrent episodes of hypersomnia, hyperphagia and hypersexuality that typically occur weeks or months apart. A 17-years-old male showed these episodes and took nocturnal polysomnography(NPSG) and multiple sleep latency test(MSLT). As results of NPSG, sleep latency was 82.5min, sleep efficiency was 82.5min, sleep efficiency was 82.5%, latency and percentage of REM sleep were 106.5min and 14.6% and percentage of slow wave sleep was 12.7%. In 4 times MLST, average of sleep latency and REM latency were 8min 7sec and 5min 20sec with 3 times sleep onset REM period(SOREMP). These findings are consistent with these of Keine-Levin syndrome. And the possible causes and classification of this syndrome were discussed.

• Journal of mucopolysaccharidosis and rare diseases
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• 제2권2호
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• pp.38-40
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• 2016

Prader-Willi syndrome (PWS) is a rare genetic disorder often caused by a deletion of the chromosome 15q11-q13 region inherited from the father or by maternal disomy 15. Growth hormone deficiency with short stature, hypogonadism, cognitive and behavioral problems, analgesia, decreased gastric motility and decreased ability to vomit with hyperphagia are common in PWS leading to severe obesity in early childhood, if not controlled. The goal of this study is to investigate the effects of recombinant human GH (rhGH, henceforth designated GH) on the gene expression related to cognitive function in the brain of PWS mouse model (Snord116del). GH restored the mRNA expression level of several genes in the cerebellum. These data suggest the effect of GH on the expression of cognitive function related genes in cerebellum may provide a mechanism for the GH-induced brain function in PWS patients.

• Journal of mucopolysaccharidosis and rare diseases
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• 제5권1호
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• pp.34-38
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• 2021

Prader-Willi syndrome is a complicated genetic disorder caused by a mutation on chromosome 15q11-13. The disease results in morbid obesity due to hyperphagia, growth disturbance, multiple endocrine problems from hypopituitarism, developmental delay, and cognitive or behavioral problems. Recombinant human growth hormone has been used to improve body composition and muscle mass, which plays a main role in treating patients with Prader-Willi syndrome. We describe previous studies showing the efficacy and safety of growth hormone treatment in children with Prader-Willi syndrome and provide treatment guidelines. Growth hormone therapy could be beneficial for children with Prader-Willi syndrome and improve their quality of life.