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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma free fatty acid (FFA) levels were measured in the mallard duck (Anas platyrhynchos) following hypothalamic lesions at various sites. The results indicate that ventromedial lesions produced hyperphagia, increased deposition of fat, and significantly elevated levels of plasma FFA. Anterior bilateral lesions resulted in aphagia, severe loss in body weight and a marked decrease in plasma FFA. Lesions in other regions of the hypothalamus produced various changes depending upon the extent of damage. The neural and neuroendocrine mechanisms which regulate FFA levels in the blood are discussed with respect to the involvement of pituitary hormones.
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PMID:Effects of hypothalamic lesions on levels of plasma free fatty acids in the mallard duck. 5 44

I have described a 21-year-old man who had biopsy-proven hypothalamic sarcoidosis and polyphagia with a weight increase to 393 lb (178.6 kg) on a 5 ft 4 inch frame during a seven-year follow-up. This morbid obesity appears to be due to sarcoid invasion of the satiety center in the ventral medial nucleus of the hypothalamus. In addition, sarcoid invasion of the supraoptic nucleus produced partial diabetes insipidus. Anterior pituitary deficiency, with complete gonadotropin and growth hormone deficiency, as well as partial ACTH and TSH deficiency, were also present.
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PMID:Hypothalamic sarcoidosis: a new cause of morbid obesity. 273 38

Experiment and clinical evidence of hypothalamic influence on autonomic function has accumulated since the early part of this century. Localization of hypothalamic lesions is difficult, and damage must be bilateral to produce symptoms. Caloric balance may be altered, with ventromedial lesions causing hyperphagia, and lateral hypothalamic lesions producing a syndrome of aphagia and weight loss in experimental animals. Gastric ulcerations are associated with brainstem lesions, including the diencephalon. Anterior hypothalamic lesions cause hyperthermia, while posterior lesions result in hypothermia, often accompanied by disturbance of sweating mechanisms. Disorders of sleep and wakefulness are seen clinically in encephalitis lethargica and Wernicke's syndrome, both associated with hypothalamic damage. The hypothalamus is the regulator and co-ordinator of central autonomic activity.
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PMID:Vegetative dysfunctions of the hypothalamus. 399 47

Prader-Willi syndrome (PWS) is a well-defined syndrome of childhood-obesity which can serve as a model for investigating early onset childhood obesity. Many of the clinical features of PWS (e.g., hyperphagia, hypogonadotropic hypogonadism, growth hormone deficiency) are hypothesized to be due to abnormalities of the hypothalamus and/or pituitary gland. Children who become severely obese very early in life (i.e., before age 4 years) may also have a genetic etiology of their obesity, perhaps with associated neuroendocrine and hypothalamo-pituitary defects, as infants and very young children have limited access to environmental factors that contribute to obesity. We hypothesized that morphologic abnormalities of the pituitary gland would be seen in both individuals with PWS and other subjects with early onset morbid obesity (EMO). This case-control study included individuals with PWS (n = 27, age 3 months to 39 years), patients with EMO of unknown etiology (n = 16, age 4-22 years; defined as body mass index greater than the 97th centile for age before age 4 years), and normal weight siblings (n = 25, age 7 months to 43 years) from both groups. Participants had 3-dimensional magnetic resonance imaging to evaluate the pituitary gland, a complete history and physical examination, and measurement of basal pituitary hormones. Subjects with PWS and EMO had a higher prevalence of pituitary morphological abnormalities than did control subjects (74% PWS, 69% EMO, 8% controls; P < 0.001). Anterior pituitary hormone deficiencies were universal in individuals with PWS (low IGF-1 in 100%, P < 0.001 PWS vs. controls; central hypothyroidism in 19%, P = 0.052, and hypoplastic genitalia or hypogonadotropic hypogonadism in 100%, P < 0.001), and was often seen in individuals with EMO (6%, P = 0.89 vs. control, 31%, P = 0.002, and 25%, P = 0.018, respectively). The presence of a hypoplastic pituitary gland appeared to correlate with the presence of anterior pituitary hormone deficiencies in individuals with EMO, but no correlation was apparent in individuals with PWS. In conclusion, the high frequency of both morphological and hormonal abnormalities of the pituitary gland in both individuals with PWS and EMO suggests that abnormalities in the hypothalamo-pituitary axis are features not only of PWS, but also frequently of EMO of unknown etiology.
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PMID:Pituitary abnormalities in Prader-Willi syndrome and early onset morbid obesity. 1743 97