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Query: UMLS:C0026827 (hypotonia)
 5,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity occurs in both clinical and animal forms in a variety of specific models which allow study of its underlining endocrine and mechanistic features. Among the neuroendocrine varieties of obesity, polycystic ovaries are probably the most common. The importance of the gonadal feedback system for regulation of food intake and obesity is indicated by the effects of castration in experimental animals which is a widely used mechanism for producing experimental obesity. Cushing syndrome and hypothalamic obesity are rare clinical syndromes. The current evidence suggests that there are two types of hypothalamic obesity from a mechanistic point of view--one associated with hyperphagia as a necessary and sufficient cause and a disturbance of the autonomic nervous system without hyperphagia as a second mechanism. Although genetic factors underlie most types of human obesity, there are several dymorphic forms of obesity including the Prader-Willy syndrome, Cohen's syndrome, Carpenter's syndrome, Ahlstrom's syndrome and the Bardet-Biedel syndrome. The Prader-Willi syndrome is characterized by obesity hypotonia hypogonadism and mental retardation. In animals, a dominant form of inheritance of obesity is seen in the yellow mouse. Current evidence suggests that this syndrome can be explained by reduced acetylation of MSH in the pituitary and/or hypothalamus. Several recessively inherited forms of obesity exist including the obese mouse, the diabetes mouse, fatty rat, the fat mouse, tubby mouse and the corpulent rat. In addition, there are a number of polygenic types of experimental obesity. The final mechanistic classification of obesity are those due to dietary manipulation. For both human beings and animals, a highly fat diet appears to be particularly problematic for the development of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic, hypothalamic and endocrine features of clinical and experimental obesity. 148 Jul 57

Structural differences between noncorticotropic ACTH peptides result in marked differences in their effects on regenerating nerve and muscle in rats. The ACTH/MSH(4-10) analog BIM 22015 was administered IP in dosages from 0.1 to 40 micrograms/kg/48 h for 5, 7, or 11 days after peroneal nerve crush, and characteristics of extensor digitorum longus (EDL) muscle were studied and compared with ACTH/MSH(4-10). Eleven days postcrush 40 micrograms/kg BIM 22015 increases rate of development of tetanic tension and amplitude of contraction of indirectly stimulated EDL. In a 21-day study, reinnervated BIM 22015-treated muscles retain tetanic strength, whereas ACTH/MSH(4-10)-treated muscles are significantly weakened. Both peptides show neurotrophic characteristics in their stimulation of endplate nerve terminal branching. However, in contrast to ACTH/MSH(4-10), BIM 22015 also prevents denervation atrophy of the EDL. This dual neurotrophic and myotrophic role for BIM 22015 accords it a clinical potential for degenerative myopathies of either pure or mixed origin, such as muscular dystrophy, infantile spinal atrophy, and hypotonia.
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PMID:ACTH/MSH(4-10) analog BIM 22015 aids regeneration via neurotrophic and myotrophic attributes. 838 88