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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Muscle and fat development are regulated by opposite and also cooperating factors. Adipo-muscular ratio is the result of those forces. The need of a determined fat mass and of its corollary a determined muscle mass is an important physiologic parameter. Sexual differentiation is the main factor adipo-muscular ratio. Feminine fat is twice as big as masculine fat: it predominates in the lower body, masculine fat in the upper body. Brachio-femoral adipo-muscular ratio is, among others, a good index of fat sexual differentiation. Android obesity, predominating in both sexes in the upper body, is, with genetic predispositions, the main factor of non insulin dependent diabetes carbohydrate sensitive hyperlipoproteinemia, hyperuricemia, atherosclerosis. Easy determination on fat topography before the age of 30 is, particularly in women, the best tool for an efficacious prophylaxis of obesity's metabolic complications.
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PMID:[Sexual differentiation of the adipose tissue-muscle ratio. Its metabolic impact]. 276 1

Obesity stands as a public health issue. Obesity prevalence is increasing throughout every industrialized country. Android obesity is linked with an increased cardiovascular mortality and with type 2 diabetes mellitis, thus calling for an early management of this disease. Several studies showed a significant association between an android fat distribution and an increased cortisol secretion, raising the still debated question of a causal relationship between the development of android obesity and hypercorticism. Moreover, android obese subjects exhibit reduced plasma testosterone and growth hormone levels, meaning complex hormonal abnormalities in these subjects. Current hypotheses suggest that android fat distribution depends on the association of these hormonal abnormalities. Android obese patients have supranormal free fatty acid plasma concentrations. Visceral fat tissue, through its portal drainage, could be an important source for free fatty acids that may exert complex metabolic effects: involvement in hepatic lipogenesis, increase in hepatic neoglucogenic flux, reduction in insulin metabolic clearance and involvement in peripheral insulin resistance through a competition mechanism described by Randle. Technics in vitro (isolated adipocytes) and in vivo in human (labelled fatty acid flux) showed that visceral fatty acid flux was increased in obese patients and subcutaneous adipose tissue, as opposed to common opinion, was also involved in free fatty acid pool in obese patients. Thus, visceral obesity and diabetes could be linked through an enhanced fatty acid availability from adipose tissues (visceral and subcutaneous) in otherwise genetically type 2 diabetes-prone individuals.
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PMID:[Metabolic difference between visceral fat and subcutaneous abdominal fat]. 1094 44

Android obesity is often associated with a metabolic syndrome characterized, in particular, by a type 2 diabetes and cardiovascular problems. This could be induced by an excess of local production of glucocorticoids (GC) by adipose tissue (or other tissues). This production of GC by its target tissues depends on the 11beta-hydroxysteroid dehydrogenase type 1 (11betaHSD1) enzyme. Our aim was to characterize some mechanisms which control the expression of the human 11betaHSD1 gene (hHSD11B1) in preadipocytes. By using different luciferase constructs containing fragments of the hHSD11B1 promoter, we demonstrate that two members of the CCAAT/enhancer-binding protein family, C/EBPalpha and C/EBPbeta, are required for the basal transcriptional activity of HSD11B1 in 3T3-L1 preadipocyte cells. This effect depends on the binding of each isoform to specific binding sites. Mutation of either one of these sites induced a 40-50% decrease of the constitutive activity of the hHSD11B1 promoter. A forskolin treatment of 3T3-L1 preadipocyte cells induced an increased endogenous expression of HSD11B1. By transfection studies using the hHSD11B1 luciferase constructs, it appears that C/EBPbeta was strongly involved in this induction, as the forskolin stimulation was suppressed after mutation of the C/EBPbeta binding site. Part of the mechanism involved the increase of nuclear C/EBPbeta protein levels induced by forskolin and a phosphorylation step associated with an enhanced binding of the transcription factor to its site. These data indicate that members of the C/EBP family control intracellular levels of GC in preadipocytes via the regulation of the constitutive and cAMP-dependent expressions of HSD11B1.
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PMID:CCAAT/enhancer-binding proteins (C/EBPs) regulate the basal and cAMP-induced transcription of the human 11beta-hydroxysteroid dehydrogenase encoding gene in adipose cells. 1683 16