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MeSH Review

Fat Body

 
 
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Disease relevance of Fat Body

 

Psychiatry related information on Fat Body

 

High impact information on Fat Body

  • This involves TSC/TOR signaling in the fat body, and a remote inhibition of organismal growth via local repression of PI3-kinase signaling in peripheral tissues [11].
  • Amino acids and the humoral regulation of growth: fat bodies use slimfast [12].
  • Remarkably, downregulation of slimfast specifically within the fat body causes a global growth defect similar to that seen in Drosophila raised under poor nutritional conditions [11].
  • Estrogen, lipid oxidation, and body fat [13].
  • After one year, the subjects in both intervention groups had reached or closely approached NCEP Step 1 dietary goals and reduced their mean body fat significantly (range of reduction in mean fat weight, 4.0 to 7.8 kg) [14].
 

Chemical compound and disease context of Fat Body

  • A longitudinal mixed-model regression for weight change controlling for age, race, sex, body mass index, and percent body fat estimated that zonisamide treatment over the 16-week study duration was associated with significantly greater weight loss than was placebo (t = 6.4; P<.001) [15].
  • IMPLICATIONS: Further research should focus on alternative endocrinologic mechanisms for risk associated with obesity and body fat distribution and for the biologic relevance of the increased risk associated with androstenedione in both premenopausal and postmenopausal disease [16].
  • CONCLUSIONS: Body weight, total body fat mass, and proportion of android fat are increased in postmenopausal women with primary hyperparathyroidism; these unexplained factors may be relevant to the increased incidence of cardiovascular disease in this condition [17].
  • During the 4 weeks of parenteral nutrition, body weight, total body fat, and total body potassium, but not total body nitrogen, increased significantly in the study group (p less than 0.001) [18].
  • Since the leptin receptor gene is a candidate gene for obesity, and because of its proximity to D1S198, a marker previously linked to insulin secretion, the LEPR gene was sequenced in 20 non-diabetic Pima Indians chosen for extremes in percent body fat and in their acute insulin response to intravenous glucose [19].
 

Biological context of Fat Body

 

Anatomical context of Fat Body

  • Vitellogenins are yolk protein precursors that are synthesised in the liver of lower vertebrates in response to ovarian hormones, and in the fat body tissue of insects, under the influence, in most species, of juvenile hormone (JH) from the corpora allata (CA) [25].
  • The correlation of fat distribution with age, gender, total body fat, energy balance, adipose tissue lipoprotein lipase and lipolytic activity, adipose tissue receptors, and genetic characteristics are discussed [26].
  • Relationship between skeletal muscle insulin resistance, insulin-mediated glucose disposal, and insulin binding. Effects of obesity and body fat topography [27].
  • The genes are strongly expressed in fat body and hemocytes after injection of bacteria, the CecA genes being much more active than CecB in the fat body [28].
  • To determine whether the depletion of body fat caused by adenovirus-induced hyperleptinemia is mediated via the hypothalamus, we used as a "bioassay" for hypothalamic leptin activity the hypothalamic expression of a leptin-regulated peptide, cocaine- and amphetamine-regulated transcript (CART) [29].
 

Associations of Fat Body with chemical compounds

  • We conclude that HDL2 levels are inversely correlated with truncal fat, plasma insulin levels, and the presence of glucose intolerance and are not independently associated with sex or total body fat [30].
  • In insects, on the other hand, because the CA of adults of both sexes are active, it appeared that male fat body could not normally respond to JH by synthesising vitellogenin [25].
  • Analysis of the fat-reducing gene inactivations in insulin, serotonin and tubby signalling mutants of C. elegans, which have increased body fat, identifies a core set of fat regulatory genes as well as pathway-specific fat regulators [31].
  • Imaginal disks were cultured in a new medium in vitrol Optimal growth occurred when the medium was supplemented with insulin and a juvenile hormone analog and conditioned by larval fat body [32].
  • To determine the relationship between lipid profiles and the type of weight training and to assess the effects of anabolic-androgenic steroids on lipids, bodybuilders and powerlifters of similar age, body fat, and testosterone levels were studied before and after androgen use [33].
 

Gene context of Fat Body

  • In response to infection, two Rel proteins, Dif and Dorsal, translocate from the cytoplasm to the nuclei of larval fat-body cells [34].
  • Indy was most abundantly expressed in the fat body, midgut, and oenocytes: the principal sites of intermediary metabolism in the fly [35].
  • Suppression of body fat accumulation in myostatin-deficient mice [36].
  • Here we show that a conditional knockout of insulin receptor substrate 2 (Irs2) in mouse pancreas beta cells and parts of the brain--including the hypothalamus--increased appetite, lean and fat body mass, linear growth, and insulin resistance that progressed to diabetes [37].
  • A single copy of the three sites is sufficient to direct the sex and fat body specificities of Yp transcription [38].
 

Analytical, diagnostic and therapeutic context of Fat Body

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