PubMed · 3467139
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C P Maguire. 1986. Suction assisted lipectomy.. https://pubmed.ncbi.nlm.nih.gov/3467139/
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Decellularized tissues provide biological cues owing to the wealth of structural and regulatory factors that promote angiogenesis, adipogenesis, and myogenesis and facilitate neurite outgrowth. Here, we demonstrated the advantages of decellularized adipose tissue (adipoECM) over defined collagen-based biomaterials for host tissue integration. Three batches of human adipose tissue were decellularized using a rapid decellularization protocol and analyzed using mass spectrometry. To assess the biological activity of the decellularized materials, adipoECM and a reference standard of care biomaterial (Integra®DRT, also containing collagen I and glycosaminoglycans) were implanted subcutaneously, but far from the wound bed (in anatomical potential spaces) of immunocompetent BALB/c mice. The mice were euthanized in the acute (1 day) and chronic (day 60) inflammatory reaction phases, followed by biomaterial excision and Masson’s trichrome immunohistofluorescence imaging of the paraffin-embedded specimens. Each batch of processed tissue passed a quality control check, showing a low level of donor genomic DNA, lack of nuclei, lipids, endotoxins, and bacterial contamination. Mass spectrometry revealed that all batches of decellularized tissue mainly contained collagen I and, to a lesser degree, collagen III, collagen IV, collagen V, laminin, fibrillin, fibronectin, tenascin, and elastin. No acute inflammatory reaction was observed in either material one day post-transplantation. At 60 days post-implantation, different cell types were detected in adipoECM specimens, whereas Integra®DRT remained acellular. Additional immunohistochemical staining of adipoECM revealed CD31-positive cells in the blood vessels. Mesenchymal (CD90 positive) and myeloid (CD14 positive) cells were also detected. Primary cell types involved in soft tissue healing and remodeling were found in the adipoECM-treated group. The ingrowth of blood vessels and mesenchymal cells confirmed the effective integration of adipoECM with host tissues. Our results demonstrate that decellularized adipose tissue implanted away from the wound bed possesses contextual biological activities that promote efficient integration with host tissues.
The interaction between tris(4-chlorophenyl)methanol (TCPM), an environmental contaminant of uncertain origin, and the human androgen receptor was examined in vitro using a previously characterized human androgen receptor reporter gene assay in which PC-3 LUC(AR+) cells respond to 5alpha-dihydrotestosterone (DHT) with enhanced luciferase activity. In two preliminary studies, TCPM (1 microM) had no effect on androgen receptor activation in the absence of DHT (50 pM), but DHT-mediated activation of the androgen receptor was decreased more than 90% by TCPM at 1 microM. This was not due to an effect of TCPM on cell viability since, with TCPM concentrations of 0.1 and 1.0 microM, cell viability was 111 and 102%, respectively, but at 10 microM TCPM, cell viability was reduced to 60% compared with controls. For kinetic studies of the effects of TCPM on androgen receptor activation, DHT was added at 0, 5, 25, 50, 75, 100, 250 and 500 pM and the TCPM concentrations used were 0, 1, 10, 100, 300 and 1000 nM. This range incorporated the levels of TCPM in human adipose tissue, where concentrations up to 55 nM (20 ng/g lipid) have been measured. TCPM increased the value of the K(m(app)) of the androgen receptor for DHT 4-6-fold with little or no effect on the V(max(app)). Slope and intercept replots revealed that TCPM inhibited the DHT-mediated activation of the androgen receptor in a competitive manner with K(i(app)) values of 0.26, 0.26 and 0.20 microM compared with respective K(m(app)) values of 9.8, 3.1 and 3.9 pM. Thus, TCPM is a competitive antagonist of human androgen receptor activation and the value of the K(i(app)) indicates that TCPM would be approximately 10-50 times more potent as an inhibitor than the previously identified androgen receptor antagonists p,p'-DDE and vinclozilin and also, the K(i(app)) values (200-260 nM) are very close to the concentration of TCPM found in the adipose tissue of some humans (55 nM).
Antiretroviral therapy in human immunodeficiency virus (HIV)-positive patients can induce a lipodystrophy syndrome of peripheral fat wasting and central adiposity, dyslipidemia, and insulin resistance. To test whether in this syndrome insulin resistance is associated with abnormal muscle handling of fatty acids, 12 HIV-1 patients (8 females/4 males, age = 26 +/- 2 yr, HIV duration = 8 +/- 1 yr, body mass index = 22.0 +/- 1.0 kg/m(2), on protease inhibitors and nucleoside analog RT inhibitors) and 12 healthy subjects were studied. HIV-1 patients had a total body fat content (assessed by dual-energy X-ray absorptiometry) similar to that of controls (22 +/- 1 vs. 23 +/- 2%; P = 0.56), with a topographic fat redistribution characterized by reduced fat content in the legs (18 +/- 2 vs. 32 +/- 3%; P < 0.01) and increased fat content in the trunk (25 +/- 2 vs. 19 +/- 2%; P = 0.03). In HIV-positive patients, insulin sensitivity (assessed by QUICKI) was markedly impaired (0.341 +/- 0.011 vs. 0.376 +/- 0.007; P = 0.012). HIV-positive patients also had increased total plasma cholesterol (216 +/- 20 vs. 174 +/- 9 mg/dl; P = 0.05) and triglyceride (298 +/- 96 vs. 87 +/- 11 mg/dl; P = 0.03) concentrations. Muscular triglyceride content assessed by means of (1)H NMR spectroscopy was higher in HIV patients in soleus [92 +/- 12 vs. 42 +/- 5 arbitrary units (AU); P < 0.01] and tibialis anterior (26 +/- 6 vs. 11 +/- 3 AU; P = 0.04) muscles; in a stepwise regression analysis, it was strongly associated with QUICKI (R(2) = 0.27; P < 0.0093). Even if the basal metabolic rate (assessed by indirect calorimetry) was comparable to that of normal subjects, postabsorptive lipid oxidation was significantly impaired (0.30 +/- 0.07 vs. 0.88 +/- 0.09 mg x kg(-1) x min(-1); P < 0.01). In conclusion, lipodystrophy in HIV-1 patients in antiretroviral treatment is associated with intramuscular fat accumulation, which may mediate the development of the insulin resistance syndrome.