PubMed · 5469756
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J W Jhung, F F Ferguson. 1970. Isolated mesenteric lipodystrophy.. https://pubmed.ncbi.nlm.nih.gov/5469756/
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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.
Hyperinsulinemia and increased visceral/abdominal fat (VF) are common features of human aging. To examine the relationships among VF, peripheral, and hepatic insulin sensitivity, we studied 4- and 18-mo-old male Sprague-Dawley rats (n = 42) fed ad libitum (4 AL and 18 AL) or moderately calorie restricted (18 CR) up to 18 mo of age. Total fat mass (FM) and VF were decreased in 18 CR to approximately one-third of that of 18 AL (P < 0.001), while lean body mass (LBM) was unchanged. Most important, 18 CR had more FM (65+/-6 vs. 45+/-6 g) but less VF (7.8+/-0.6 vs. 12.3+/-3.3 g) compared with 4 AL (P < 0.01 for both). Thus, the effects of variable VF on HIS could be assessed, independent of FM and age. Marked hepatic insulin resistance ensued with aging (18 AL) and CR restored hepatic insulin sensitivity to the levels of young rats, while peripheral insulin sensitivity remained unchanged (by insulin clamp of 18 mU/kg/min). In fact, the rates of insulin infusion required to maintain basal hepatic glucose production in the presence of pancreatic clamp were 0.75+/-0.10, 1.41+/-0.13, and 0.51+/-0.12 mU/kg . min, in 4 AL, 18 AL, and 18 CR, respectively (P < 0.01 between all groups), and in 18 CR rats infused with insulin at similar rates as in the 18 AL (1.4 mU/kg/min) hepatic glucose production was decreased by 32% (P < 0. 005). Furthermore, when 18 CR rats were fed AL for 14 d, VF rapidly and selectively increased and severe hepatic insulin resistance was induced. We propose that in this animal model the age-associated decrease in hepatic (rather than peripheral) insulin action is the major determinant of fasting hyperinsulinemia and that increased visceral adiposity plays the major role in inducing hepatic insulin resistance. Thus, interventions designed to prevent the accumulation of VF are likely to represent an effective mean to improve carbohydrate metabolism in aging.
Previous studies have suggested that the peptide galanin (GAL) in the hypothalamus is related to the preference of an animal for dietary fat. The present report investigates this relationship further to identify the specific GAL-synthesizing cell groups involved and to characterize their association to circulating glucose or hormones and their possible contribution to body fat deposition. Male albino Sprague Dawley rats were tested in different feeding paradigms with diets containing the macronutrients, fat, carbohydrate, or protein. These studies, using multiple techniques, identify a cell group in the hypothalamus that expresses GAL and that shows a shift in peptide activity in close relation to dietary fat, circulating glucose, and body fat. In all paradigms, a rise in fat intake, from 10 to 30%, is associated with reduced levels of insulin and corticosterone and normal glucose levels, whereas a further increase in fat ingestion (>30%) leads to hyperglycemia along with greater adiposity. In the hypothalamus, GAL gene expression, peptide production, and peptide release rise significantly (by 40%) in association with fat ingestion, showing no relation to either carbohydrate or protein ingestion. This change is highly site specific, evident predominantly in GAL-synthesizing neurons in the anterior parvocellular region of the paraventricular nucleus (aPVN) and in GAL-containing terminals in the external zone of the median eminence (ME). Positive correlations detected between mRNA abundance in the aPVN and GAL peptide in the ME support the existence of an aPVN-ME projection system related to fat intake and fat deposition. When activated by dietary fat, the contribution of this projection to body fat is suggested by consistent positive correlations between aPVN-ME GAL and either dietary fat, circulating glucose, or body fat and by significantly higher GAL levels (+30%) in obesity-prone compared with obesity-resistant rats. This evidence supports a role for this hypothalamic GAL projection system in the development of obesity produced by the overconsumption of fat.