Relevance of omental pericellular adipose tissue collagen in the pathophysiology of human abdominal obesity and related cardiometabolic risk.

BACKGROUND: Adipose tissue fibrosis is a relatively new notion and its relationship with visceral obesity and cardiometabolic alterations remains unclear, particularly in moderate obesity. OBJECTIVE: Our objective was to examine if total and pericellular collagen accumulation are relevant for the pathophysiology of visceral obesity and related cardiometabolic risk. SUBJECTS AND METHODS: Surgical omental (OM) and subcutaneous (SC) fat samples were obtained in 56 women (age: 47.2±5.8 years; body mass index (BMI): 27.1±4.4 kg/m2). Body composition and fat distribution were measured by dual-energy X-ray absorptiometry and computed tomography, respectively. Total and pericellular collagen were measured using picrosirius red staining. CD68+ cells (total macrophages) and CD163+ cells (M2-macrophages) were identified using immunohistochemistry. RESULTS: We found that only pericellular collagen percentage, especially in OM fat, was associated with higher BMI, body fat mass and adipose tissue areas as well as lower radiologic attenuation of visceral adipose tissue and altered cardiometabolic risk variables. Strong correlations between peri-adipocyte collagen percentage and total or M2-macrophage percentages were observed in both depots. Total collagen percentage in either compartment was not related to adiposity, fat distribution or cardiometabolic risk. CONCLUSIONS: As opposed to whole tissue-based assessments of adipose tissue fibrosis, collagen deposition around the adipocyte, especially in the OM fat compartment is related to total and regional adiposity as well as altered cardiometabolic risk profile.

Arginine plus proline supplementation elicits metabolic adaptation that favors wound healing in diabetic rats.

Diabetic patients with wounds are at risk of protein malnutrition, have low arginine plasma levels, and suffer from delayed wound healing. We sought to determine the efficacy of arginine plus proline supplementation on protein and amino acid metabolism and on wound repair in a model of diabetic rats. Eighteen 11-wk-old Zucker diabetic fatty fa/fa male rats underwent a 7-cm abdominal skin incision with implantation of sponges and daily excision of full-thickness round sections of dorsal skin for 5 days. They were randomized to be fed with either a standard formula (S group, Clinutren Iso), a high-protein and arginine (ARG) plus proline (PRO)-enriched formula (ARG+PRO group, Clinutren Repair), or an isonitrogenous isoenergetic control formula (IC group). Nitrogen balance was calculated daily. The rats were euthanized on day 5, and plasma glucose, insulin, amino acids, skin epithelialization, and angiogenesis were measured. In macrophages, we assessed inducible nitric oxide synthase (iNOS) and arginase expression, production of nitric oxide (NO) and amino acid metabolism. Both the ARG+PRO and IC groups showed improved nitrogen balance. ARG plus PRO supplementation increased proline and branched-chain amino acid plasma concentrations and improved angiogenesis. Arginase and iNOS expressions in macrophages were reduced, together with NO and citrulline production. In diabetic rats, ARG plus PRO supplementation improves wound angiogenesis and favors whole body protein metabolism. Low macrophage iNOS expression at day 5 may reflect a low inflammatory state in the wounds, favoring wound closure.

Preferential reduction of very low density lipoprotein-1 particle number by fenofibrate in type IIB hyperlipidemia: consequences for lipid accumulation in human monocyte-derived macrophages.

The combined (mixed) type IIB phenotype is typically associated with premature atherosclerosis and characterised by concomitant elevation of plasma levels of atherogenic triglyceride-rich lipoproteins, consisting of very low density lipoprotein (VLDL)-1 (Sf 60-400), VLDL-2 (Sf 20-60), and intermediate density lipoprotein (IDL) (Sf 12-20), as well as small dense LDL. After dietary stabilisation, type IIB patients received micronised fenofibrate (267 mg/day) for up to 12 months. At baseline (T0), patients (n=11) displayed fasting triglyceride, cholesterol and apoB levels of 308+/-13, 350+/-17 and 187+/-9 mg/dl, respectively. Micronised fenofibrate (M-fenofibrate) induced marked reductions in plasma triglyceride (TG) (-61%, P<0.0001), total cholesterol (-32%, P=0.0005) and apolipoprotein (apo) B (-33%, P<0.001) at 12 months (T12); similar effects were seen after 3 months (T3) of treatment. These changes resulted from significant reductions in VLDL-1 (-75%, P=0.00001), VLDL-2 (-46%, P=0.002) and LDL (-33%, P<0.0003); IDL concentrations were unchanged. At baseline, VLDL-1 constituted the major TG-rich lipoprotein (TRL) fraction (50% of total mass), but only 25% at T12. These drug effects were accompanied by marked increase in HDL-C (+20%, P=0.018). Quantitative changes in triglyceride-rich lipoproteins were accompanied by significant qualitative modifications in particle size and chemical composition (VLDL-1: TG, -10.7%, P<0.001; FC, +59%, P=0.0002; PL, +19%, P=0.033; VLDL-2: FC, +11%, P=0.027; IDL: FC, +14%, P=0.0004; PL, +12%, P=0.002). Reduction in the TG content of VLDL-1 was reflected in a shift of particle size distribution to smaller diameters (mean 45.4 and 42.3 nm, respectively, at T0 and T12). We evaluated the relative atherogenicity of TRL subfractions by determining their capacity, when normalised to equal particle numbers (as apoB 100 content), to induce lipid accumulation in human monocyte-derived macrophages. Among TRL subfractions, VLDL-1 (100 microg apoB/ml) possessed the highest capacity to induce macrophage lipid loading (up to sevenfold increase in TG content, P<0.001; free cholesterol, up to 1.7-fold; P<0.05). At 100 microg apoB/ml, cellular TG loading from VLDL-1 was twofold greater than that for VLDL-2 (P<0.01), and fivefold greater than for IDL (P<0.01). Despite drug-induced changes in the qualitative properties of TRL subfractions, the activity of VLDL-1, VLDL-2 and IDL as ligands which lead to induction of macrophage lipid accumulation, at equivalent particle numbers, was not detectably altered. By contrast, the fibrate-mediated reduction in the number of circulating VLDL-1 and VLDL-2 particles (four and twofold, respectively) resulted in marked decrease in cellular lipid loading. Considered together, these findings suggest that fenofibrate may act at systemic and arterial levels to reduce the cardiovascular risk associated with VLDL subfractions in patients with a combined hyperlipidemic (type IIB) phenotype. Indeed, we speculate that reductions in circulating levels of VLDL-1 and VLDL-2 may diminish intimal penetration of these particles and thus their propensity to enhance arterial macrophage lipid accumulation and foam cell formation. Finally, fenofibrate further attenuated the atherogenic lipid profile in these patients by inducing marked reduction in LDL and elevation in cardioprotective HDL.

Evaluation of combinations of titanium, zirconia, and alumina implants with 2 bone fillers in the dog.

The quality of the tissue-implant interface was evaluated using light and scanning electron microscopy with morphometric analysis. Nine dogs were implanted with 3 types of dental implants (titanium, zirconia, or alumina). A total of 24 dental implants was placed in mandibular bone previously filled with coral carbonate calcium (corail) or hydroxyapatite. The study results in breaking the concept of osseointegration into 2 phases: "osseocoaptation," which concerns only the interface (physical contact between the implants and the bone without interpenetration process), and "osseocoalescence," which relies on an interpenetration of the bioactive material, which almost entirely disappears, being substituted by newly formed bone. There was no significant statistical difference between the 3 types of implants. Both fillings showed good ossecoalescence properties. However, hydroxyapatite led to fibrous encystment, preventing osseocoaptation of implants. In contrast with calcium carbonate filling.

[Benign anal granular cell tumor. Apropos of a case]. / Tumeur anale bénigne à cellules granuleuses. A propos d'un cas.

A case of benign granular cell tumor of the perianal region is presented. The patient was treated by local excision of the tumor. This is an unusual site. Superficial biopsy specimens may indicate an incorrect diagnosis of squamous cell carcinoma.

[Histopathologic lesions of the accessory salivary glands in Gougerot-Sjögren syndrome: re-evaluation of the diagnostic criteria of Chisholm and Mason and of Chometter et al]. / Lésions histopathologiques des glandes salivaires accessoires (G.S.A.) au cours du syndrome de Gougerot-Sjögren: réévaluation des critères diagnostiques de Chisholm et Mason et de Chomette et coll.

In a retrospective study, we used a series of 29 patients with Sjögren's Syndrome diagnosed according to the new European criteria (Cl. Vitali, S. Bombardieri, H. M. Moutsopoulos et al.) (8). (Arthritis Rheum 1993; 36:340-7). A labial biopsy technique allowed to classify these patients into the anatomical "scores" formerly related by Chisholm and Mason and Chomette et al. Referring to these criteria, only 45% of patients presented a characteristic histopathological pattern. If another complementary criterium, i.e. ductal tropism of lymphoid infiltrates, was added, that percentage remained low (50% only). Thus, these results would suggest the following considerations: the classical histopathological criteria do not seem sufficiently specific; other histological criteria such as ductal lesions previously noted by Leroy et al. must in addition be looked for; thus it would seem to be of considerable value to use in the future complementary quantitative studies by means of morphometric methods.

[Fibroblasts of the normal human periodontium. Morphology and functional behavior in lattice collagen]. / Le fibroblaste du parodonte humain normal. Morphologie et comportement fonctionnel en lattis de collagène.

In this preliminary report, we studied human periodontal normal fibroblasts cultured on a fibrillary tridimensional net of collagen (lattice). As demonstrated by scanning and transmission electron microscope, cells were closely binded to this fibrillar net. They kept their functional activities (oxidatives enzymes, leucine aminopeptidase). As seen in monolayer cultures by immunocytochemical methods, the majority of these cells secreted type I collagen (70 to 80% of them: 15 to 25% secreting type III collagen). Besides, the capacity of retraction of collagen lattices, quite similar to that of skin lattices, was expressed by a decreasing curve up to the 8th day. In order to study the possible role of fibroblastic biological changes in periodontal disease, later on we shall compare the characteristics of normal fibroblast to those of fibroblast taken in periodontal disease.