Fat Pads Of Rats Research Articles

Automatic tracing and segmentation of rat mammary fat pads in MRI image sequences based on cartoon-texture model

The growth patterns of mammary fat pads and glandular tissues inside the fat pads may be related with the risk factors of breast cancer. Quantitative measurements of this relationship are available after segmentation of mammary pads and glandular tissues. Rat fat pads may lose continuity along image sequences or adjoin similar intensity areas like epidermis and subcutaneous regions. A new approach for automatic tracing and segmentation of fat pads in magnetic resonance imaging (MRI) image sequences is presented, which does not require that the number of pads be constant or the spatial location of pads be adjacent among image slices. First, each image is decomposed into cartoon image and texture image based on cartoon-texture model. They will be used as smooth image and feature image for segmentation and for targeting pad seeds, respectively. Then, two-phase direct energy segmentation based on Chan-Vese active contour model is applied to partitioning the cartoon image into a set of regions, from which the pad boundary is traced iteratively from the pad seed. A tracing algorithm based on scanning order is proposed to accurately trace the pad boundary, which effectively removes the epidermis attached to the pad without any post processing as well as solves the problem of over-segmentation of some small holes inside the pad. The experimental results demonstrate the utility of this approach in accurate delineation of various numbers of mammary pads from several sets of MRI images.

Effect of continuous local microdose norethisterone enanthate on the epididymis of adult rat.

Unilateral implantation of a small silastic capsule containing crystalline Norethisterone Enanthate (NE, average observed rate of release, 17-22 micrograms/24 h) into the epididymal fat-pad of adult rats induced drastic impairment of epididymal functional anatomy in the adjacent epididymis six weeks later without affecting the contralateral epididymis. Tubular elements in the ipsilateral epididymis were highly shrunken with their luminal epithelial height greatly reduced and the lumen devoid of spermatozoa as compared with the normal epididymis (full of spermatozoa) on the sham operated contralateral side.

An Experimental Design to Study Adipocyte Stem Cells for Reconstruction of Calvarial Defects

Autogenous osteogenic differentiated rat adipose stromal cells (ASCs) were used to repopulate cadaveric processed bone in a critical calvarial defect model to improve bone healing as compared with the standard treatment of cadaveric bone implantation alone. Forty-two skeletally mature Sprague-Dawley rats were randomized to 5 groups including bone graft only, bone/osteogenic differentiated ASCs, fibrin glue/osteogenic differentiated ASCs, and bone/fibrin glue/osteogenic differentiated ASCs; 2 animal calvarias were left empty. Adipose stromal cells were isolated from the inguinal fat pad of rats and differentiated into osteogenic cells, verified using von Kossa and alkaline phosphatase staining, and osteocalcin immunohistochemistry. These cells were added to sterilized, 8-mm cadaveric bone graft disks and placed back into calvarial defect for 6 weeks. The rat calvarias then underwent bone density analysis and histology. Intact cells were observed in the bone graft of the bone/osteogenic differentiated ASC group only. Islands of bone were seen in the bone-graft-only group, the bone/osteogenic differentiated ASC group, and the bone/fibrin/osteogenic differentiated ASC group. The bone-graft-only group and bone/osteogenic differentiated ASC group were similar in bone mineral density (1397 +/- 184.5 vs 1365 +/- 160.4). The bone/fibrin/osteogenic differentiated ASC group density was less than the bone and bone/osteogenic differentiated ASC groups at 835.2 +/- 319.5 (P < 0.001). Allograft bone scaffolds with autogenous osteogenic differentiated ASCs showed cellularity within the bone grafts and had larger bone islands. The presence of osteogenic differentiated ASCs did not increase overall bone density compared with bone graft only.

Pref-1 and adipokine expression in adipose tissues of GK and Zucker rats

In view of the central role of preadipocyte factor-1, adiponectin and leptin in white adipose tissue function, the aim of the present study was to analyze the mRNA expression of these proteins and of the inflammatory markers interleukin-6 and tumor necrosis factor-alpha in visceral and subcutaneous fat pads of rats with different metabolic disorders. We demonstrated highly divergent expression of preadipocyte factor-1, upregulated expression of adiponectin, interleukin-6 and TNF-alpha mRNA in adipose tissues of the diabetic Goto Kakizaki rat compared to the obese Zucker rat. This was correlated to an increased number of large adipocytes and serum levels of adiponectin. Furthermore, in all four strains studied (as above plus Wistar Furth and Zucker Lean), significant heterogeneity was evident in adipokine expression within specific adipose tissues previously defined as belonging to the visceral or subcutaneous fat depots. These results suggest that significantly increased levels of inflammation and redistribution of adipocyte size are mechanisms contributing to the development of type 2 diabetes in the GK rat.

Effects of Conjugated Linoleic Acid Supplementation on Fatty Acid Composition in the Plasma, Liver, and Epididymal Fat Pads of Male-Sprague Dawley Rats

The purpose of this study was to investigate the effects of conjugated linoleic acid (CLA) on the fatty acid composition of plasma, liver, and epididymal fat pads in rats. Seventy-two male Sprague-Dawley rats were divided into four groups and received beef tallow (BT), fish oil (FO), beef tallow with CLA (BTC), and fish oil with CLA (FOC). All the rats were fed an experimental diet containing 12% (wt/wt) total fat, including CLA at 1%, for 30 weeks. The fatty acid analyses of the plasma, liver, and epididymal fat pads were performed by the one-step methylation method, followed by gas chromatography. Monounsaturated fatty acid (MUFA) levels in the plasma were significantly reduced in the BTC group as compared to the BT group. The levels of C18:1 and C20:4 in the liver were significantly lower in the BTC group than in the BT group (P < .05). CLA was detected in the epididymal fat pads of the rats that did not receive supplemental CLA (the BT and FO groups), indicating de novo synthesis. CLA caused significant decreases in C18:1 fatty acid levels in both the BTC and FOC groups in epididymal fat pads. C22:6 was significantly higher in the liver microsomes of the BTC group, as compared to the BT group. MUFA was stored at higher levels in the epididymal fat pads and was significantly lower in level in the CLA-supplemented (BTC and FOC) groups as compared to the BT and FO groups (P < .05). In conclusion, dietary CLA supplementation in rats altered fatty acid composition in a tissue-specific manner. CLA was stored mainly in the epididymal fat pad. The results also suggested that CLA may inhibit the conversions of C18:0 to C18:1 and C18:2 to C20:4 fatty acid, resulting in significantly lower levels of C18:1 and C20:4 in the livers of the BTC group as compared to the BT group.

Serum Leptin, Lipids, Free Fatty Acids, and Fat Pads in Long-Term Dehydroepiandrosterone-Treated Zucker Rats

Abstract. The obese Zucker rat has a genetically flawed leptin system and is a model of hyperphagia, obesity, hyperlipidemia, and markedly elevated leptin levels. Dehydroepiandrosterone (DHEA) administration reduces hyperphagia, hyperlipidemia, and obesity in Zucker rats. Since serum leptin levels are associated with body fat, we wondered what the effects of fat pad weight reduction from DHEA administration would have on leptin levels. This experiment investigated the effects of DHEA on intra-abdominal fat pads, serum lipids, and peripheral leptin in male lean and obese Zucker rats that were administered DHEA in their food from 4 weeks of age to 20 weeks. Lean and obese rats received plain chow or chow containing DHEA. Additional chow-fed groups of lean and obese weight-matched controls and obese pair-fed rats helped to control for the reduced body weight, food intake, and fat pad weights seen with DHEA administration. DHEA administration to lean Zucker rats reduced body weight and fat pad weights, but leptin levels showed a lower trend. Among obese rats, both DHEA treatment and pair-feeding reduced body weight and fat pad weights, but only DHEA lowered leptin levels. The weight-matched controls had reductions in fat pad weights similar to the DHEA-treated group, but with increased leptin levels. Thus, DHEA may exert a small, independent effect on leptin levels in this animal model, but the reduction is less than what would be expected.

Maternal protein restriction during early lactation induces GLUT4 translocation and mTOR/Akt activation in adipocytes of adult rats

Epidemiological and experimental studies have demonstrated that early postnatal nutrition has been associated with long-term effects on glucose homeostasis in adulthood. Recently, our group demonstrated that undernutrition during early lactation affects the expression and activation of key proteins of the insulin signaling cascade in rat skeletal muscle during postnatal development. To elucidate the molecular mechanisms by which undernutrition during early life leads to changes in insulin sensitivity in peripheral tissues, we investigated the insulin signaling in adipose tissue. Adipocytes were isolated from epididymal fat pads of adult male rats that were the offspring of dams fed either a normal or a protein-free diet during the first 10 days of lactation. The cells were incubated with 100 nM insulin before the assays for immunoblotting analysis, 2-deoxyglucose uptake, immunocytochemistry for GLUT4, and/or actin filaments. Following insulin stimulation, adipocytes isolated from undernourished rats presented reduced tyrosine phosphorylation of IR and IRS-1 and increased basal phosphorylation of IRS-2, Akt, and mTOR compared with controls. Basal glucose uptake was increased in adipocytes from the undernourished group, and the treatment with LY294002 induced only a partial inhibition both in basal and in insulin-stimulated glucose uptake, suggesting an involvement of phosphoinositide 3-kinase activity. These alterations were accompanied by higher GLUT4 content in the plasma membrane and alterations in the actin cytoskeleton dynamics. These data suggest that early postnatal undernutrition impairs insulin sensitivity in adulthood by promoting changes in critical steps of insulin signaling in adipose tissue, which may contribute to permanent changes in glucose homeostasis.

Signaling the Signal, Cyclic AMP-dependent Protein Kinase Inhibition by Insulin-formed H2O2 and Reactivation by Thioredoxin

Catecholamines in adipose tissue promote lipolysis via cAMP, whereas insulin stimulates lipogenesis. Here we show that H(2)O(2) generated by insulin in rat adipocytes impaired cAMP-mediated amplification cascade of lipolysis. These micromolar concentrations of H(2)O(2) added before cAMP suppressed cAMP activation of type IIbeta cyclic AMP-dependent protein kinase (PKA) holoenzyme, prevented hormone-sensitive lipase translocation from cytosol to storage droplets, and inhibited lipolysis. Similarly, H(2)O(2) impaired activation of type IIalpha PKA holoenzyme from bovine heart and from that reconstituted with regulatory IIalpha and catalytic alpha subunits. H(2)O(2) was ineffective (a) if these PKA holoenzymes were preincubated with cAMP, (b) if added to the catalytic alpha subunit, which is active independently of cAMP activation, and (c) if the catalytic alpha subunit was substituted by its C199A mutant in the reconstituted holoenzyme. H(2)O(2) inhibition of PKA activation remained after H(2)O(2) elimination by gel filtration but was reverted with dithiothreitol or with thioredoxin reductase plus thioredoxin. Electrophoresis of holoenzyme in SDS gels showed separation of catalytic and regulatory subunits after cAMP incubation but a single band after H(2)O(2) incubation. These data strongly suggest that H(2)O(2) promotes the formation of an intersubunit disulfide bond, impairing cAMP-dependent PKA activation. Phylogenetic analysis showed that Cys-97 is conserved only in type II regulatory subunits and not in type I regulatory subunits; hence, the redox regulation mechanism described is restricted to type II PKA-expressing tissues. In conclusion, phylogenetic analysis results, selective chemical behavior, and the privileged position in holoenzyme lead us to suggest that Cys-97 in regulatory IIalpha or IIbeta subunits is the residue forming the disulfide bond with Cys-199 in the PKA catalytic alpha subunit. A new molecular point for cross-talk among heterologous signal transduction pathways is demonstrated.

Intralymphatic Chemotherapy Using a Hyaluronan–Cisplatin Conjugate

Breast cancers typically spread to regional lymph nodes once they disseminate from the primary tumor, thus adequate evaluation and treatment of the axillary lymph nodes is paramount in early stage disease. One significant problem with current therapy is the side effects chemotherapy agents create systemically, either alone or in combination. The purpose of this study is to determine whether lymphatically targeted cisplatin carriers will increase the localized dose in lymphatic metastases without systemic toxicities. Hyaluronan (HA) is a highly biocompatible polymer that follows lymphatic drainage from the interstitial spaces. We formed complexes of HA and cisplatin by non-covalent conjugation. Complexes were injected subcutaneously into the upper mammary fat pad of female rats, and the tissue distribution determined. Cisplatin-HA contained up to 0.25 w/w of Pt and released drug with a half-life of 10 h in saline. Cisplatin-HA conjugates had high anti-tumor activity in vitro similar to the free drug: cisplatin-HA IC50 7 microg/mL in MCF7 and MDA-MB-231 human breast cancer cells (free cisplatin IC50 7 microg/mL). Cisplatin-HA conjugates were well tolerated in rodents with no signs of injection site morbidity or major organ toxicity after 96 h. The area-under-the-curve of cisplatin in the axially lymph nodes after injection with cisplatin-HA increased 74% compared with normal cisplatin. This study demonstrates a novel intralymphatic drug delivery method in breast cancer to preferentially treat at-risk regional lymph nodes and avoid systemic toxicities. Further in vivo testing related to efficacy of this approach with regard to survival, toxicity, and pharmacokinetics is warranted to support its use in human trials.

Mast cell mediators increase endothelial cell MMP‐2 production in a β‐catenin‐dependent manner

In skeletal muscle, mast cells reside in close proximity to capillaries and may be activated in response to muscle stretch. Angiogenesis may be initiated by factors released from mast cells including vascular endothelial growth factor (VEGF) and histamine. Both VEGF and histamine increase endothelial permeability, and as our results show, regulate matrix metalloproteinase (MMP)‐2 production and induce nuclear translocation of β‐catenin. Our objective is to determine how VEGF and histamine increase MMP‐2 production in endothelial cells isolated from the fat pad of rats. We have found that histamine acts through its H2 receptor as stimulation with the H2 receptor agonist dimaprit induced a significant increase in MMP‐2 mRNA levels and promoter activity (4.1±0.5 vs control, p&lt; 0.05, n=3, 1.4±0.1 vs control, p&lt;0.05, n=3). To determine if β‐catenin mediates transcription of MMP‐2, rat endothelial cells were transduced with Ad‐ICAT or Ad‐Bgal prior to growth factor stimulation. Transduction of ICAT blocked the VEGF induced increase in MMP‐2 mRNA levels (1.8±0.04 VEGF vs 1.0 for Bgal, p&lt;0.05 n=3, 0.95±0.1 ICAT + VEGF vs Bgal, p&lt;0.05 n=3). These results indicate a role for β‐catenin in the induction of endothelial cell MMP‐2 expression following VEGF and histamine stimulation. Funding by NSERC.

Type of dietary protein regulates gene expression pattern in adipose tissue

Dietary protein plays an important role in the regulation of lipogenesis in liver and secretion of insulin by pancreas, however it is not known whether the type of protein exerts an effect in adipose tissue functionality. Thus, the aim of this study was to analyze the gene expression pattern of adipose tissue in obese rats fed casein or soy protein diet. Results indicate that adipose tissue from retroperitoneal fat pads of rats fed soy protein presented a significant decrease in the expression of leptin, tumor necrosis factor alpha and its receptor, angiotensinogen, genes involved in inflammatory response, genes of signaling mediators and genes involved in cholesterol metabolism compared with rats fed casein diet. These results suggest that soy protein improves adipose tissue functionality in a model of diet induced obesity. This work was supported by grant # 46135M, CONACYT.

Protein Kinase Cϵ Mediates Polymeric Fibronectin Assembly on the Surface of Blood-borne Rat Breast Cancer Cells to Promote Pulmonary Metastasis

Malignant breast cancer cells that have entered the blood circulation from primary mammary fat pad tumors or are grown in end-over-end suspension culture assemble a characteristic, multi-globular polymeric fibronectin (polyFn) coat on their surfaces. Surface polyFn is critical for pulmonary metastasis, presumably by facilitating lung vascular arrest via endothelial dipeptidylpeptidase IV (CD26). Here, we show that cell-surface polyFn assembly is initiated by the state of suspension, is dependent upon the synthesis and secretion of cellular Fn, and is augmented in a dose- and time-dependent manner by plasma Fn. PolyFn assembly is regulated by protein kinase Cepsilon (PKCepsilon), which translocates rapidly and in increasing amounts from the cytosol to the plasma membrane and is phosphorylated. PolyFn assembly is impeded by select inhibitors of this kinase, i.e. bisindolylmaleimide I, Ro-32-0432, Gö6983, and Rottlerin, by the phorbol 12-myristate 13-acetate-mediated and time-dependent loss of PKCepsilon protein and decreased plasma membrane translocation, and more specifically, by stable transfection of lung-metastatic MTF7L breast cancer cells with small interfering RNA-PKCepsilon and dominant-negative PKCepsilon constructs (e.g. RD-PKCepsilon). The inability to assemble a cell surface-associated polyFn coat by knockdown of endogenous Fn or PKCepsilon impedes cancer cells from metastasis to the lungs. The present studies identify a novel regulatory mechanism for polyFn assembly on blood-borne breast cancer cells and depict its effect on pulmonary metastasis.

Fat tissue as a new vascular carrier for prefabrication in reconstructive surgery: experimental study in rats

Several vascular carriers for different tissues were used for the purpose of fat tissue prefabrication. However, the inguinal fat pad in rats can be elevated with a vascular pedicle and considered as a vascular carrier. To the best of our knowledge, the fat tissue in rats as a vascular carrier has not been reported in any experimental studies to date. In our study, we aimed to describe a new prefabrication model in rats in which skin prefabrication was accomplished using the inguinal fat pad as a vascular carrier. Inguinal fat pads in rats were elevated over a superficial epigastric vessel pedicle in the pilot study. The contralateral inguinal fat pads were prepared as grafts. After 1 week, we compared the histopathological findings of the inguinal fat pad flaps and grafts and determined that the inguinal fat pad can be safely elevated over the vascular pedicle. In the experimental group, bilateral vascularised inguinal fat pads were transferred to the lower abdomen for skin prefabrication. After 3 weeks, bilateral fat-skin composite flaps including prefabricated lower abdomen skin were elevated over the vascular pedicles. One side was used as a composite flap while pedicle of the other side was transected at its origin at the femoral vessels to create the composite graft. Composite flap and graft were inserted at their original positions. One week later, the composite flaps were stained with India ink, perfused by fluorescein, and filled with contrast material for microangiographic study. In the histological examination, fat and skin tissues of the composite flaps were viable while those of the composite grafts were necrotic. Based on these findings, we can conclude that the fat tissue as a vascular carrier can be successfully used for tissue prefabrication in plastic surgery.

고지방 식이로 유도된 비만쥐에서 녹차 Catechin이 체지방 조성 및 지방조직에 미치는 영향

The current study examined the effects of catechin on lipid composition of serum and liver and adipocyte of epididymal fat pads in obese rats fed high fat diet. Sprague-Dawley male rats weighing 100±10 g were randomly divided into eight groups, four normal diet groups and four high fat diet groups according to the level of dietary catechin supplement. The rats were fed ad libitum experimental diets for 4 weeks and then they were sacrificed. Body weight in HF group was heavier than that of NC group, but HFCM and HFCH groups were significantly reduced compared to HF group. Relative body weight to abdominal weight and relative body weight to epididymal weight in HF group were increased to 103% and 106%, respectively, compared to NC group, but HFCM and HFCH groups were significantly reduced as compared to HF group. The levels of serum triglyceride, total cholesterol, LDL?cholesterol and atherogenic index in HFCH groups were significantly lower than those of HF group, whereas HDL?cholesterol levels were increased. Total lipid contents of liver in HF group was significantly higher than that of NC group, but HFCH group maintained the NC level. There were no significant difference in hepatic triglyceride contents of high fat diet groups. Contents of hepatic cholesterol in HF group was 29% higher than that of NC group, but HFCM and HFCH groups were significantly reduced as compared to HF group. Cell number and cell size of epididymal fat pads in HFCM and HFCH groups were significantly reduced, respectively, compared to HF group. Improved lipid metabolism observed in rats fed catechin may be caused by an alteration of number and size in epididymal fat pad and lipid composition.

천연소재 흔합물의 보충급여가 부고환 지방세포 크기에 미치는 영향

천연소재 흔합물의 보충급여가 부고환 지방세포 크기에 미치는 영향

Difference of NPY and its Receptor Gene Expressions between Obesity and Obesity-resistant Rats in Response to High-fat Diet

To investigate the effect of high-fat diet on expressions of hypothalamic neuropeptide Y (NPY) and Y1, Y2, Y5 receptors and the mechanism relative to the susceptibility of obesity. Thirty-six female SD rats were randomly divided into high-fat diet group (HF, n=27) and chow food group (CF, n=9), and given either HF or CF diet for 13 weeks. Then the HF diet group was subdivided into dietary induced obesi-ty (DIO) and dietary induced obesity resistant (DIO-R) rat according to the final body weight. Body weight, caloric intake, energy efficiency, visceral fat pads were measured and compared. The levels of plasma and hypothalamic NPY were determined by Radioimmunoassay. Real-time Polymerase Chain Reaction (PCR) was used to measure the gene expression of NPY and its receptors in hypothalamus. Body weight, caloric intake, energy efficiency and visceral fat pads in DIO rats were higher significantly than those in CF or DIO-R rats (p<0.01). No difference in plasma NPY level was detected among the three groups (p>0.05); the hypothalamic NPY level was significantly higher in DIO group than in CF or DIO-R group (p<0.01). Gene expression levels of NPY and Y1, Y2, Y5 receptors were higher significantly in DIO group than in CF or DIO-R group (p<0.01), while no significant difference was found between DIO-R and CF rats (p>0.05), except that Y2 receptor was lower in DIO-R rats (p<0.01). SD rat fed with a HF diet showed different susceptibility to obesity, and up-regulated hypothalamic NPY and Y1, Y2, Y5 receptor gene expressions were closely associated with being predisposed to obesity and overeating of DIO rats.

In Situ Regeneration of Adipose Tissue in Rat Fat Pad by Combining a Collagen Scaffold with Gelatin Microspheres Containing Basic Fibroblast Growth Factor

In Situ Regeneration of Adipose Tissue in Rat Fat Pad by Combining a Collagen Scaffold with Gelatin Microspheres Containing Basic Fibroblast Growth Factor

In Situ Regeneration of Adipose Tissue in Rat Fat Pad by Combining a Collagen Scaffold with Gelatin Microspheres Containing Basic Fibroblast Growth Factor

This study is an investigation to evaluate in situ adipose tissue regeneration in fat pads. Gelatin microspheres with different water contents were prepared for the controlled release of basic fibroblast growth factor (bFGF). After a collagen sponge scaffold was incorporated by the microspheres containing 0, 0.01, 0.1, 1, and 10 microg of bFGF with or without syngeneic rat preadipocytes (1 x 10(5) cells/site) into a defect of rat fat pad, adipogenesis at the implanted site of scaffold was evaluated histologically. in situ formation of adipose tissue accompanied with angiogenesis was observed in the scaffold implanted with the microspheres containing 1.0 microg of bFGF, although the extent was less at the lower and higher bFGF doses. The in situ formation induced by the microspheres containing bFGF was significantly higher than that induced by free bFGF of the same dose. Adipogenesis was enhanced with time after implantation up to 4 weeks and thereafter leveled off. Such in situ adipogenesis was reproducibly induced by implantation of collagen scaffold incorporating gelatin microspheres containing 1 microg of bFGF, whereas addition of rat syngeneic preadipocytes did not promote the adipogenesis. The degradation of microspheres and the consequent FGF release became faster with an increase in the water content of gelatin microspheres. Less in situ formation of adipose tissue was observed at the lower water content of microspheres, which showed longer-term bFGF release. We conclude that combination of scaffold collagen with an appropriate controlled release of bFGF was essential to achieve the in situ formation of adipose tissue even without preadipocytes.

Biocompatibility of subsieve‐size capsules versus conventional‐size microcapsules

Biocompatibility of cell-enclosing capsules, defined as suppression of pericapsular cellular reactions, is one of the factors governing the success of enclosed cell transplantation in in vivo cell therapy. Agarose capsules of subsieve size, less than 100 microm in diameter, and conventional size, approximately 300-1,000 microm in diameter, were implanted into the peritoneal cavity and epididymal fat pads of mice and rats, respectively, to determine the effect of a reduction in diameter to subsieve size. The degree of cellular reaction to the subsieve-size capsules was much lower than that of the conventional-size microcapsules, independent of implantation site. The frequency of overgrown subsieve-size capsules retrieved from the peritoneal cavities was less than 5% in contrast to approximately 20% for capsules 387 microm in diameter. In addition, no increase in floating cells, which are generated through capsule stimulation, was observed in the peritoneal cavity only with subsieve-size capsules. From these results, we concluded that subsieve-size capsules are more biocompatible than microcapsules of conventional size.

Action of low-level laser therapy on living fatty tissue of rats

Little is known about the action of laser rays on normal adipose cells. The present study attempts to observe the behavior of fatty cells submitted to laser therapy. Dorsal fat pads of normal adult rats were submitted to low-level laser irradiation applied locally through intact skin, with four different dose schedules (4, 8, 12, and 16 J/cm(2)), with a further group being sham-irradiated. Histology, morphometry, immunofluorescence, and electron microscopy were all used to analyze irradiated tissues. Changes were restricted to the brown fatty tissue, in which a tendency was shown for multivacuolar cells to be transformed into the unilocular type. The number of cells which exhibited enlargement and fusion of small vacuoles was greater in the 4- and 16-J/cm(2) groups (p<0.05). Increased vascular proliferation and congestion was another more evident finding in laser-treated animals compared to nontreated animals. Low-level laser rays cause brown adipose fat droplets to coalesce and fuse. Additionally, they stimulated proliferation and congestion of capillaries in the extracellular matrix.