OBJECTIVETo investigate the role of the expression of PPAR-gamma gene in the adipogenesis in hemangioma evolution.

METHODSRoutine immunohistochemistry staining of Perilipin A, the marker antigen of adipocytes, was performed to observe the adipogenesis in hemangioma. Immunofluorescence staining of PPAR-gamma, the important transcription factor in promoting adipogenesis, was carried out to observe its location in hemangioma tissue, with the co-staining of alpha-SMA and CD31. And RT-PCR was used to examine the expression of PPAR-gamma gene in hemangioma in different stages.

RESULTSIn the evolution of hemangioma, the number of adipocytes increased continuously. And the tumor was replaced by fibrofatty tissue finally. PPAR-gamma was located in the nuclei of perivascular cell in hemangioma tissue. The expression of PPAR-gamma gene in hemangioma increased in the evolution of hemangioma, but still was lower than that in normal fat tissue from children.

CONCLUSIONThe expression of PPAR-gamma in the perivascular cells suggests that they may contribute to the adipogenesis in hemangioma involution.

Adipogenesis ; Adipose Tissue ; metabolism ; pathology ; Hemangioma ; metabolism ; pathology ; Humans ; PPAR gamma ; metabolism

Obesity, which underlies various metabolic and cardiovascular diseases, is a growing public health challenge for which established therapies are inadequate. Given the current obesity epidemic, there is a pressing need for more novel therapeutic strategies that will help adult individuals to manage their weight. One promising therapeutic intervention for reducing obesity is to enhance energy expenditure. Investigations into human brown fat and the recently discovered beige/brite fat have galvanized intense research efforts during the past decade because of their pivotal roles in energy dissipation. In this review, we summarize the evolution of human brown adipose tissue (hBAT) research and discuss new in vivo methodologies for evaluating energy expenditure in patients. We highlight the differences between human and mouse BAT by integrating and comparing their cellular morphology, function, and gene expression profiles. Although great advances in hBAT biology have been achieved in the past decade, more cellular models are needed to acquire a better understanding of adipose-specific processes and molecular mechanisms. Thus, this review also describes the development of a human brown fat cell line, which could provide promising mechanistic insights into hBAT function, signal transduction, and development. Finally, we focus on the therapeutic potential and current limitations of hBAT as an anti-glycemic, anti-lipidemic, and weight loss-inducing 'metabolic panacea'.
Adipose Tissue, Beige ; metabolism ; pathology ; Adipose Tissue, Brown ; metabolism ; pathology ; Animals ; Cell Line ; Energy Metabolism ; Humans ; Mice ; Obesity ; metabolism ; pathology ; therapy

Brown adipose tissue (BAT) plays a fundamental role in maintaining body temperature by producing heat. BAT that had been know to exist only in mammals and the human neonate has received great attention for the treatment of obesity and diabetes due to its important function in energy metabolism, ever since it is recently reported that human adults have functional BAT. In addition, beige adipocytes, brown adipocytes in white adipose tissue (WAT), have also been shown to take part in whole body metabolism. Multiple lines of evidence demonstrated that transplantation or activation of BAT or/and beige adipocytes reversed obesity and improved insulin sensitivity. Furthermore, many genes involved in BATactivation and/or the recruitment of beige cells have been found, thereby providing new promising strategies for future clinical application of BAT activation to treat obesity and metabolic diseases. This review focuses on recent advances of BAT function in the metabolic aspect and the relationship between BAT and cancer cachexia, a pathological process accompanied with decreased body weight and increased energy expenditure in cancer patients. The underlying possible mechanisms to reduce BAT mass and its activity in the elderly are also discussed.
Adipose Tissue, Brown ; metabolism ; Aging ; metabolism ; Animals ; Cachexia ; metabolism ; pathology ; Disease Models, Animal ; Energy Metabolism ; Humans ; Metabolic Syndrome ; metabolism ; Neoplasms ; metabolism ; pathology ; Obesity ; metabolism ; Thermogenesis

Diabetes mellitus is a complex metabolic disorder characterized by chronic hyperglycemia due to absolute or relative lack of insulin. Though great efforts have been made to investigate the pathogenesis of diabetes, the underlying mechanism behind the development of diabetes and its complications remains unexplored. Cumulative evidence has linked mitochondrial modification to the pathogenesis of diabetes and its complications and they are also observed in various tissues affected by diabetes. Proteomics is an attractive tool for the study of diabetes since it allows researchers to compare normal and diabetic samples by identifying and quantifying the differentially expressed proteins in tissues, cells or organelles. Great progress has already been made in mitochondrial proteomics to elucidate the role of mitochondria in the pathogenesis of diabetes and its complications. Further studies on the changes of mitochondrial protein specifically post-translational modifications during the diabetic state using proteomic tools, would provide more information to better understand diabetes.
Adipose Tissue ; metabolism ; Diabetes Complications ; Diabetes Mellitus ; metabolism ; pathology ; Humans ; Insulin ; metabolism ; Insulin-Secreting Cells ; cytology ; metabolism ; Liver ; metabolism ; Mitochondria ; metabolism ; Muscle, Skeletal ; metabolism ; Proteome ; metabolism ; Proteomics

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver dysfunction and a significant global health problem with substantial rise in prevalence over the last decades. It is becoming increasingly clear that NALFD is not only predominantly a hepatic manifestation of metabolic syndrome, but also involves extra-hepatic organs and regulatory pathways. Therapeutic options are limited for the treatment of NAFLD. Accordingly, a better understanding of the pathogenesis of NAFLD is critical for gaining new insight into the regulatory network of NAFLD and for identifying new targets for the prevention and treatment of NAFLD. In this review, we emphasize on the current understanding of the inter-organ crosstalk between the liver and peripheral organs that contributing to the pathogenesis of NAFLD.
Adipose Tissue ; pathology ; Animals ; Extracellular Vesicles ; metabolism ; Humans ; Hypothalamus ; metabolism ; Intestines ; microbiology ; pathology ; Non-alcoholic Fatty Liver Disease ; etiology ; metabolism ; microbiology ; pathology

Central obesity with visceral fat accumulation and the amount of skeletal muscle mass may influence insulin sensitivity via its capacity for glucose load uptake. We investigated the relationships among the following metabolic variables: ratio of fat area to skeletal muscle area (VMR), percent ideal body weight, body mass index, waist-to-hip circumference (WHR) and visceral fat to subcutaneous fat ratio (VSR) in 114 nondiabetic middle-aged women. Anthropometric parameters, lipid profiles and sex hormone- binding globulin were measured. Visceral and subcutaneous fat areas at the umbilical level and the skeletal muscle area at the mid-thigh level were measured and computed. 75-gram OGTT tests were performed, along with measuring plasma glucose, insulin and free fatty acid levels, according to which area under the curve of glucose (Glu-AUC), insulin (Ins-AUC), free fatty acid (FFA-AUC) and glucose/insulin ratio (GIR=Glu- AUC/Ins-AUC), were calculated. 1) Triglyceride was more correlated with VSR than VMR. 2) The independent anthropometric parameters for each metabolic variable were In conclusion, VMR for Ins-AUC, WHR for Glu-AUC and total cholesterol, and VSR for triglyceride. 3) For subjects with higher VMR, age, Ins-AUC and triglyceride were significantly higher. 4) Subjects with higher VMR were older and showed higher Ins-AUC and lower GIR than the subjects with lower VMR. In conclusion, VMR is an anthropometric parameter that reflects insulin resistance concerning glucose metabolism, and VSR is thought to be a good parameter that that reflects the serum lipid levels. Further prospective studies are necessary to reevaluate the visceral fat vs. skeletal muscle relationship.
Adipose Tissue/*metabolism/*pathology ; Adult ; Body Constitution ; *Body Mass Index ; Female ; Human ; *Insulin Resistance ; Menopause ; Middle Aged ; Muscle, Skeletal/*metabolism ; Obesity/metabolism/pathology ; Postmenopause ; Viscera

Adenoma, Pleomorphic ; metabolism ; pathology ; surgery ; Adipose Tissue ; pathology ; Female ; Follow-Up Studies ; Humans ; Immunohistochemistry ; Male ; Membrane Proteins ; metabolism ; Metaplasia ; pathology ; Middle Aged ; Parotid Gland ; metabolism ; pathology ; surgery ; Parotid Neoplasms ; metabolism ; pathology ; surgery ; S100 Proteins ; metabolism

Obesity is characterized by abnormal and excessive adipose tissue accumulated in the body. Compared with peripheral obesity (the accumulation of subcutaneous adipose tissue), abdominal obesity (the accumulation of visceral adipose tissue) is associated with increased risk of the metabolic syndrome, such as diabetes, hypertension, atherosclerosis, and dyslipidemia. Adipose tissue is a highly heterogeneous endocrine organ. Adipose tissue depots differ significantly in anatomy, cell biology, glucose and lipid metabolism as well as in endocrine regulation. Visceral adipose tissue has a stronger metabolic activity and secrets a larger amount of free fat acids, adipocytokines, hormones and inflammatory factors, which flux into the liver directly via the hepatic portal vein. These characteristics indicate that visceral adiposity may lead to the metabolic syndrome and thus visceral adipose tissue might be the clinical target for the prevention and treatment of obesity.
Adipose Tissue ; pathology ; Humans ; Intra-Abdominal Fat ; pathology ; Lipid Metabolism ; Metabolic Syndrome ; physiopathology ; Obesity ; physiopathology ; Obesity, Abdominal ; physiopathology ; Subcutaneous Fat ; pathology

OBJECTIVETo investigate the influence of lipopolysaccharide (LPS) on adipose metabolism in liver during shock stage of scalded rats.

METHODSSixty adult Wistar rats were inflicted with 30% TBSA full thickness scald and were randomly divided into 3 groups: i. e. sham group (control, n = 20), simple scald group [(n = 20) and LPS group (n = 20, with intra-peritoneal injection of 3.0 mg/kg LPS at 2 postscald hour (PSH)]. The contents of LPS, tumor necrosis factor alpha (TNF-alpha), free fatty acids (FFA) in plasma and adenosine triphosphate (ATP), triglyceride (TG), malonaldehyde (MDA) in liver in each group were determined at 24 and 48 PSH. The histological changes in hepatic tissue in each group were also observed.

RESULTSThe plasma contents of FFA in LPS group at 24 and 48 PSH were 2.3 +/- 0.3 mmol/L and 2.5 +/- 0.4 mmol/L, respectively, which were obviously higher than those in control (0.4 +/- 0.3 mmol/L, 0.5 +/- 0.3 mmol/L) and scald (0.9 +/- 0.3, 1.2 +/- 0.5 mmol/L, P <0.01) groups. Meanwhile, there was obvious difference in the contents of TG and ATP in liver between LPS group (TG: 530 +/- 30 mmol/g, ATP: 1.7 +/- 0.5 micromol/g) and scald group (TG: 242 +/- 27 mmol/g, ATP: 6.0 +/- 2.4 micromol/g, P < 0.01). Pathological examination revealed that adipose denaturalization and injury to mitochondria in hepatocytes in scald group were significantly milder than those in LPS group. The morphology of hepatocyte in control group appeared normal.

CONCLUSIONLPS challenge to burn subjects could induce impairment in utilizing fat derived energy, and it would aggravate adipose denaturalization in the liver.

Adenosine Triphosphate ; metabolism ; Adipose Tissue ; metabolism ; Animals ; Burns ; metabolism ; pathology ; Disease Models, Animal ; Fatty Acids ; blood ; Lipopolysaccharides ; toxicity ; Liver ; metabolism ; pathology ; Male ; Rats ; Rats, Wistar ; Shock ; metabolism ; pathology ; Triglycerides ; metabolism

The purpose of the present study was to determine whether chronic high-fat diet (HF) induces insulin resistance independently of obesity. We randomly divided 40 rats into two groups and fed them either with a HF or with a high-carbohydrate diet (HC) for 8 weeks. Whole body glucose disappearance rate (Rd) was measured using a euglycemic hyperinsulinemic clamp. Firstly, we defined whether insulin resistance by HF was associated with obesity. Plasma glucose and triglyceride concentrations were significantly increased in HF. Rd was decreased (10.6+/-0.2 vs. 9.1+/-0.2 mg/kg/min in HC and HF, respectively) and the hepatic glucose output rate (HGO) was increased in HF (2.2+/-0.3 vs. 4.5+/-0.2 mg/kg/min in HC and HF, respectively). Rd was significantly correlated with %VF (p<0.01). These results implicate that visceral obesity is associated with insulin resistance induced by HF. In addition, to define whether dietary fat induces insulin resistance regardless of visceral obesity, we compared Rd and HGO between groups 1) after matching %VF in both groups and 2) using an ANCOVA to adjust for %VF. After matching %VF, Rd in HF was significantly decreased by 14% (p<0.001) and HGO was significantly increased by 110% (p<0.001). Furthermore, statistical analyses using an ANCOVA also showed Rd for HF was significantly decreased even after adjusting %VF. In conclusion, we suggest that dietary fat per se could induce insulin resistance in rats fed with chronic HF independently of obesity.
Adipose Tissue/*pathology ; Animal ; Dietary Carbohydrates/administration &age ; Dietary Fats/*administration &age ; Fatty Acids, Nonesterified/metabolism ; Female ; *Insulin Resistance ; Obesity/etiology ; Rats ; Rats, Sprague-Dawley ; Viscera