This study was conducted to examine the effects of dietary xylooligosaccharides on lipoprotein lipase (LPL) activitiy in epididymal adipose tissue and lipid composition in serum of rats fed normal or high fat diet. Male Sprague-Dawley male rats weighing 100 $\pm$ 10 g were randomly divided into four groups, two normal diets and two high fat diets containing 1% cholesterol and 10% lard. Two normal diets were classified into a basal diet (normal group) and that with 10% xylooligosaccharide diet (NX group). The high fat diet groups were classified into a HF group without xylooligosaccharides diet and HFX group supplemented with 10% xylooligosacchride diet. Experimental diets were fed ad libitum to the rats for 4 weeks and then they were sacrificed. Body weight, epididymal weight and abdominal weight in HF group were hevier than the those of normal group, but HFX group was significantly reduced compared to HF group. Relative body weight to epididymal weight and relative body weight to abdominal weight in HF group were increased to 50%, 51%, respectively, compared to normal group, but HFX group was reduced 22%, 16%, respectively, compared to HF group. The levels of serum triglyceride, total cholesterol, LDL-cholesterol and atherogenic index in HFX groups were significantly lower than those of HF group, whereas HDL-cholesterol levels were significant increased. Triglyceride contents of epididymal adipose tissue in HF group was increased to 39%, compared to normal group, but HFX group was reduced to 15.8%, compared to HF group. Cholesterol contents of epididymal adipose tissue in HF group was increased 121%, compared to normal group, but HFX group was reduced to 26%, compared to HF group. The activity of LPL in epididymal adipose tissue was increased to 259% in HF group, compared to normal group and HFX group was reduced to 66%, compared to HF group. These result of this study suggested that improved lipid metabolism observed in rats fed xylooligosaccharides may be caused by an alteration of LPL activity in epididymal adipose tissue and lipid composition in serum.
Seo, Dong-Joo;Chung, Mi-Ja;Kim, Dae-Jung;Choe, Myeon
Journal of the Korean Society of Food Science and Nutrition
/
v.38
no.11
/
pp.1522-1527
/
2009
We investigated the effects of feeding diet containing medicinal plant water extracts (MPWEs) on body weight, epididymal adipose tissue weight, adipocyte size of epididymal adipose tissue and plasma lipid levels in high fat (HF) diet-induced obese mice. To test antiobese effects of diet containing the MPWEs, C57BL/6J mice were fed with HF diet for 11 weeks. In the last 6 weeks, the HF diet was supplemented with 0 (HFD) or MPWEs (5 g/kg, HFD+MPWEs) or orlistat [0.5 g/kg, HFD+orlistat (antiobesity drug)]. The HF-free diet group was fed normal chow for 11 weeks. Eleven-weeks feeding with HFD resulted in significant increase in lipid levels, body weight, liver and epididymal adipose tissue weights, compared with the HF-free group. Diet containing MPWEs significantly reduced plasma total cholesterol, LDL-cholesterol, triglyceride and glucose concentrations as well as body weight, liver weight and epididymal adipose tissue weight. Plasma triglyceride levels were significantly lower in the HFD+Forlistat group after 6 weeks and a similar effect was found with HFD+MPWEs group. The adipocyte size of epididymal adipose tissue in HFD group was significantly larger than those of HF-free group. MPWEs and orlistat (positive control) significantly decreased the size of epididymal adipocytes but orlistat was slightly more effective than MPWEs. These results suggest that oral feeding of the MPWEs may have antiobesity effects by suppressing body weight gain, adipose tissue formation and adipocyte size increase.
Obesity can be defined as a metabolic disease due to a increased state of fat tissue caused by an imbalance of calorie intake and use. To define genes that affected by different nutrient, we study gene expression from mice which were fed different nutrient. Epididymal and retro-peritineal adipose tissue were increase in high fat diet feeding mice compared with control, but liver and spleen were not. In serum, total cholesterol were differently increase in high fat diet feeding mice but total triglyceride and free fatty acid were not. That was maybe result of energy balance regulation in vivo system. aP2, PPART2 and FAS genes that were increased during adipogenesis were inclosed in high fat diet fed mice compared with control. In microarray assay, 1.4% of total genes were affected in epididymal adipose tissue by different nutrient. 1.1% of total genes were decreased down 0.5 fold and 0.3% were increased over 2 fold. These results indicated that many genes are affected in adipose tissue by nutrient.
Objectives : The purpose of this study was to investigate how Rhei Radix et Rhizoma affects on insulin resistance and adipose tissue inflammatory response in high fat diet induced obese C57BL/6 mice. Methods : Obesity was induced in C57BL/6 mice by high fat diet for 12 weeks. Models were divided into 3 groups (n=6) of normal diet, high fat diet (HFD), and high fat diet with Rhei Radix et Rhizoma and investigated for 12 weeks. We measured body weight, FBS and oral glucose tolerance test (OGTT), serum insulin, homeostatic model assessment-insulin resistance (HOMA-IR), weight of liver and epididymal fat pad. Inflammatory markers such as adipose tissue macrophage (ATM), tumor necrosis factor-${\alpha}$ and interlukin-10 and CD68 of epididymal adipocyte were determined to evaluate the effect of Rhei Radix et Rhizoma on adipose tissue inflammation. Results : Compared with the HFD group, we observed loss of body weight and epididymal fat pad weight, improvement of glucose level and HOMA-IR, reduction of ATM and gene expression of TNF-${\alpha}$, CD68 in the high fat diet with Rhei Radix et Rhizoma group. Conclusions : This study suggests that Rhei Radix et Rhizoma has effects on insulin resistance and adipose tissue inflammatory response in high fat diet induced obese mice.
The adipogenesis is a maturation process of pre-adipocyte cell into mature lipid-filled adipocyte cell. The adipogenesis begins at the late prenatal stage and continues until the early postnatal age. Because the adipogenesis and formation of adipose tissue persist during postnatal period and are precisely regulated by the action of numerous gene products, the present research was attempted to determine the expressional patterns of adipose tissue-associated genes in the rat epididymal fat pad at different postnatal ages, from 7 days to 2 years of ages, using a quantitative real-time PCR analysis. The basal expression levels of CCAAT/enhancer binding protein gamma, sterol regulatory element binding transcription factor 1, fatty acid binding protein 4, adiponectin, leptin, and resistin at the early postnatal ages were significantly lower than those at the elderly ages, even though a fluctuation of expressional levels was observed at some ages. The lowest expressional level of delta like non-canonical Notch ligand 1 was detected at 44 days and 5 months of ages. The expression of peroxisome proliferator-activated receptor gamma ($PPAR{\gamma}$) was the highest at 44 days of age, followed by a diminished expression of $PPAR{\gamma}$ at the elderly ages. These results indicate the existence of a complex regulatory mechanism(s) for expression of adipose tissueassociated genes in the rat epididymal fat during postnatal period.
The risk of inflammatory conditions caused by obesity is associated with an increased predisposition for additional pathological conditions, including cardiovascular risk factors. Adipose tissue stores energy and contributes to endocrine and immune functions that regulate homeostasis throughout the body. The effects of honokiol on vascular homeostasis in adipose tissue in high-fat diet (HFD)-induced obese mice are unclear. This study examined the protective effect of honokiol, an extract of traditional alkaloid herbs, on vascular endothelial cells in epididymal adipose tissue (EAT) and its regulatory effect on other metabolic parameters, such as the lipid droplet diameter, macrophage infiltration, and inflammation in HFD-induced obese mice. A HFD increased the density of platelet endothelial cell adhesion molecule-1 (PECAM-1)-1-positive vascular endothelial cells in EAT, which was decreased significantly by the honokiol treatment. Honokiol ameliorated the HFD-induced increase in lipid droplet diameter and increased macrophage infiltration in adipose tissue. Honokiol ameliorated the up-regulation of pro-inflammatory molecules and F4/80-positive macrophage infiltration in the adipose tissue of HFD-induced obese mice. Obese mice administered honokiol exhibited reduced mRNA expression of M1 macrophage (F4/80, TNF-α, mIL-1β, CD11c, and CCL2) and M2 macrophage (Arginase-1, FIZZ1, CD206, and TGF-β1) markers in EAT. The vascular permeability was detected by Evans blue dye leakage in EAT of obese mice and treated mice with honokiol. These data suggest that honokiol regulates the angiogenic effects in adipose tissue and inflammation in HFD-induced obese mice.
The current study was undertaken to determine the effects of the ratios of dietary fat to carbohydrate and energy restriction on insulin sensitivity in the growing rats. Male rats weighting 80-90g were fed experimental diets for two weeks. Rats were killed and epiddymal adipose tissue were removed and sliced. Explants of adipose tissues were incubated for 2 hours in KRB(Krebs-Ringer bicarbonate) buffer containing various concentrations of human insulin and [U-14C]glucose. Insulin sensitivity was determined as glucose conversion to total lipids (lipogenesis) during 2 hr incubation. Exp't I : Effects of Ratios of Fat to Carbohydrate on Insulin Sensitivity. Eighteen male rats were fed 3 diets for 2 weeks. Diet 1 was low fat-high carbohydrate (4% soybean oil and 66.5% cornstarch) ; diet 2, medium fat-medium sarbohydrate(12% soybean oil and 58.5% cornstarch) ; diet 3, high fat-low carbohydrate (20% soybean oil and 50.5% cornstarch). Insulin sensitivity was higher in the order of LF-HC, MF-HC and HF-LC diet groups (p<0.05), i.e, lipogenesis was higher at all insuline concentration in the explants from rats fed LF-HC diet. However, thers was no significant difference in body weight gain and epididymal adipose tissue weight among treatments. Exp't II ; Effects of Energy Restriction on Insulin Sensitivity. Twelve rats were grouped into ad libitum feeding and restricted feeding(70% of ad libitum). The experimental diet was medium fat-medium carbohydrat diet as used in the Exp't I. Restricted feeding group tended to show higher insulin sensitivity compared to ad libitum group. However, there was no statistical difference between two groups. As expected, body weight gain and epididymal adipose tissue were higher in the ad libitum group. In summary, the resutls of the current study showed that the epididymal adipose tissue taken from the rats fed low fat-high carbohydrate diet showed higher insulin sensitivity compared to those fed high fat-low carbohydrate, and that resticted feeding tended to elevate insulin sensitivity in these tissues.
We investigated the anti-obesity effect of berberine in mice fed a high fat diet and focused on the analysis of adipogenesis in epdidymal adipose tissue. Male C57BL/6J mice were divided into three groups, which were fed either a normal diet (Nor), a high fat diet (HFD), or a high fat diet plus orally administered berberine (0.2 g /kg body weight) (HFD+B) for 8 weeks. Relative to mice in the HFD group, mice in the HFD+B group showed significant reductions in weight gain and adipose tissue weight. Serum triglyceride levels in mice from the HFD+B group were significantly lower than those of the HFD mice, as were the levels of serum insulin and leptin. An effect of berberine to reduce epididymal adipose mass was revealed by H&E staining. Berberine inhibited the high fat diet-induced increase in levels of the proteins CD36 and CCAAT/enhancer-binding protein $\alpha$ ($C/EBP{\alpha}$) observed in epididymal adipose tissues of mice from the HFD group. These results suggest that berberine has an anti-obesity effect in mice and that the effect is mediated by inhibition of adipogenesis.
BACKGROUND/OBJECTIVES: The steamed ginger has been shown to have antioxidative effects and a protective effect against obesity. In the present study, we investigated the effects of ethanolic extract of steamed ginger (SGE) on adipogenesis in 3T3-L1 preadipocytes and diet-induced obesity (DIO) mouse model. MATERIALS/METHODS: The protective effects of SGE on adipogenesis were examined in 3T3-L1 adipocytes by measuring lipid accumulations and genes involved in adipogenesis. Male C57BL/6J mice were fed a normal diet (ND, 10% fat w/w), a high-fat diet (HFD, 60% fat w/w), and HFD supplemented with either 40 mg/kg or 80 mg/kg of SGE for 12 weeks. Serum chemistry was measured, and the expression of genes involved in lipid metabolism was determined in the adipose tissue. Histological analysis and micro-computed tomography were performed to identify lipid accumulations in epididymal fat pads. RESULTS: In 3T3-L1 cells, SGE significantly decreased lipid accumulation, with concomitant decreases in the expression of adipogenesis-related genes. SGE significantly attenuated the increase in body, liver, and epididymal adipose tissue weights by HFD. Serum total cholesterol and triglyceride levels were significantly lower in SGE fed groups compared to HFD. In adipose tissue, SGE significantly decreased adipocyte size than that of HFD and altered adipogenesis-related genes. CONCLUSIONS: In conclusion, steamed ginger exerted anti-obesity effects by regulating genes involved in adipogenesis and lipogenesis in 3T3-L1 cell and epididymal adipose tissue of DIO mice.
It is now well-accepted that obesity-induced inflammation plays an important role in the development of insulin resistance and type 2 diabetes. A key source of the inflammation is the murine epididymal and human visceral adipose tissue. The current paradigm is that obesity activates multiple proinflammatory immune cell types in adipose tissue, including adipose-tissue macrophages (ATMs), T Helper 1 (Th1) T cells, and natural killer (NK) cells, while concomitantly suppressing anti-inflammatory immune cells such as T Helper 2 (Th2) T cells and regulatory T cells (Tregs). A key feature of the current paradigm is that obesity induces the anti-inflammatory M2 ATMs in lean adipose tissue to polarize into proinflammatory M1 ATMs. However, recent single-cell transcriptomics studies suggest that the story is much more complex. Here we describe the single-cell genomics technologies that have been developed recently and the emerging results from studies using these technologies. While further studies are needed, it is clear that ATMs are highly heterogeneous. Moreover, while a variety of ATM clusters with quite distinct features have been found to be expanded by obesity, none truly resemble classical M1 ATMs. It is likely that single-cell transcriptomics technology will further revolutionize the field, thereby promoting our understanding of ATMs, adipose-tissue inflammation, and insulin resistance and accelerating the development of therapies for type 2 diabetes.
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