(−)-Cedrol isolated from Juniperus chinensis reduces diet-induced obesity through increased uncoupling protein expression in the visceral adipose tissue of mice

2009 ◽  
Vol 25 ◽  
pp. S13
Author(s):  
T. Park ◽  
H.I. Jung ◽  
H.W. Kim
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Visceral Adipose Tissue ◽  
Uncoupling Protein ◽  
Diet Induced Obesity ◽  
Juniperus Chinensis ◽  
Visceral Adipose

Trans-palmitoleic Acid Reduces Adiposity via Increased Lipolysis in a Rodent Model of Diet-Induced Obesity

2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Palmitoleic Acid ◽  
Rodent Model ◽  
Adipocyte Size ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Visceral Adipose

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.

scholarly journals Systems-wide effects of short-term feed deprivation in obese mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Daniel Andersen ◽  
Henrik Munch Roager ◽  
Li Zhang ◽  
Janne Marie Moll ◽  
Henrik Lauritz Frandsen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Butyric Acid ◽  
Visceral Adipose Tissue ◽  
Animal Studies ◽  
Uncoupling Protein ◽  
Metabolic Changes ◽  
Obese Mice ◽  
Short Term ◽  
Feed Deprivation ◽  
Visceral Adipose

AbstractWhile prolonged fasting induces significant metabolic changes in humans and mice, less is known about systems-wide metabolic changes in response to short-term feed deprivation, which is used in experimental animal studies prior to metabolic challenge tests. We here performed a systems biology-based investigation of connections between gut bacterial composition and function, inflammatory and metabolic parameters in the intestine, liver, visceral adipose tissue, blood and urine in high-fat fed, obese mice that were feed deprived up to 12 h. The systems-wide analysis revealed that feed deprivation linked to enhanced intestinal butyric acid production and expression of the gene encoding the pro-thermogenic uncoupling protein UCP1 in visceral adipose tissue of obese mice. Ucp1 expression was also positively associated with Il33 expression in ileum, colon and adipose tissue as well as with the abundance of colonic Porphyromonadaceae, the latter also correlating to cecal butyric acid levels. Collectively, the data highlighted presence of a multi-tiered system of inter-tissue communication involving intestinal, immune and metabolic functions which is affected by feed deprivation in obese mice, thus pointing to careful use of short-feed deprivation in metabolic studies using obese mice.

scholarly journals Systems-wide effects of short-term feed deprivation in obese mice

2020 ◽  
Author(s):  
Daniel Andersen ◽  
Henrik Munch Roager ◽  
Li Zhang ◽  
Janne Marie Moll ◽  
Henrik Lauritz Frandsen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Butyric Acid ◽  
Visceral Adipose Tissue ◽  
Animal Studies ◽  
Uncoupling Protein ◽  
Metabolic Changes ◽  
Obese Mice ◽  
Short Term ◽  
Feed Deprivation ◽  
Visceral Adipose

Abstract Background While prolonged fasting induces significant metabolic changes in humans and mice, less is known about systems-wide metabolic changes in response to short-term feed deprivation, which traditionally has been used in experimental animal studies prior to metabolic challenge tests. Methods We here performed a systems biology-based investigation of connections between gut bacterial composition and function, inflammatory and metabolic parameters in the intestine, liver, visceral adipose tissue, blood and urine in obese mice that were feed deprived for varying durations up to 12 hours. Results Our analysis revealed that increased duration of feed deprivation linked to enhanced intestinal butyric acid production and expression of the gene encoding the pro-thermogenic uncoupling protein UCP1 in visceral adipose tissue of obese mice. Ucp1 expression was also positively associated with Il33 expression in ileum, colon and adipose tissue as well as with the abundance of colonic Porphyromonadaceae, the latter also correlating to cecal butyric acid levels. Conclusions The data highlighted presence of a three-tiered system of inter-tissue communication involving intestinal, immune and metabolic functions which is affected by the duration of feed deprivation in obese mice.

scholarly journals Systems-wide Effects of Short-term Feed Deprivation in Obese Mice

2020 ◽  
Author(s):  
Daniel Andersen ◽  
Henrik Roager ◽  
Li Zhang ◽  
Janne Moll ◽  
Henrik Frandsen ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Butyric Acid ◽  
Visceral Adipose Tissue ◽  
Animal Studies ◽  
Uncoupling Protein ◽  
Metabolic Changes ◽  
Obese Mice ◽  
Short Term ◽  
Feed Deprivation ◽  
Visceral Adipose

Abstract While prolonged fasting induces significant metabolic changes in humans and mice, less is known about systems-wide metabolic changes in response to short-term feed deprivation, which is used in experimental animal studies prior to metabolic challenge tests, and hence, information on the effects of varying length of feed deprivation is warranted. We here performed a systems biology-based investigation of connections between gut bacterial composition and function, inflammatory and metabolic parameters in the intestine, liver, visceral adipose tissue, blood and urine in obese mice that were feed deprived for varying durations up to 12 hours. The systems-wide analysis revealed that increased duration of feed deprivation linked to enhanced intestinal butyric acid production and expression of the gene encoding the pro-thermogenic uncoupling protein UCP1 in visceral adipose tissue of obese mice. Ucp1 expression was also positively associated with Il33 expression in ileum, colon and adipose tissue as well as with the abundance of colonic Porphyromonadaceae, the latter also correlating to cecal butyric acid levels. Collectively, the data highlighted presence of a three-tiered system of inter-tissue communication involving intestinal, immune and metabolic functions which is affected by the duration of feed deprivation in obese mice, thus pointing to careful use of short-feed deprivation in metabolic studies using mice.

Genetic Deficiency of TRAF5 Promotes Adipose Tissue Inflammation and Aggravates Diet-Induced Obesity in Mice

2021 ◽  
Author(s):  
Mark Colin Gissler ◽  
Nathaly Anto-Michel ◽  
Jan Pennig ◽  
Philipp Scherrer ◽  
Xiaowei Li ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
Obese Patients ◽  
Adipose Tissue Inflammation ◽  
Metabolic Complications ◽  
Tissue Inflammation ◽  
Diet Induced Obesity ◽  
Genetic Deficiency ◽  
Obesity In Mice ◽  
Visceral Adipose

Objective: The accumulation of inflammatory leukocytes is a prerequisite of adipose tissue inflammation during cardiometabolic disease. We previously reported that a genetic deficiency of the intracellular signaling adaptor TRAF5 (TNF [tumor necrosis factor] receptor–associated factor 5) accelerates atherosclerosis in mice by increasing inflammatory cell recruitment. Here, we tested the hypothesis that an impairment of TRAF5 signaling modulates adipose tissue inflammation and its metabolic complications in a model of diet-induced obesity in mice. Approach and Results: To induce diet-induced obesity and adipose tissue inflammation, wild-type or Traf5 −/− mice consumed a high-fat diet for 18 weeks. Traf5 −/− mice showed an increased weight gain, impaired insulin tolerance, and increased fasting blood glucose. Weight of livers and peripheral fat pads was increased in Traf5 −/− mice, whereas lean tissue weight and growth were not affected. Flow cytometry of the stromal vascular fraction of visceral adipose tissue from Traf5 −/− mice revealed an increase in cytotoxic T cells, CD11c + macrophages, and increased gene expression of proinflammatory cytokines and chemokines. At the level of cell types, expression of TNFα, MIP (macrophage inflammatory protein)-1α, MCP (monocyte chemoattractant protein)-1, and RANTES (regulated on activation, normal T-cell expressed and secreted) was significantly upregulated in Traf5 -deficient adipocytes but not in Traf5 -deficient leukocytes from visceral adipose tissue. Finally, Traf5 expression was lower in adipocytes from obese patients and mice and recovered in adipose tissue of obese patients one year after bariatric surgery. Conclusions: We show that a genetic deficiency of TRAF5 in mice diet-induced obesity and its metabolic derangements by a proinflammatory response in adipocytes. Our data indicate that TRAF5 may promote anti-inflammatory and obesity-preventing signaling events in adipose tissue.

scholarly journals Long-term hypercortisolism induces lipogenesis promoting palmitic acid accumulation and inflammation in visceral adipose tissue compared with HFD-induced obesity

2020 ◽  
Vol 318 (6) ◽  
pp. E995-E1003
Author(s):  
Guillermo García-Eguren ◽  
Aleix Sala-Vila ◽  
Oriol Giró ◽  
Arturo Vega-Beyhart ◽  
Felicia A. Hanzu
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Mouse Model ◽  
Acid Composition ◽  
Visceral Adipose Tissue ◽  
Diet Induced Obesity ◽  
Visceral Adipose ◽  
Composition Changes

Glucocorticoids (GCs) play critical roles in adipose tissue metabolism. Here, we compare in a mouse model the effects of chronic glucocorticoid excess and diet-induced obesity on white adipose tissue mass and distribution, by focusing on visceral adipose tissue (VAT) fatty acid composition changes, the role of de novo lipogenesis (DNL) and the inflammatory state. We used a noninvasive mouse model of hypercortisolism to compare GC-induced effects on adipose tissue with diet-induced obesity [high-fat diet (HFD) 45%] and control mice after 10 wk of treatment. Subcutaneous adipose tissue (SAT) and VAT mass and distribution were measured by nuclear magnetic resonance imaging (NMRI). Fatty acid composition in VAT was analyzed by NMR spectroscopy and gas chromatography. Gene expression of key enzymes involved in DNL was analyzed in liver and VAT. Macrophage infiltration markers and proinflammatory cytokines were measured by gene expression in VAT. HFD or GC treatment induced similar fat mass expansion with comparable distribution between SAT and VAT depots. However, in VAT, GCs induce DNL, higher palmitic acid (PA), macrophage infiltration, and proinflammatory cytokine levels, accompanied by systemic nonesterified fatty acid (NEFA) elevation, hyperinsulinemia, and higher homeostatic model assessment for insulin resistance (HOMA-IR) levels compared with diet-induced obesity. Thus, chronic hypercortisolism induces DNL and fatty acid composition changes toward increased SFA and reduced polyunsaturated fatty acid (PUFA) levels in VAT, promoting macrophage recruitment and proinflammatory cytokines, suggesting a worse cardiometabolic profile even compared with HFD mice.

Adipocyte triglyceride lipase expression in human obesity

2007 ◽  
Vol 293 (4) ◽  
pp. E958-E964 ◽  
Author(s):  
Gregory R. Steinberg ◽  
Bruce E. Kemp ◽  
Matthew J. Watt
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Mrna Expression ◽  
Visceral Adipose Tissue ◽  
Lipase Activity ◽  
Subcutaneous Adipose Tissue ◽  
Lipolytic Enzymes ◽  
Obese Subjects ◽  
Visceral Adipose ◽  
Subcutaneous Adipose

We have investigated the gene and protein expression of adipose triglyceride lipase (ATGL) and triglyceride (TG) lipase activity from subcutaneous and visceral adipose tissue of lean and obese subjects. Visceral and subcutaneous adipose tissue was obtained from 16 age-matched lean and obese subjects during abdominal surgery. Tissues were analyzed for mRNA expression of lipolytic enzymes by real-time quantitative PCR. ATGL protein content was assessed by Western blot and TG lipase activity by radiometric assessment. Subcutaneous and visceral adipose tissue of obese subjects had elevated mRNA expression of PNPLA2 (ATGL) and other lipases including PNPLA3, PNPLA4, CES1, and LYPLAL1 ( P < 0.05). Surprisingly, ATGL protein expression and TG lipase activity were reduced in subcutaneous adipose tissue of obese subjects. Immunoprecipitation of ATGL reduced total TG lipase activity in adipose lysates by 70% in obese and 83% in lean subjects. No significant differences in the ATGL activator CGI-58 mRNA levels ( ABHD5) were associated with obesity. These data demonstrate that ATGL is important for efficient TG lipase activity in humans. They also demonstrate reduced ATGL protein expression and TG lipase activity despite increased mRNA expression of ATGL and other novel lipolytic enzymes in obesity. The lack of correlation between ATGL protein content and in vitro TG lipase activity indicates that small decrements in ATGL protein expression are not responsible for the reduction in TG lipase activity observed here in obesity, and that posttranslational modifications may be important.

RIP140 Gene and Protein Expression Levels are Downregulated in Visceral Adipose Tissue in Human Morbid Obesity

2009 ◽  
Vol 19 (6) ◽  
pp. 771-776 ◽  
Author(s):  
Victoria Catalán ◽  
Javier Gómez-Ambrosi ◽  
Amaia Lizanzu ◽  
Amaia Rodríguez ◽  
Camilo Silva ◽  
...  
Keyword(s):  
Morbid Obesity ◽  
Adipose Tissue ◽  
Protein Expression ◽  
Visceral Adipose Tissue ◽  
Expression Levels ◽  
Gene And Protein Expression ◽  
Visceral Adipose

scholarly journals PO-280 Effects of different exercise on autophagy and inflammation in visceral adipose tissue of obese

2018 ◽  
Vol 1 (5) ◽  
Author(s):  
Yongjun Zhao ◽  
Jing Wang ◽  
Yuxiu He
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Visceral Adipose Tissue ◽  
Exercise Intervention ◽  
Intervention Group ◽  
Diet Group ◽  
Normal Diet ◽  
Fat Reduction ◽  
Visceral Adipose ◽  
The Relationship

Objective To compare the effectiveness of endurance exercise and resistance exercise in fat reduction, then to examine the impact of exercise on autophagy activity and inflammation response in visceral adipose tissue in obesity, finally to explore the relationship between autophagy and inflammation in adipose tissue after exercise. Methods 42 obese mice were randomly divided into four groups as follows: high fat diet group (HC, n=9), normal diet group (NC, n=9), normal diet combined with endurance exercise intervention group (NE, n=12), and normal diet combined with resistance exercise intervention group (NR, n=12). NE and NR group conducted treadmill and ladder climbing exercise respectively for 8 weeks. Then to detect the gene and protein expression of autophagy, inflammation, ER stress and antioxidant markers using RT-PCR and WB, in addition, TEM and IHC were used to observe the autophagosome in visceral adipose tissue. Results BW, Lee’s index and BFI were significantly decreased in all three intervention groups, and there is a great decreasing in the two exercise group, but no difference between them. Atg5, Becn1 expression and LC3II/I were decreased significantly in NE and NR group compared with HC, meanwhile p62 expression were significantly increased. When compared with NC group, p62 expression were significantly increased in NE and not happened in NR group. Becn1 mRNA expression increased and p62 protein expression decreased significantly in NR group when compared with NE group. IL-1β was decreased significantly in NC, NE and NR group compared with HC. In addition, IL-6 and IL-10 protein expression increased significantly both in NE and NR group. When compared with NC group, IL-6 and IL-10 protein expression increased and IL-1β was decreased significantly both in NE and NR group except IL-6 protein expression in NR group. IL-6 increased and IL-10 decreased significantly in NR group when compared with NE group. Finally we found that IL-10 showed a negative correlation with almost every autophagy markers used in this study. Conclusions The effectiveness of 8wks different exercise intervention had no difference in fat reduction. The autophagic activity of visceral adipose tissue was inhibited after exercise, especially after aerobic exercise. Autophagy and inflammation enjoy the same trend before and after exercise intervention in visceral adipose tissue in obesity, and the IL-10 is the most sensitive factor in reflecting the relationship between autophagy and inflammation.

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