scholarly journals High-Fat Diet in the Absence of Obesity Does Not Aggravate Surgically Induced Lymphoedema in Mice

2017 ◽  
Vol 58 (3-4) ◽  
pp. 180-192 ◽  
Author(s):  
Epameinondas Gousopoulos ◽  
Sinem Karaman ◽  
Steven T. Proulx ◽  
Kristin Leu ◽  
Dorina Buschle ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Vascular Function ◽  
Lymphatic Vessel ◽  
Immune Cell ◽  
Control Group ◽  
High Fat ◽  
Lymphatic Vasculature ◽  
Morphological Differences ◽  
Surgically Induced

Background: Lymphoedema represents the cardinal manifestation of lymphatic dysfunction and is associated with expansion of the adipose tissue in the affected limb. In mice, high-fat diet (HFD)-induced obesity was associated with impaired collecting lymphatic vessel function, and adiposity aggravated surgery-induced lymphoedema in a mouse model. The aim of the current study was to investigate whether adiposity is necessary to impair lymphatic function or whether increased lipid exposure alone might be sufficient in a surgical lymphoedema model. Methods: To investigate the role of increased lipid exposure in lymphoedema development we used a well-established mouse tail lymphoedema model. Female mice were subjected to a short-term (6 weeks) HFD, without development of obesity, before surgical induction of lymphedema. Lymphoedema was followed over a period of 6 weeks measuring oedema, evaluating tissue histology and lymphatic vascular function. Results: HFD increased baseline angiogenesis and average lymphatic vessel size in comparison to the chow control group. Upon induction of lymphedema, HFD-treated mice did not exhibit aggravated oedema and no morphological differences were observed in the blood and lymphatic vasculature. Importantly, the levels of fibro-adipose tissue deposition were comparable between the 2 groups and lymphatic vessel function was not impaired as a result of the HFD. Although the net immune cell infiltration was comparable, the HFD group displayed an increased infiltration of macrophages, which exhibited an M2 polarization phenotype. Conclusions: These results indicate that increased adiposity rather than dietary influences determines predisposition to or severity of lymphedema.

scholarly journals Anti-Obesity and Hypocholesterolemic Actions of Protamine-Derived Peptide RPR (Arg-Pro-Arg) and Protamine in High-Fat Diet-Induced C57BL/6J Mice

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2501
Author(s):  
Maihemuti Mijiti ◽  
Ryosuke Mori ◽  
Bingyu Huang ◽  
Kenichiro Tsukamoto ◽  
Keisuke Kiriyama ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Fecal Excretion ◽  
Control Group ◽  
High Fat ◽  
Tissue Weight ◽  
Cholesterol Levels ◽  
Adipose Tissue Weight ◽  
Fas Mrna ◽  
Hypocholesterolemic Peptide

Dietary protamine can ameliorate hyperlipidemia; however, the protamine-derived active peptide and its hypolipidemic mechanism of action are unclear. Here, we report the discovery of a novel anti-obesity and hypocholesterolemic peptide, RPR (Arg-Pro-Arg), derived from protamine in mice fed a high-fat diet for 50 days. Serum cholesterol levels were significantly lower in the protamine and RPR groups than in the control group. White adipose tissue weight was significantly decreased in the protamine and RPR groups. The fecal excretion of cholesterol and bile acid was significantly higher in the protamine and RPR groups than in the control group. We also observed a significant decrease in the expression of hepatic SCD1, SREBP1, and adipocyte FAS mRNA, and significantly increased expression of hepatic PPARα and adipocyte PPARγ1 mRNA in the protamine group. These findings demonstrate that the anti-obesity effects of protamine are linked to the upregulation of adipocyte PPARγ1 and hepatic PPARα and the downregulation of hepatic SCD1 via SREBP1 and adipocyte FAS. RPR derived from protamine has a crucial role in the anti-obesity action of protamine by evaluating the effective dose of adipose tissue weight loss.

scholarly journals Systemic Overexpression of GDF5 in Adipocytes but Not Hepatocytes Alleviates High-Fat Diet-Induced Nonalcoholic Fatty Liver in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Yan Yang ◽  
Wenting Zhang ◽  
Xiaohui Wu ◽  
Jing Wu ◽  
Chengjun Sun ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Fatty Liver ◽  
High Fat Diet ◽  
Lentiviral Vector ◽  
Cell Model ◽  
Control Group ◽  
High Fat ◽  
Fatty Acid Binding ◽  
Nonalcoholic Fatty Liver

Objective. Our recent study demonstrated that growth differentiation factor 5 (GDF5) could promote white adipose tissue thermogenesis and alleviate high-fat diet- (HFD-) induced obesity in fatty acid-binding protein 4- (Fabp4-) GDF5 transgenic mice (TG). Here, we further investigated the effects of systemic overexpression of the GDF5 gene in adipocytes HFD-induced nonalcoholic fatty liver disease (NAFLD). Methods. Fabp4-GDF5 TG mice were administered an HFD feeding. NAFLD-related indicators associated with lipid metabolism and inflammation were measured. A GDF5 lentiviral vector was constructed, and the LO2 NAFLD cell model was induced by FFA solution (oleic acid and palmitic acid). The alterations in liver function, liver lipid metabolism, and related inflammatory indicators were analyzed. Results. The liver weight was significantly reduced in the TG group, which was in accordance with the significantly downregulated expression of TNFα, MCP1, Aim2, and SREBP-1c and significantly upregulated expression of CPT-1α and ACOX2 in TG mouse livers. Compared to that of cells in the FAA-free control group, LO2 cells with in situ overexpression of GDF5 developed lipid droplets after FFA treatment; the levels of triglycerides, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly increased in both the GDF5 lentivirus and control lentivirus groups compared with those of the FAA-free group. Additionally, the levels of FAS, SREBP-1, CPT-1α, and inflammation-associated genes, such as ASC and NLRC4, were unaltered despite GDF5 treatment. Conclusion. Systemic overexpression of GDF5 in adipose tissue in vivo significantly reduced HFD-induced NAFLD liver damage in mice. The overexpression of GDF5 in hepatocytes failed to improve lipid accumulation and inflammation-related reactions induced by mixed fatty acids, suggesting that the protective effect of GDF5 in NAFLD was mainly due to the reduction in adipose tissue and improvements in metabolism. Hence, our study suggests that the management of NAFLD should be targeted to reduce the overall amount of body fat and improve metabolic status before the progression to nonalcoholic steatohepatitis occurs.

scholarly journals PO-043 The Effects of One-Time High Intensity Intermittent Training on Expression of LC3 Gene in Rats’ White Adipose Tissue

2018 ◽  
Vol 1 (3) ◽  
Author(s):  
Qishu Zhou ◽  
Chunyu Liang ◽  
Yafei Li ◽  
Yi Yan
Keyword(s):  
Adipose Tissue ◽  
White Adipose Tissue ◽  
High Intensity ◽  
High Fat Diet ◽  
Intermittent Exercise ◽  
Diet Group ◽  
Control Group ◽  
High Fat ◽  
Subcutaneous White Adipose Tissue ◽  
White Fat

Objective  To investigate the effect of one-time high-intensity intermittent exercise in white fat autophagy in obese rats and provide a theoretical basis of the molecular mechanism of exercise fat loss. Methods  Eighteen male 3-weeks-old rats were selected and divided into control group fed with normal diet (C), high-fat diet group fed with high fat diet (H). After 16 weeks, there were twelve obesity rats that divided into diet group (HS) and exercise group (HE). The other six control group rats of 19 weeks age were used as the standard (CS group). OE group did the high intensity intermittent exercise once. The CS group and the CS group were kept quietly. Three groups were taken subcutaneous white adipose tissue(S) and epididymal white adipose tissue (E) immediately after exercise. Mensurate the expression of LC3 gene in the tissue using the fluorescent quantitative PCR. Results 1. The expression of LC3 mRNA from white fat tissue was different to the tissues, which the expression of epididymal white adipose tissue of each group was higher than that in subcutaneous white adipose tissue (P <0.01). 2. Compared with CS group, the expression of epididymal white fat adipose tissue LC3 mRNA decreased (P<0.01) and the expression of the subcutaneous white adipose tissue increased from HS group (P <0.05). 3. Compared with OS group, the expression of epididymal white fat adipose tissue LC3 mRNA decreased (P<0.05) and the expression of subcutaneous white adipose tissue decreased from OS group. Conclusions The expression of LC3mRNA in epididymal white fat adipose tissue of rats was significantly higher than that of subcutaneous white fat. The changes of LC3mRNA expression of adipose tissue caused by high-fat diet have tissue differences. One-time high-intensity intermittent exercise can reduce the expression of LC3mRNA in fat tissue of obese rats. Its regulatory mechanism needs to be further studied.

scholarly journals Maternal separation enhances anticontractile perivascular adipose tissue function in male rats on a high-fat diet

2018 ◽  
Vol 315 (6) ◽  
pp. R1085-R1095 ◽  
Author(s):  
Analia S. Loria ◽  
Frank T. Spradley ◽  
Ijeoma E. Obi ◽  
Bryan K. Becker ◽  
Carmen De Miguel ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Life Stress ◽  
Vascular Function ◽  
Maternal Separation ◽  
Male Rats ◽  
Protective Effects ◽  
Ang Ii ◽  
High Fat ◽  
Perivascular Adipose Tissue

Clinical studies have shown that obesity negatively impacts large arteries’ function. We reported that rats exposed to maternal separation (MatSep), a model of early life stress, display enhanced angiotensin II (ANG II)-induced vasoconstriction in aortic rings cleaned of perivascular adipose tissue (PVAT) under normal diet (ND) conditions. We hypothesized that exposure to MatSep promotes a greater loss of PVAT-mediated protective effects on vascular function and loss of blood pressure (BP) rhythm in rats fed a high-fat diet (HFD) when compared with controls. MatSep was performed in male Wistar-Kyoto rats from days 2 to 14 of life. Normally reared littermates served as controls. On ND, aortic rings from MatSep rats with PVAT removed showed increased ANG II-mediated vasoconstriction versus controls; however, rings from MatSep rats with intact PVAT displayed blunted constriction. This effect was exacerbated by an HFD in both groups; however, the anticontractile effect of PVAT was greater in MatSep rats. Acetylcholine-induced relaxation was similar in MatSep and control rats fed an ND, regardless of the presence of PVAT. HFD impaired aortic relaxation in rings without PVAT from MatSep rats, whereas the presence of PVAT improved relaxation in both groups. On an HFD, immunolocalization of vascular smooth muscle-derived ANG-(1–7) and PVAT-derived adiponectin abundances were increased in MatSep. In rats fed an HFD, 24-h BP and BP rhythms were similar between groups. In summary, MatSep enhanced the ability of PVAT to blunt the heightened ANG II-induced vasoconstriction and endothelial dysfunction in rats fed an HFD. This protective effect may be mediated via the upregulation of vasoprotective factors within the adipovascular axis.

scholarly journals Interscapular and Perivascular Brown Adipose Tissue Respond Differently to a Short-Term High-Fat Diet

2019 ◽  
Author(s):  
Peter Aldiss ◽  
Jo Lewis ◽  
David Boocock ◽  
Amanda Miles ◽  
Ian Bloor ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Vascular Function ◽  
Rna Degradation ◽  
Whole Body ◽  
Anatomical Location ◽  
High Fat ◽  
Short Term ◽  
Brown Adipose

Brown adipose tissue (BAT) function may depend on its anatomical location and developmental origin. Interscapular BAT (iBAT) regulates acute macronutrient metabolism, whilst perivascular BAT (PVAT) regulates vascular function. Although phenotypically similar, whether these depots respond differently to acute nutrient excess is unclear. Given their distinct anatomical locations and developmental origins and we hypothesised that iBAT and PVAT would respond differently to brief period of nutrient excess. Sprague-Dawley rats aged 12 weeks (n = 12) were fed either a standard (10% fat, n = 6) or high fat diet (HFD: 45% fat, n = 6) for 72 h and housed at thermoneutrality. Following an assessment of whole body physiology, fat was collected from both depots for analysis of gene expression and the proteome. HFD consumption for 72 h induced rapid weight gain (c. 2.6%) and reduced serum NEFA with no change in either total adipose or depot mass. In iBAT, an upregulation of genes involved in insulin signalling and lipid metabolism was accompanied by enrichment of lipid-related processes and functions, plus glucagon and PPAR signalling pathways. In PVAT, HFD induced a pronounced down-regulation of multiple metabolic pathways which was accompanied with increased abundance of proteins involved in apoptosis (e.g. Hdgf and Ywaq) and toll-like receptor signalling (Ube2n). There was also an enrichment of DNA-related processes and functions (e.g., nucleosome assembly and histone exchange) and RNA degradation and cell adhesion pathways. In conclusion, we show that iBAT and PVAT elicit divergent responses to short-term nutrient excess highlighting early adaptations in these depots before changes in fat mass.

scholarly journals Interscapular and Perivascular Brown Adipose Tissue Respond Differently to a Short-Term High-Fat Diet

Nutrients ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 1065 ◽  
Author(s):  
Peter Aldiss ◽  
Jo E. Lewis ◽  
David J. Boocock ◽  
Amanda K. Miles ◽  
Ian Bloor ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Vascular Function ◽  
Rna Degradation ◽  
Whole Body ◽  
Anatomical Location ◽  
High Fat ◽  
Short Term ◽  
Brown Adipose

Brown adipose tissue (BAT) function may depend on its anatomical location and developmental origin. Interscapular BAT (iBAT) regulates acute macronutrient metabolism, whilst perivascular BAT (PVAT) regulates vascular function. Although phenotypically similar, whether these depots respond differently to acute nutrient excess is unclear. Given their distinct anatomical locations and developmental origins and we hypothesised that iBAT and PVAT would respond differently to brief period of nutrient excess. Sprague-Dawley rats aged 12 weeks (n=12) were fed either a standard (10% fat, n=6) or high fat diet (HFD: 45% fat, n=6) for 72h and housed at thermoneutrality. Following an assessment of whole body physiology, fat was collected from both depots for analysis of gene expression and the proteome. HFD consumption for 72h induced rapid weight gain (c. 2.6%) and reduced serum non-esterified fatty acids (NEFA) with no change in either total adipose or depot mass. In iBAT, an upregulation of genes involved in insulin signalling and lipid metabolism was accompanied by enrichment of lipid-related processes and functions, plus glucagon and peroxisome proliferator-activated receptor (PPAR) signalling pathways. In PVAT, HFD induced a pronounced down-regulation of multiple metabolic pathways which was accompanied with increased abundance of proteins involved in apoptosis (e.g., Hdgf and Ywaq) and toll-like receptor signalling (Ube2n). There was also an enrichment of DNA-related processes and functions (e.g., nucleosome assembly and histone exchange) and RNA degradation and cell adhesion pathways. In conclusion, we show that iBAT and PVAT elicit divergent responses to short-term nutrient excess highlighting early adaptations in these depots before changes in fat mass.

scholarly journals Impact of weight loss and partial weight regain on immune cell and inflammatory markers in adipose tissue in male mice

2020 ◽  
Vol 129 (4) ◽  
pp. 909-919
Author(s):  
Alexander T. Sougiannis ◽  
Brandon N. VanderVeen ◽  
Taryn L. Cranford ◽  
Reilly T. Enos ◽  
Kandy T. Velazquez ◽  
...  
Keyword(s):  
Weight Loss ◽  
Adipose Tissue ◽  
Immune Cells ◽  
High Fat Diet ◽  
Inflammatory Markers ◽  
Weight Regain ◽  
Immune Cell ◽  
High Fat ◽  
Inflammatory Status ◽  
Partial Weight

We examined the immune and inflammatory status of adipose tissue in mice after they underwent weight loss followed by partial weight regain. We show an increase in selected immune cells and inflammatory mediators, in high-fat diet-fed mice that had prior exposure to a high-fat diet. Although weight fluctuations appear to exacerbate immune cell abundance and inflammation in adipose tissue, severity is less than in mice that were exposed to sustained high-fat diet feedings.

scholarly journals Time-Restricted Feeding Restores Obesity-Induced Alteration in Adipose Tissue Immune Cell Phenotype

Nutrients ◽  
2021 ◽  
Vol 13 (11) ◽  
pp. 3780
Author(s):  
Youngyoon Lee ◽  
Yelim Kim ◽  
Minam Lee ◽  
Dayong Wu ◽  
Munkyong Pae
Keyword(s):  
Adipose Tissue ◽  
Weight Gain ◽  
High Fat Diet ◽  
Immune Cell ◽  
Cell Phenotype ◽  
Mrna Levels ◽  
Restricted Feeding ◽  
High Fat ◽  
Low Fat Diet ◽  
Adipose Tissue Macrophages

Studies suggest that time-restricted feeding (TRF) may prevent obesity and its commodities. At present, little is known about how TRF impacts immune cells, and whether such an effect is linked to altered metabolic parameters under condition of a high-fat diet (HFD)-induced obesity. To address these issues, we conducted a study in which we determined whether TRF has therapeutic efficacy against weight gain, adiposity, as well as associated immune cell disturbance found in obese mice. Six-week-old male C57BL/6 mice were fed a low-fat diet (LFD) or HFD ad libitum for six weeks, after which time a subgroup of HFD mice was switched to the 10 h TRF paradigm (HFD-TRF) for additional eight weeks. We found that TRF intervention reduced HFD-induced weight gain. Even with comparable fat mass and mean adipocyte area, the HFD-TRF group had lower mRNA levels of proinflammatory cytokine Tnfα and chemokine Ccl8, along with reduced numbers of adipose tissue macrophages (ATM), CD11c+ ATM, and CD8+ T cell compared to the HFD group, while maintaining CD8+ to CD4+ ratio at levels similar to those in the LFD group. Furthermore, TRF intervention was effective in improving glucose tolerance and reducing HOMA-IR. Taken together, our findings suggest that TRF restores the obesity-induced alteration in immune cell composition, and this effect may in part contribute to health benefits (including insulin sensitivity) of practicing TRF.

scholarly journals Endothelin-1 Receptor A Blockade Attenuates Metabolic and Proinflammatory Profile in Mice Fed a High Fat Diet

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A41-A42
Author(s):  
Osvaldo Rivera-Gonzalez ◽  
Erin Taylor ◽  
Joshua S Speed
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Visceral Adipose Tissue ◽  
High Fat Diet ◽  
Immune Cell ◽  
Ppar Gamma ◽  
High Fat ◽  
Endothelin 1 ◽  
Eta Receptor ◽  
Visceral Adipose

Abstract Endothelin-1 (ET-1) is elevated in patients with obesity; however, its contribution to the pathophysiology related to obesity is not fully understood. Obesity is associated with dyslipidemia and insulin resistance, which may in part be mediated by inflammation and alterations to immune cell subsets within the adipose tissue. ET-1 promotes inflammation via the ET-1 type A (ETA) receptor, and blockade of ETA receptors improves dyslipidemia in patients with chronic kidney disease. We hypothesized that ET-1 causes dyslipidemia and inflammation within the adipose tissue of obese mice. To test this hypothesis, C57BL/6J mice were fed either normal diet (NMD) or high fat diet (HFD) for 8 weeks followed by 2 weeks of treatment with either vehicle or atrasentan (ETA receptor antagonist, 10mg/kg/day). HFD mice had significantly higher fat mass than NMD mice, with no significant effect of treatment with atrasentan. HFD mice had significantly higher circulating non-esterified free fatty acids, an effect that was ameliorated in mice treated with atrasentran (1.03±0.07 vs 0.58±0.02 mEq/L, p&lt;0.05). Atrasentan-treated mice had significantly attenuated increase in liver triglycerides compared to non-treated HFD mice (3.8±0.7 vs 7.5±1.3mg/dL respectively, p&lt;0.05). Mice treated with atrasentan had significantly improved glucose tolerance (10150±1031 vs 6563±975 AUC, p&lt;0.05) and insulin tolerance (-2796±386 vs -9825±319 AUC, p&lt;0.05) compared to non-treated insulin-resistant HFD mice. Plasma adiponectin, an insulin sensitizing adipokine that is inversely associated with adiposity and insulin resistance, was significantly increased in atrasentan-treated mice compared to non-treated HFD (4.8±0.1326 vs 6.5±0.3 µg/ml, p&lt;0.05), with no differences in plasma insulin levels. Gene expression analysis of visceral fat showed improved expression of genes negatively associated with insulin resistance that were downregulated in non-treated HFD mice vs. NMD (IRS-1, PPAR-gamma, GLUT4, and adiponectin). Flow cytometric analyses of visceral adipose tissue indicated that HFD mice had a significantly higher number of both CD4+ and CD8+ T cells compared to NMD mice, which was attenuated by treatment with atrasentan. Further, eosinophils, which are important in maintaining adipose tissue health and reducing inflammation, were significantly decreased in HFD mice compared to NMD. Atrasentan treatment abolished the decrease in eosinophils. Taken together, these data indicate that ETA receptor blockade improves peripheral glucose homeostasis, dyslipidemia, and liver triglyceride levels, and also attenuates the proinflammatory immune profile in visceral adipose tissue. These data suggest a potential use for ETA receptor blockers in the treatment of obesity-associated dyslipidemia and insulin resistance.

scholarly journals Supplementation of Non-Dairy Creamer-Enriched High-Fat Diet with D-Allulose Ameliorated Blood Glucose and Body Fat Accumulation in C57BL/6J Mice

2019 ◽  
Vol 9 (13) ◽  
pp. 2750 ◽  
Author(s):  
Ga Young Do ◽  
Eun-Young Kwon ◽  
Yun Jin Kim ◽  
Youngji Han ◽  
Seong-Bo Kim ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Blood Glucose ◽  
Body Fat ◽  
High Fat Diet ◽  
Fasting Blood Glucose ◽  
Control Group ◽  
High Fat ◽  
Food Component ◽  
Fat Accumulation

D-allulose, which has 70% of the sweet taste of sucrose but nearly no calories, has been reported to inhibit the absorption of lipids and suppress body weight gain in obese mice. Fats in non-dairy creamer consist of highly saturated fatty acids, which can cause various lipid disorders when consumed over a long period. We investigated whether D-allulose supplementation alleviates the effects of a non-dairy creamer-enriched high-fat diet on lipid metabolism. High-fat diets enriched with non-dairy creamer were administered to C57BL/6J mice with or without D-allulose supplementation for eight weeks by the pair-feeding design. Lipid metabolic markers were compared between the non-dairy creamer control group (NDC) and non-dairy creamer allulose group (NDCA). Body, adipose tissue, and liver weights, and fasting blood glucose levels, were significantly lower in the NDCA group than in the NDC group. Fecal fatty acid and triglyceride levels were significantly higher in the NDCA group than in the NDC group. Supplementing a non-dairy creamer-enriched high-fat diet with D-allulose improved overall lipid metabolism, including the plasma and hepatic lipid profiles, hepatic and adipose tissue morphology, and plasma inflammatory adipokine levels in mice. These results suggest that D-allulose can be used as a functional food component for preventing body fat accumulation from a high-fat diet that includes hydrogenated plant fats.

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