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.

Inhibition of Adipose Tissue Angiogenesis Prevents Rebound Weight Regain after Calorie Restriction Independent of Hypothalamic Melanocortin System in Obese Mice Fed a High-Fat Diet

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 287-LB
Author(s):  
HYE-JIN LEE ◽  
MUN-GYU SONG ◽  
NA-HEE HA ◽  
BO-YEONG JIN ◽  
SANG-HYUN CHOI ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Calorie Restriction ◽  
High Fat Diet ◽  
Weight Regain ◽  
Obese Mice ◽  
High Fat ◽  
Melanocortin System

The Effects Of Short-term Weight Loss And Partial Weight Regain On Systemic Inflammatory Markers

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S268
Author(s):  
R S. Rector ◽  
Erik J. Stites ◽  
Brianne L. Giles ◽  
Brian W. Toedebusch ◽  
Matt W. McClanahan ◽  
...  
Keyword(s):  
Weight Loss ◽  
Inflammatory Markers ◽  
Weight Regain ◽  
Short Term ◽  
Partial Weight

The Effects Of Short-term Weight Loss And Partial Weight Regain On Systemic Inflammatory Markers

2005 ◽  
Vol 37 (Supplement) ◽  
pp. S268
Author(s):  
R S. Rector ◽  
Erik J. Stites ◽  
Brianne L. Giles ◽  
Brian W. Toedebusch ◽  
Matt W. McClanahan ◽  
...  
Keyword(s):  
Weight Loss ◽  
Inflammatory Markers ◽  
Weight Regain ◽  
Short Term ◽  
Partial Weight

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 The Absence of Adiponectin Alters Niacin’s Effects on Adipose Tissue Inflammation in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2427
Author(s):  
Emily C. Graff ◽  
Han Fang ◽  
Desiree Wanders ◽  
Robert L. Judd
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Inflammatory Markers ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Low Fat Diet ◽  
Expression Of Genes ◽  
Ccl2 Expression ◽  
Anti Inflammatory

Obesity is an immunometabolic disease associated with chronic inflammation and the dysregulation of pro- and anti-inflammatory cytokines. One hallmark of obesity is reduced concentrations of the anti-inflammatory adipokine, adiponectin. Pharmacologic doses of niacin produce multiple metabolic benefits, including attenuating high-fat diet (HFD)-induced adipose tissue inflammation and increasing adiponectin concentrations. To determine if adiponectin mediates the anti-inflammatory effects of niacin, male C57BL/6J (WT) and adiponectin null (Adipoq-/-) mice were maintained on a low-fat diet (LFD) or HFD for 6 weeks, before being administered either vehicle or niacin (360 mg/kg/day) for 5 weeks. HFD-fed mice had increased expression of genes associated with macrophage recruitment (Ccl2) and number (Cd68), and increased crown-like structure (CLS) number in adipose tissue. While niacin attenuated Ccl2 expression, there were no effects on Cd68 or CLS number. The absence of adiponectin did not hinder the ability of niacin to reduce Ccl2 expression. HFD feeding increased gene expression of inflammatory markers in the adipose tissue of WT and Adipoq-/- mice. While niacin tended to decrease the expression of inflammatory markers in WT mice, niacin increased their expression in HFD-fed Adipoq-/- mice. Therefore, our results indicate that the absence of adiponectin alters the effects of niacin on markers of adipose tissue inflammation in HFD-fed mice, suggesting that the effects of niacin on tissue cytokines may involve adiponectin.

scholarly journals TNF-α Represses β-Klotho Expression and Impairs FGF21 Action in Adipose Cells: Involvement of JNK1 in the FGF21 Pathway

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4238-4245 ◽  
Author(s):  
Julieta Díaz-Delfín ◽  
Elayne Hondares ◽  
Roser Iglesias ◽  
Marta Giralt ◽  
Carme Caelles ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Mouse Embryonic Fibroblast ◽  
Fibroblast Growth Factor 21 ◽  
High Fat ◽  
Fgf Receptor ◽  
Inflammatory Status ◽  
Tnf Α

Fibroblast growth factor 21 (FGF21) is a member of the FGF family that reduces glycemia and ameliorates insulin resistance. Adipose tissue is a main target of FGF21 action. Obesity is associated with a chronic proinflammatory state. Here, we analyzed the role of proinflammatory signals in the FGF21 pathway in adipocytes, evaluating the effects of TNF-α on β-Klotho and FGF receptor-1 expression and FGF21 action in adipocytes. We also determined the effects of rosiglitazone on β-Klotho and FGF receptor-1 expression in models of proinflammatory signal induction in vitro and in vivo (high-fat diet-induced obesity). Because c-Jun NH2-terminal kinase 1 (JNK1) serves as a sensing juncture for inflammatory status, we also evaluated the involvement of JNK1 in the FGF21 pathway. TNF-α repressed β-Klotho expression and impaired FGF21 action in adipocytes. Rosiglitazone prevented the reduction in β-Klotho expression elicited by TNF-α. Moreover, β-Klotho levels were reduced in adipose tissue from high-fat diet-induced obese mice, whereas rosiglitazone restored β-Klotho to near-normal levels. β-Klotho expression was increased in white fat from JNK1−/− mice. The absence of JNK1 increased the responsiveness of mouse embryonic fibroblast-derived adipocytes and brown adipocytes to FGF21. In conclusion, we show that proinflammatory signaling impairs β-Klotho expression and FGF21 responsiveness in adipocytes. We also show that JNK1 activity is involved in modulating FGF21 effects in adipocytes. The impairment in the FGF21 response machinery in adipocytes and the reduction in FGF21 action in response to proinflammatory signals may play important roles in metabolic alterations in obesity and other diseases associated with enhanced inflammation.

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<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<0.05). Mice treated with atrasentan had significantly improved glucose tolerance (10150±1031 vs 6563±975 AUC, p<0.05) and insulin tolerance (-2796±386 vs -9825±319 AUC, p<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<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.

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