Selective Leptin Resistance in Brain but Not in Adipose-Tissue Macrophages Following High-Fat Feeding

2011 ◽  
pp. P2-429-P2-429
Author(s):  
Diana Athonvarangku ◽  
Kehao Zhang ◽  
Weijie Li ◽  
Preeti Kishore ◽  
Meredith Hawkins
Keyword(s):  
Adipose Tissue ◽  
Leptin Resistance ◽  
High Fat ◽  
Adipose Tissue Macrophages ◽  
Fat Feeding

scholarly journals High fat feeding impairs select features of M1 polarization in CD11c+ adipose tissue macrophages

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Grace Bennett ◽  
Merav E. Shaul ◽  
Katherine J. Strissel ◽  
Jason Defuria ◽  
Andrew S. Greenberg ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat ◽  
Adipose Tissue Macrophages ◽  
M1 Polarization ◽  
Fat Feeding

A Tale of Three Systems: Toward a Neuroimmunoendocrine Model of Obesity

2021 ◽  
Vol 37 (1) ◽  
pp. 549-573
Author(s):  
Conan J.O. O'Brien ◽  
Emma R. Haberman ◽  
Ana I. Domingos
Keyword(s):  
Adipose Tissue ◽  
Energy Homeostasis ◽  
Current Knowledge ◽  
Neural Circuitry ◽  
Leptin Resistance ◽  
Direct Role ◽  
Adipose Tissues ◽  
Adipose Tissue Macrophages ◽  
Prevalence Of Obesity ◽  
Established Role

The prevalence of obesity is on the rise. What was once considered a simple disease of energy imbalance is now recognized as a complex condition perpetuated by neuro- and immunopathologies. In this review, we summarize the current knowledge of the neuroimmunoendocrine mechanisms underlying obesity. We examine the pleiotropic effects of leptin action in addition to its established role in the modulation of appetite, and we discuss the neural circuitry mediating leptin action and how this is altered with obesity, both centrally (leptin resistance) and in adipose tissues (sympathetic neuropathy). Finally, we dissect the numerous causal and consequential roles of adipose tissue macrophages in obesity and highlight recent key studies demonstrating their direct role in organismal energy homeostasis.

scholarly journals Loss of Oncostatin M Signaling in Adipocytes Induces Insulin Resistance and Adipose Tissue Inflammation in Vivo

2016 ◽  
Vol 291 (33) ◽  
pp. 17066-17076 ◽  
Author(s):  
Carrie M. Elks ◽  
Peng Zhao ◽  
Ryan W. Grant ◽  
Hardy Hang ◽  
Jennifer L. Bailey ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cell Types ◽  
Oncostatin M ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Fat Feeding

Oncostatin M (OSM) is a multifunctional gp130 cytokine. Although OSM is produced in adipose tissue, it is not produced by adipocytes. OSM expression is significantly induced in adipose tissue from obese mice and humans. The OSM-specific receptor, OSM receptor β (OSMR), is expressed in adipocytes, but its function remains largely unknown. To better understand the effects of OSM in adipose tissue, we knocked down Osmr expression in adipocytes in vitro using siRNA. In vivo, we generated a mouse line lacking Osmr in adiponectin-expressing cells (OSMRFKO mice). The effects of OSM on gene expression were also assessed in vitro and in vivo. OSM exerts proinflammatory effects on cultured adipocytes that are partially rescued by Osmr knockdown. Osm expression is significantly increased in adipose tissue T cells of high fat-fed mice. In addition, adipocyte Osmr expression is increased following high fat feeding. OSMRFKO mice exhibit increased insulin resistance and adipose tissue inflammation and have increased lean mass, femoral length, and bone volume. Also, OSMRFKO mice exhibit increased expression of Osm, the T cell markers Cd4 and Cd8, and the macrophage markers F4/80 and Cd11c. Interestingly, the same proinflammatory genes induced by OSM in adipocytes are induced in the adipose tissue of the OSMRFKO mouse, suggesting that increased expression of proinflammatory genes in adipose tissue arises both from adipocytes and other cell types. These findings suggest that adipocyte OSMR signaling is involved in the regulation of adipose tissue homeostasis and that, in obesity, OSMR ablation may exacerbate insulin resistance by promoting adipose tissue inflammation.

scholarly journals FTO is necessary for the induction of leptin resistance by high-fat feeding

2015 ◽  
Vol 4 (4) ◽  
pp. 287-298 ◽  
Author(s):  
Y.C. Loraine Tung ◽  
Pawan Gulati ◽  
Che-Hsiung Liu ◽  
Debra Rimmington ◽  
Rowena Dennis ◽  
...  
Keyword(s):  
Leptin Resistance ◽  
High Fat ◽  
Fat Feeding

scholarly journals Reduced Vascular Nitric Oxide–cGMP Signaling Contributes to Adipose Tissue Inflammation During High-Fat Feeding

2011 ◽  
Vol 31 (12) ◽  
pp. 2827-2835 ◽  
Author(s):  
Priya Handa ◽  
Sanshiro Tateya ◽  
Norma O. Rizzo ◽  
Andrew M. Cheng ◽  
Vicki Morgan-Stevenson ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Cgmp Signaling ◽  
Fat Feeding

scholarly journals Chronic High-Fat Feeding Affects the Mesenchymal Cell Population Expanded From Adipose Tissue but Not Cardiac Atria

2015 ◽  
Vol 4 (12) ◽  
pp. 1403-1414 ◽  
Author(s):  
Filippo Perbellini ◽  
Renata S.M. Gomes ◽  
Silvia Vieira ◽  
Dougal Buchanan ◽  
Sophia Malandraki-Miller ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cell Population ◽  
Mesenchymal Cell ◽  
High Fat ◽  
Fat Feeding

scholarly journals Perinatal Overnutrition Exacerbates Adipose Tissue Inflammation Caused by High-Fat Feeding in C57BL/6J Mice

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0121954 ◽  
Author(s):  
Brandon D. Kayser ◽  
Michael I. Goran ◽  
Sebastien G. Bouret
Keyword(s):  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Fat Feeding

Adipose tissue metabolism of obese mice on standard and high-fat diets

1961 ◽  
Vol 201 (1) ◽  
pp. 23-26 ◽  
Author(s):  
Serene Lochaya ◽  
Nicole Leboeuf ◽  
Jean Mayer ◽  
Bernard Leboeuf
Keyword(s):  
Adipose Tissue ◽  
Obese Mice ◽  
High Fat ◽  
Carbon Incorporation ◽  
Adipose Tissue Metabolism ◽  
Glucose Carbon ◽  
Low Carbohydrate ◽  
High Fat Diets ◽  
Fat Diets ◽  
Fat Feeding

Adipose tissue metabolism in vitro was studied, after substitution for several weeks of synthetic low-carbohydrate, high-fat (saturated or unsaturated) diets for the standard chow diet, in obese hyperglycemic mice and in their nonobese littermates. In tissue from nonobese mice fed the high-fat diets, glucose metabolism to CO2 and to fatty acids was diminished in the absence of added hormone, while glucose carbon incorporation to glyceride-glycerol was increased. Under insulin (0.1 unit/ml) stimulation, total glucose uptake was relatively decreased by the diets, as was glucose metabolism to CO2, to fatty acids, and to glycogen; however, glucose carbon incorporation to glyceride-glycerol was unaltered. Under epinephrine stimulation, the sum of glucose carbon recovery was less after high-fat feeding. No effect of high-fat feeding was detected on base-line rates of free fatty acid release nor on the effects of insulin or epinephrine on this process. No differences were found between the effects of saturated- or unsaturated-fat diets on any parameters. The metabolism of adipose tissue from obese mice was slightly, if at all, affected by high-fat feeding. These results are discussed in reference to the normal adaptation to low-carbohydrate, high-fat diets and to the metabolic abnormalities present in obese hyperglycemic mice.

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