scholarly journals Moderate exercise training provides modest protection against adipose tissue inflammatory gene expression in response to high-fat feeding

2014 ◽  
Vol 2 (7) ◽  
pp. e12071 ◽  
Author(s):  
Melissa A. Linden ◽  
Yair Pincu ◽  
Stephen A. Martin ◽  
Jeffrey A. Woods ◽  
Tracy Baynard
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Exercise Training ◽  
Moderate Exercise ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Fat Feeding ◽  
Moderate Exercise Training

scholarly journals Exercise Training Effects on Inflammatory Gene Expression in White Adipose Tissue of Young Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Tracy Baynard ◽  
Victoria J. Vieira-Potter ◽  
Rudy J. Valentine ◽  
Jeffrey A. Woods
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Exercise Training ◽  
White Adipose Tissue ◽  
Training Effects ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Young Mice

Pro-inflammatory gene expression in adipose tissue in patients with atherosclerosis

2016 ◽  
Vol 252 ◽  
pp. e174 ◽  
Author(s):  
S. Čejková ◽  
I. Králová Lesná ◽  
J. Froněk ◽  
A. Králová ◽  
R. Poledne
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

scholarly journals Maternal high-fat diet induces sex-specific changes to glucocorticoid and inflammatory signaling in response to corticosterone and lipopolysaccharide challenge in adult rat offspring

2019 ◽  
Author(s):  
Sanoji Wijenayake ◽  
Mouly F. Rahman ◽  
Christine M.W. Lum ◽  
Wilfred C. De Vega ◽  
Aya Sasaki ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Fat Diet ◽  
Maternal Obesity ◽  
Inflammatory Responses ◽  
Physiological Stress ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Genes ◽  
Inflammatory Gene ◽  
Rat Offspring

ABSTRACTBackgroundAcute elevations in endogenous corticosterone (CORT) with psychosocial stress or exogenous administration potentiate inflammatory gene expression. Maternal obesity as a result of high-fat diet (HFD) consumption has been linked to higher basal levels of neuroinflammation, including increased expression of pro-inflammatory genes in the amygdala. These findings suggest that exposure to maternal HFD may elicit pro-inflammatory responses in the presence of an immune stressor such as lipopolysaccharide (LPS), a component of gram-negative bacteria, as well as acute elevated CORT.MethodsRat offspring were exposed to maternal HFD or control diet (CHD) throughout pre and postnatal development until weaning, when all offspring were provided CHD until adulthood. In adulthood, offspring were ‘challenged’ with administration of exogenous CORT, to simulate an acute physiological stress, LPS, to induce an immune stress, or both. qPCR was used to measure transcript abundance of CORT receptors and downstream inflammatory genes in the amygdala, hippocampus and prefrontal cortex, brain regions that mediate neuroendocrine and behavioral responses to stress.ResultsHFD female offspring exhibited elevations in anti-inflammatory transcripts, whereas HFD male offspring responded with greater pro-inflammatory gene expression to simultaneous CORT and LPS administration.ConclusionsThese findings suggest that exposure to maternal HFD leads to sex-specific alterations that may alter inflammatory responses in the brain, possibly as an adaptive response to basal inflammation.

scholarly journals Dietary Sodium Nitrite Causes Similar Modifications to Splenic Inflammatory Gene Expression as a High-Fat Diet

2021 ◽  
Vol 67 (6) ◽  
pp. 404-416
Author(s):  
Motoko OARADA ◽  
Yuushi OKUMURA ◽  
Katsuya HIRASAKA ◽  
Kosuke SUGIURA ◽  
Nobuhiko TACHIBANA ◽  
...  
Keyword(s):  
Gene Expression ◽  
Sodium Nitrite ◽  
High Fat Diet ◽  
Dietary Sodium ◽  
High Fat ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Inflammation, but not recruitment, of adipose tissue macrophages requires signalling through Mac-1 (CD11b/CD18) in diet-induced obesity (DIO)

2017 ◽  
Vol 117 (02) ◽  
pp. 325-338 ◽  
Author(s):  
Dennis Wolf ◽  
Nora Bukosza ◽  
David Engel ◽  
Marjorie Poggi ◽  
Felix Jehle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Adipose Tissue Inflammation ◽  
Inflammatory Gene Expression ◽  
Tissue Inflammation ◽  
Inflammatory Gene ◽  
Diet Induced Obesity ◽  
Adipose Tissue Macrophages ◽  
Cell Accumulation

SummaryCell accumulation is a prerequisite for adipose tissue inflammation. The leukocyte integrin Mac-1 (CD11b/CD18, αMβ2) is a classic adhesion receptor critically regulating inflammatory cell recruitment. Here, we tested the hypothesis that a genetic deficiency and a therapeutic modulation of Mac-1 regulate adipose tissue inflammation in a mouse model of diet-induced obesity (DIO). C57Bl6/J mice genetically deficient (Mac-1-/-) or competent for Mac-1 (WT) consumed a high fat diet for 20 weeks. Surprisingly, Mac-1-/- mice presented with increased diet-induced weight gain, decreased insulin sensitivity in skeletal muscle and in the liver in insulin-clamps, insulin secretion deficiency and elevated glucose levels in fasting animals, and dyslipidaemia. Unexpectedly, accumulation of adipose tissue macrophages (ATMs) was unaffected, while gene expression indicated less inflamed adipose tissue and macrophages in Mac-1-/- mice. In contrast, inflammatory gene expression at distant locations, such as in skeletal muscle, was not changed. Treatment of ATMs with an agonistic anti-Mac-1 antibody, M1/70, induced pro-inflammatory genes in cell culture. In vivo, treatment with M1/70 induced a hyper-inflammatory phenotype with increased expression of IL-6 and MCP-1, whereas accumulation of ATMs did not change. Finally, inhibition of Mac-1’s adhesive interaction to CD40L by the peptide inhibitor cM7 did not affect myeloid cell accumulation in adipose tissue. We present the surprising finding that adhesive properties of the leukocyte integrin Mac-1 are not required for macrophage accumulation in adipose tissue. Instead, Mac-1 modulates inflammatory gene expression in macrophages. These findings question the net effect of integrin blockade in cardio-metabolic disease.D. W., N. B., and D. E. equally contributed to this work.K. P., E. L., and A. Z. share senior authorship.Note: The review process for this manuscript was fully handled by Gregory Y. H. Lip, Editor in Chief.Supplementary Material to this article is available online at www.thrombosis-online.com.

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