Role of brown adipose tissue in modulating adipose tissue inflammation and insulin resistance in high-fat diet fed mice

2019 ◽  
Vol 854 ◽  
pp. 354-364 ◽  
Author(s):  
Kripa Shankar ◽  
Durgesh Kumar ◽  
Sanchita Gupta ◽  
Salil Varshney ◽  
Sujith Rajan ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Brown Adipose

scholarly journals Luteolin Improves Insulin Resistance in Postmenopausal Obese Mice by Altering Macrophage Polarization (FS12-01-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Yunjung Baek ◽  
Mi Nam Lee ◽  
Dayong Wu ◽  
Munkyong Pae
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Ovarian Function ◽  
Body Weight Gain ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Ovariectomized Mice

Abstract Objectives Previously, we showed that loss of ovarian function in mice fed high-fat diet exacerbated insulin resistance and adipose tissue inflammation. In the current study, we tested whether consumption of luteolin, an anti-inflammatory flavonoid, could mitigate adipose tissue inflammation and insulin resistance in obese ovariectomized mice. Methods Nine-week-old ovariectomized C57BL/6 mice were fed a low-fat diet (LFD), high-fat diet (HFD), or HFD supplemented with 0.005% luteolin (HFD + L) for 16 weeks. The anti-inflammatory drug salicylate was used as a positive control. Fasting blood glucose, insulin, and insulin resistance index HOMA-IR were measured every 4 weeks. Adipose tissue and spleen were characterized for tissue inflammation by real-time PCR and immune cell populations by flow cytometry after 16 weeks of feeding. Results HFD resulted in more body weight gain than LFD in ovariectomized mice and supplementing HFD with 0.005% luteolin did not affect the body weight gain. In addition, HFD elicited a significant elevation in fat mass, which were comparable between HFD and HFD + L groups. However, luteolin supplementation resulted in a significant decrease in CD11c+ macrophages in gonadal adipose tissue, as well as a trend of decrease in macrophage infiltration. Luteolin supplementation also significantly decreased mRNA expression of inflammatory and M1 markers MCP-1, CD11c, TNF-a, and IL-6, while maintaining expression of M2 marker MGL1. We further found that luteolin treatment protected mice from insulin resistance induced by HFD consumption; this improved insulin resistance was correlated with reductions in CD11c+ adipose tissue macrophages. Conclusions Our findings indicate that dietary luteolin supplementation attenuates adipose tissue inflammation and insulin resistance found in mice with loss of ovarian function coupled with a HFD intake, and this effect may be partly mediated through suppressing M1-like polarization of macrophages in adipose tissue. These results have clinical implication in implementing dietary intervention for prevention of metabolic syndrome associated with postmenopause and obesity. Funding Sources Supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIP) (NRF-2018R1A1A1A05078886).

Abstract 537: Dock2 Deficiency Mitigates High-Fat Diet-Induced Obesity by Reducing Adipose Tissue Inflammation While Increasing Energy Expenditure

2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Xia Guo ◽  
Feifei Li ◽  
Zaiyan Xu ◽  
Shi-You Chen
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Energy Expenditure ◽  
High Fat Diet ◽  
Inflammatory Diseases ◽  
Body Weight Gain ◽  
Public Health Problem ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation

Obesity is a public health problem as its association with type 2 diabetes, cardiovascular disorders and many other diseases. Adipose tissue inflammation is frequently observed and plays a vital role in obesity and insulin resistance. Dedicator of cytokinesis 2 (DOCK2) has shown proinflammatory effect in several inflammatory diseases, but its role in obesity remain unknown. To explore the function of DOCK2 in obesity and insulin resistance, wild-type (WT) and DOCK2 knockout (DOCK2-/-) mice were fed with chow or high-fat diet (HFD) for 12 weeks. Metabolic, biochemical and histologic analyses were performed. DOCK2 expression was robustly up-regulated in adipose tissue in WT mice given HFD. DOCK2-/- mice were protected against HFD-enhanced body weight gain with an improved metabolic homeostasis and insulin resistance. In addition, DOCK2 deficiency attenuated adipose tissue and systemic inflammation accompanied by a reduced macrophage infiltration. Moreover, DOCK2 deficiency induced the adipose tissue browning and increased energy expenditure as shown by the up-regulation of metabolic genes in DOCK2-/- mice. Our data indicated that DOCK2 deficiency can protect mice from HFD-induced obesity, metabolic disorders, and insulin resistance. Therefore, targeting DOCK2 may be a potential therapeutic strategy for treating obesity-associated diseases.

scholarly journals Nrf2 deficiency in myeloid cells is not sufficient to protect mice from high-fat diet-induced adipose tissue inflammation and insulin resistance

2012 ◽  
Vol 52 (9) ◽  
pp. 1708-1715 ◽  
Author(s):  
Akshaya K. Meher ◽  
Poonam R. Sharma ◽  
Vitor A. Lira ◽  
Masayuki Yamamoto ◽  
Thomas W. Kensler ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Myeloid Cells ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation

A single day of high fat diet feeding induces lipid accumulation and insulin resistance in brown adipose tissue in mice

2020 ◽  
Vol 315 ◽  
pp. e87
Author(s):  
M. Modder ◽  
E.N. Kuipers ◽  
N.M. Held ◽  
W. In Het Panhuis ◽  
P.M.M. Ruppert ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Lipid Accumulation ◽  
High Fat Diet ◽  
High Fat ◽  
Brown Adipose

Haploinsufficiency of the retinoblastoma protein gene reduces diet-induced obesity, insulin resistance, and hepatosteatosis in mice

2009 ◽  
Vol 297 (1) ◽  
pp. E184-E193 ◽  
Author(s):  
Josep Mercader ◽  
Joan Ribot ◽  
Incoronata Murano ◽  
Søren Feddersen ◽  
Saverio Cinti ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
High Fat Diet ◽  
Retinoblastoma Protein ◽  
Brown Adipocyte ◽  
Wild Type ◽  
High Fat ◽  
Brown Adipose

Brown adipose tissue activity dissipates energy as heat, and there is evidence that lack of the retinoblastoma protein (pRb) may favor the development of the brown adipocyte phenotype in adipose cells. In this work we assessed the impact of germ line haploinsufficiency of the pRb gene (Rb) on the response to high-fat diet feeding in mice. Rb+/− mice had body weight and adiposity indistinguishable from that of wild-type (Rb+/+) littermates when maintained on a standard diet, yet they gained less body weight and body fat after long-term high-fat diet feeding coupled with reduced feed efficiency and increased rectal temperature. Rb haploinsufficiency ameliorated insulin resistance and hepatosteatosis after high-fat diet in male mice, in which these disturbances were more marked than in females. Compared with wild-type littermates, Rb+/− mice fed a high-fat diet displayed higher expression of peroxisome proliferator-activated receptor (PPAR)γ as well as of genes involved in mitochondrial function, cAMP sensitivity, brown adipocyte determination, and tissue vascularization in white adipose tissue depots. Furthermore, Rb+/− mice exhibited signs of enhanced activation of brown adipose tissue and higher expression levels of PPARα in liver and of PPARδ in skeletal muscle, suggestive of an increased capability for fatty acid oxidation in these tissues. These findings support a role for pRb in modulating whole body energy metabolism and the plasticity of the adipose tissues in vivo and constitute first evidence that partial deficiency in the Rb gene protects against the development of obesity and associated metabolic disturbances.

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