Regulation of TNFα converting enzyme activity in visceral adipose tissue of obese mice

Kawasaki, Shuji; Motoshima, Hiroyuki; Hanatani, Satoko; Takaki, Yuki; Igata, Motoyuki; Tsutsumi, Atsuyuki; Matsumura, Takeshi; Kondo, Tatsuya; Senokuchi, Takafumi; Ishii, Norio; Kinoshita, Hiroyuki; Fukuda, Kazuki; Kawashima, Junji; Shimoda, Seiya; Nishikawa, Takeshi; Araki, Eiichi

doi:10.1016/j.bbrc.2012.12.086

Cited by 3 publications

(3 citation statements)

References 36 publications

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“…(27,28) In brief, total RNA from cultured cells and tissues was extracted using Sepasol-RNA I Super G (Nacalai Tesque), and complementary DNAs were synthesized using ReverTraAce qPCR RT Master Mix (Toyobo, Osaka, Japan). The qRT-PCR analysis was performed using Light Cycler Fast-Start DNA Master Plus SYBER Green (Roche, Basel, Switzerland) according to the manufacturer’s instructions.…”

Section: Methodsmentioning

confidence: 99%

Acetate alters expression of genes involved in beige adipogenesis in 3T3-L1 cells and obese KK-Ay mice

Hanatani

Motoshima

Takaki

et al. 2016

J. Clin. Biochem. Nutr.

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The induction of beige adipogenesis within white adipose tissue, known as “browning”, has received attention as a novel potential anti-obesity strategy. The expression of some characteristic genes including PR domain containing 16 is induced during the browning process. Although acetate has been reported to suppress weight gain in both rodents and humans, its potential effects on beige adipogenesis in white adipose tissue have not been fully characterized. We examined the effects of acetate treatment on 3T3-L1 cells and in obese diabetic KK-Ay mice. The mRNA expression levels of genes involved in beige adipocyte differentiation and genes selectively expressed in beige adipocytes were significantly elevated in both 3T3-L1 cells incubated with 1.0 mM acetate and the visceral white adipose tissue from mice treated with 0.6% acetate for 16 weeks. In KK-Ay mice, acetate reduced the food efficiency ratio and increased the whole-body oxygen consumption rate. Additionally, reduction of adipocyte size and uncoupling protein 1-positive adipocytes and interstitial areas with multilocular adipocytes appeared in the visceral white adipose tissue of acetate-treated mice, suggesting that acetate induced initial changes of “browning”. In conclusion, acetate alters the expression of genes involved in beige adipogenesis and might represent a potential therapeutic agent to combat obesity.

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Section: Methodsmentioning

confidence: 99%

Acetate alters expression of genes involved in beige adipogenesis in 3T3-L1 cells and obese KK-Ay mice

Hanatani

Motoshima

Takaki

et al. 2016

J. Clin. Biochem. Nutr.

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“…Secondly, the mRNA expression levels of key mediators were measured; protein levels should also be evaluated to enhance the physiological relevance of the study. In addition, some studies demonstrated that inhibition of the p38 pathway can lower blood glucose by improving insulin sensitivity in peripheral organs 19 , 20 , which the finding of a temporary SB203580-mediated improvement in HOMA IR is to some extent consistent with. Therefore, insulin tolerance testing and measurement of expression levels of mediators of insulin sensitivity in insulin target tissues should be carried out in a future study, to explore the role of p38 in insulin sensitivity.…”

Section: Discussionmentioning

confidence: 70%

Inhibition of p38 mitogen-activated protein kinase exerts a hypoglycemic effect by improving β cell function via inhibition of β cell apoptosis in db/db mice

Wei

Feng

et al. 2018

Journal of Enzyme Inhibition and Medicinal Chemistry

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The p38 mitogen-activated protein kinase (MAPK) pathway is involved in endoplasmic reticulum stress (ERS) and inflammation, which may play an important role in the pathogenesis of type 2 diabetes (T2DM). This study aimed to investigate whether p38 MAPK contributes to the pathogenesis of T2DM. 6-week-old female db/db mice were randomly assigned to Dmo and Dmi groups, and C57 mice were assigned as controls. The Dmi group was gavaged with the p38 MAPK inhibitor SB203580 for 9 weeks, and the effects on β cell dysfunction and apoptosis were investigated. db/db mice showed higher food intake, body mass, fasting glucose, and plasma insulin levels than C57 mice. After SB203580 administration, blood glucose was significantly lower. HOMA β and HOMA IR were improved. Islet mRNA expression levels of the ERS markers were lower. P38 MAPK inhibition reduced blood glucose and improved β cell function, at least in part by reducing β cell apoptosis.

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“…At an early stage of the development of obesity, TACE activity seems to be elevated in visceral adipose tissue, but not in liver or skeletal muscle. Interestingly, intraperitoneal injection of exogenous TNF increased TACE activity and protein expression in white adipose tissue of mice [91]. Treatment with the TACE-inhibitor marimastat improved surrogate markers for insulin sensitivity and reversed steatosis in mouse model of diet-induced obesity and leptin deficiency [92].…”

Section: Source(s) and Release Of Tnf From Adipose Tissuementioning

confidence: 99%

Obesity and Coronary Microvascular Disease – Implications for Adipose Tissue-Mediated Remote Inflammatory Response

Bagi¹,

Broskova²,

Fehér

2014

CVP

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It is believed that obesity has detrimental effects on the coronary circulation. These include immediate changes in coronary arterial vasomotor responsiveness and the development of occlusive large coronary artery disease. Despite its critical role in regulating myocardial perfusion, the altered behavior of coronary resistance arteries, which gives rise to coronary microvascular disease (CMD) is poorly understood in obesity. A chronic, low-grade vascular inflammation has been long considered as one of the main underlying pathology behind CMD. The expanded adipose tissue and the infiltrating macrophages are the major sources of pro-inflammatory mediators that have been implicated in causing inadequate myocardial perfusion and, in a long term, development of heart failure in obese patients. Much less is known the mechanisms regulating the release of these cytokines into the circulation that enable them to exert their remote effects in the coronary microcirculation. This mini review aims to examine recent studies describing alterations in the vasomotor function of coronary resistance arteries and the role of adipose tissue-derived pro-inflammatory cytokines and adipokines in contributing to CMD in obesity. We provide examples of regulatory mechanisms by which adipokines are released from adipose tissue to exert their remote inflammatory effects on coronary microvessels. We identify some of the important challenges and opportunities going forward.

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Regulation of TNFα converting enzyme activity in visceral adipose tissue of obese mice

Cited by 3 publications

References 36 publications

Acetate alters expression of genes involved in beige adipogenesis in 3T3-L1 cells and obese KK-Ay mice

Acetate alters expression of genes involved in beige adipogenesis in 3T3-L1 cells and obese KK-Ay mice

Inhibition of p38 mitogen-activated protein kinase exerts a hypoglycemic effect by improving β cell function via inhibition of β cell apoptosis in db/db mice

Obesity and Coronary Microvascular Disease – Implications for Adipose Tissue-Mediated Remote Inflammatory Response

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