Moderate alcohol intake induces thermogenic brown/beige adipocyte formation<i>via</i>elevating retinoic acid signaling

Wang, Bo; Wang, Zhixiu; Avila, Jeanene M. de; Zhu, Mei‐Jun; Zhang, Faya; Gomez, Noe Alberto; Zhao, Liang; Tian, Qiyu; Zhao, Junxing; Maricelli, Joseph; Zhang, Hui; Rodgers, Buel D.; Du, Min

doi:10.1096/fj.201700396r

Cited by 12 publications

(12 citation statements)

References 63 publications

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“…We further demonstrated that direct alcohol injection into the brain, like alcohol feeding, potently activates fat. It is worth mentioning that alcohol treatment was reported to stimulate WAT Ucp1 expression through enhancement of retinoic acid signaling (44); surprisingly, alcohol intake was also reported to suppress BAT retinoid signaling (45). Ambient temperatures, which vary among different animal facilities, are known to influence baseline activities of BAT and beige fat, which prompted us 50), we posit that the brain alcohol-sensing/sympathetic nerve/ BAT/beige fat axis likely confers a broad spectrum of health benefits beyond protection against ALD.…”

Section: Discussionmentioning

confidence: 99%

Brown fat activation mitigates alcohol-induced liver steatosis and injury in mice

Shen¹,

Jiang²,

Lin³

et al. 2019

Journal of Clinical Investigation

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Section: Discussionmentioning

confidence: 99%

Brown fat activation mitigates alcohol-induced liver steatosis and injury in mice

Shen¹,

Jiang²,

Lin³

et al. 2019

Journal of Clinical Investigation

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“…During measurement, mice were provided with the respective diets and water ad libitum (Wang et al . ). Fat and carbohydrate oxidation was calculated as described previously (Peronnet & Massicotte, ).…”

Section: Methodsmentioning

confidence: 97%

“…The tissue sections at a thickness of 5 μm were prepared for haematoxylin and eosin staining or immunocytochemical staining following deparaffinization as described previously (Wang et al . ). For measurement of the ratio of the cross‐sectional area (CSA) of the junctional/labyrinth zones and the CSA of the placenta, each zone was calculated using ImageJ (National Institutes of Health, Bethesda, MD, USA).…”

Section: Methodsmentioning

confidence: 97%

Exercise prevents the adverse effects of maternal obesity on placental vascularization and fetal growth

Son

Liu

Tian

et al. 2019

The Journal of Physiology

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Key pointsr Maternal exercise improves the metabolic health of maternal mice challenged with a high-fat diet.r Exercise intervention of obese mothers prevents fetal overgrowth. r Exercise intervention reverses impaired placental vascularization in obese mice. r Maternal exercise activates placental AMP-activated protein kinase, which was inhibited as a result of maternal obesity.Abstract More than one-third of pregnant women in the USA are obese and maternal obesity (MO) negatively affects fetal development, which predisposes offspring to metabolic diseases. The placenta mediates nutrient delivery to fetuses and its function is impaired as a result of MO. Exercise ameliorates metabolic dysfunction resulting from obesity, although its effect on placental function of obese mothers has not been explored. In the present study, C57BL/6J female mice were randomly assigned into two groups fed either a control or a high-fat diet (HFD) and then the mice on each diet were further divided into two subgroups with/without exercise. In HFD-induced obese mice, daily treadmill exercise during pregnancy reduced body weight gain, lowered serum glucose and lipid concentration, and improved insulin sensitivity of maternal mice. Importantly, maternal exercise prevented fetal overgrowth (macrosomia) induced by MO. To further examine the preventive effects of exercise on fetal overgrowth, placental vascularization and nutrient transporters were analysed. Vascular density and the expression of vasculogenic factors were reduced as a result of MO but were recovered by maternal exercise. On the other hand, the contents of nutrient transporters were not substantially altered by MO or exercise, suggesting that the protective effects of exercise in MO-induced fetal overgrowth were primarily a result of the alteration of placental vascularization and improved maternal metabolism. Furthermore, exercise enhanced downstream insulin signalling and activated AMP-activated protein kinase in HFD placenta. In sum, maternal exercise prevented fetal overgrowth induced by MO, which was Jun Seok Son received MS Degree in Kinesiology from Seoul National University. Currently, Jun Seok is a PhD student in the . His research interests focus on the impacts of maternal obesity, exercise, nutrition and other physiological conditions on fetal development and offspring health, especially the epigenetic mechanisms linking nutrients/metabolites to progenitor cell differentiation into myocytes/adipocytes. Ultimately, he aims to translate his work into clinical practice with respect to improving health outcomes for mothers and children affected by obesity.

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“…ALDH1A1 plays an important role in producing RA and inducing beige adipogenesis [ 28 ]. Mice implanted with tumor cells had higher ALDH1A1 protein contents (Figure 3A and 3B ).…”

Section: Resultsmentioning

confidence: 99%

“…Chronic alcohol intake enhances the oxidative capacity of brown adipose tissue (BAT) [ 25 – 27 ]. In addition, we recently reported that alcohol consumption induces white adipose tissue browning and activates thermogenesis by elevating peripheral retinoic acid (RA) levels [ 28 ]. Due to the lower nutrient partitioning priority for adipose tissue and skeletal muscle, the increased energy demand from BAT and beige adipocytes induced by alcohol likely deprives nutrients available for muscle and adipose tissue of cancer patients, aggravating CAC.…”

Section: Introductionmentioning

confidence: 99%

Alcohol intake aggravates adipose browning and muscle atrophy in cancer-associated cachexia

Wang

Zhang

et al. 2017

Oncotarget

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Cancer is commonly associated with cachexia, a paraneoplastic syndrome characterized by body weight loss, muscle wasting, adipose tissue atrophy and inflammation. Chronic alcohol consumption increases the risk of multiple types of cancer, and enhances cancer-associated cachexia (CAC), but the underlying mechanisms remain poorly defined. To test, C57BL/6 mice were fed with 0% or 20% (w/v) alcohol for 3 months, then inoculated with B16BL6 melanoma cells subcutaneously in the right side of the hip and continued to feed with/without alcohol for 3 or 4 weeks. Alcohol intake upregulated ALDH1A1 expression and elevated retinoic acid (RA) content in inguinal white adipose tissue (iWAT), which led to enhanced iWAT browning and brown adipose tissue (BAT) activation, accelerating fat loss. Moreover, alcohol increased muscle loss through augmenting muscle protein degradation, cell apoptosis and inflammation. In addition, alcohol reduced satellite cell density and impaired myogenesis in skeletal muscle. Taken together, alcohol aggravates cancer-associated cachexia at least partially through elevating adipose browning and muscle atrophy.

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Moderate alcohol intake induces thermogenic brown/beige adipocyte formationviaelevating retinoic acid signaling

Cited by 12 publications

References 63 publications

Brown fat activation mitigates alcohol-induced liver steatosis and injury in mice

Brown fat activation mitigates alcohol-induced liver steatosis and injury in mice

Exercise prevents the adverse effects of maternal obesity on placental vascularization and fetal growth

Alcohol intake aggravates adipose browning and muscle atrophy in cancer-associated cachexia

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