Insights into an adipocyte whitening program

Hill, Bradford G.

doi:10.4161/21623945.2014.960351

Cited by 9 publications

(8 citation statements)

References 44 publications

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“…An interesting, but largely ignored, aspect of the muscle-like characteristics of BAT is the expression of muscle-specific type II myosin heavy chains (MyH), which are known to facilitate intrinsic physical forces in cells. RNAseq comparing white adipose to brown adipose has revealed muscle-like characteristics (Figure 1F), which are resistant to high fat diet induced “whitening” (Hill, 2015). When comparing the relative abundance of MyH species in these tissues, it is evident that brown adipose tissue is enriched with MyH1, -2, -4, -7, and -11 expression (Figure S1B).…”

Section: Resultsmentioning

confidence: 99%

Actomyosin-Mediated Tension Orchestrates Uncoupled Respiration in Adipose Tissues

et al. 2018

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The activation of brown/beige adipose tissue (BAT) metabolism and the induction of uncoupling protein 1 (UCP1) expression are essential for BAT-based strategies to improve metabolic homeostasis. Here, we demonstrate that BAT utilizes actomyosin machinery to generate tensional responses following adrenergic stimulation, similar to muscle tissues. The activation of actomyosin mechanics is critical for the acute induction of oxidative metabolism and uncoupled respiration in UCP1 adipocytes. Moreover, we show that actomyosin-mediated elasticity regulates the thermogenic capacity of adipocytes via the mechanosensitive transcriptional co-activators YAP and TAZ, which are indispensable for normal BAT function. These biomechanical signaling mechanisms may inform future strategies to promote the expansion and activation of brown/beige adipocytes.

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Section: Resultsmentioning

confidence: 99%

Actomyosin-Mediated Tension Orchestrates Uncoupled Respiration in Adipose Tissues

et al. 2018

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“… 8 Activation of white adipose browning program plays a critical role in positively regulating overall systemic metabolism as Epi and SC adipose tissues are the main site of energy storage and mobilization. 9 – 13 Biochemical changes occurring during adipose browning are linked with alteration in several metabolic pathways. 14 – 15 We therefore sought to determine whether Fst expression regulates (in addition to browning) the metabolic repertoire of adipocytes and adipose tissues.…”

Section: Introductionmentioning

confidence: 99%

Metabolic profiling of follistatin overexpression: a novel therapeutic strategy for metabolic diseases

Singh¹,

Pervin²,

Lee³

et al. 2018

DMSO

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BackgroundFollistatin (Fst) promotes brown adipocyte characteristics in adipose tissues.MethodsAbdominal fat volume (CT scan), glucose clearance (GTT test), and metabolomics analysis (mass spectrometry) of adipose tissues from Fst transgenic (Fst-Tg) and wild type (WT) control mice were analyzed. Oxygen consumption (Seahorse Analyzer) and lipidomics (gas chromatography) was analyzed in 3T3-L1 cells.ResultsFst-Tg mice show significant decrease in abdominal fat content, increased glucose clearance, improved plasma lipid profiles and significant changes in several conventional metabolites compared to the WT mice. Furthermore, overexpression of Fst in 3T3-L1 cells resulted in up regulation of key brown/beige markers and changes in lipidomics profiles.ConclusionFst modulates key factors involved in promoting metabolic syndrome and could be used for therapeutic intervention.

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“…Therefore, obesity is characterized by low-grade inflammation in local and systemic sites as demonstrated by robust secretion of proinflammatory cytokines, including IL-6, as well as active recruitment of leukocytes [3]. Substantial evidence supports the hypothesis indicating that inflammation may contribute to insulin resistance, which further induces a series of diseases such as diabetes, hypertension, fatty liver disease, and coronary heart disease, thereby threatening human health [4, 5]. However, the mechanism underlying inflammation remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Autophagy-Related Protein and Cell Differentiation by High Mobility Group Box 1 Protein in Adipocytes

Feng

Zhang

et al. 2016

Mediators of Inflammation

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High mobility group box 1 protein (HMGB1) is a molecule related to the development of inflammation. Autophagy is vital to maintain cellular homeostasis and protect against inflammation of adipocyte injury. Our recent work focused on the relationship of HMGB1 and autophagy in 3T3-L1 cells. In vivo experimental results showed that, compared with the normal-diet group, the high-fat diet mice displayed an increase in adipocyte size in the epididymal adipose tissues. The expression levels of HMGB1 and LC3II also increased in epididymal adipose tissues in high-fat diet group compared to the normal-diet mice. The in vitro results indicated that HMGB1 protein treatment increased LC3II formation in 3T3-L1 preadipocytes in contrast to that in the control group. Furthermore, LC3II formation was inhibited through HMGB1 knockdown by siRNA. Treatment with the HMGB1 protein enhanced LC3II expression after 2 and 4 days but decreased the expression after 8 and 10 days among various differentiation stages of adipocytes. By contrast, FABP4 expression decreased on the fourth day and increased on the eighth day. Hence, the HMGB1 protein modulated autophagy-related proteins and lipid-metabolism-related genes in adipocytes and could be a new target for treatment of obesity and related metabolic diseases.

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Insights into an adipocyte whitening program

Cited by 9 publications

References 44 publications

Actomyosin-Mediated Tension Orchestrates Uncoupled Respiration in Adipose Tissues

Actomyosin-Mediated Tension Orchestrates Uncoupled Respiration in Adipose Tissues

Metabolic profiling of follistatin overexpression: a novel therapeutic strategy for metabolic diseases

Regulation of Autophagy-Related Protein and Cell Differentiation by High Mobility Group Box 1 Protein in Adipocytes

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