2018
DOI: 10.3390/ijms19113335
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Abstract: Caloric restriction (CR) delays the onset of many age-related pathophysiological changes and extends lifespan. White adipose tissue (WAT) is not only a major tissue for energy storage, but also an endocrine tissue that secretes various adipokines. Recent reports have demonstrated that alterations in the characteristics of WAT can impact whole-body metabolism and lifespan. Hence, we hypothesized that functional alterations in WAT may play important roles in the beneficial effects of CR. Previously, using microa… Show more

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Cited by 27 publications
(18 citation statements)
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References 76 publications
(105 reference statements)
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“…The transcriptional cofactor, Pgc1α, is important for mitochondrial biogenesis. The regulation of Pgc1α expression enhances mitochondrial biogenesis through Srebp-1c upregulation [ 31 , 32 ]. The present study found that only GiA-7 induced Srebp-1c and Pgc1α .…”
Section: Resultsmentioning
confidence: 99%
“…The transcriptional cofactor, Pgc1α, is important for mitochondrial biogenesis. The regulation of Pgc1α expression enhances mitochondrial biogenesis through Srebp-1c upregulation [ 31 , 32 ]. The present study found that only GiA-7 induced Srebp-1c and Pgc1α .…”
Section: Resultsmentioning
confidence: 99%
“…In adipose tissue, the mRNA levels of lipogenic genes did not change in animals using a Srebp1c loss of function or gain of function approach, thus indicating that in this tissues Srebp1c is not essential for DNL activation [58]. By contrast, mice under caloric restriction (CR) showed an SREBP1c/PGC1a-dependant induction of DNL in adipose tissue giving to Srebp1c an role on activating this metabolic pathway under this specific nutritional condition [100]. Finally, CREG1 has been described as an inducer of Ucp1 and FGF21 expression in an adipocyte P2–Creg1-transgenic (Tg) mice and globally of BAT adipogenesis and browning [101,102].…”
Section: Discussionmentioning
confidence: 99%
“…Many metabolic intermediates such as pyruvate kinase M2, sterol regulatory element-binding protein 1c, and peroxisome proliferator-activated receptors γ (PPARγ) are differentially regulated in obesity [8,9,10]. These factors have been implicated in reprogramming in the tumor microenvironment (TME) and have been shown to promote breast cancer proliferation and migration and even alter epigenetics leading to increased cancer incidence [11,12,13]. Data demonstrates targeting metabolic reprogramming with agents, such as statins or thiazolidinediones, can be as chemoprevention in rats [14,15].…”
Section: Introductionmentioning
confidence: 99%