Abstract
The increasing prevalence of obesity and its associated comorbidities has gained attention in developing effective treatments and strategies that promote energy expenditure and the conversion of fat from a white to a brite phenotype. Capsaicin, bioactive component of chili peppers and a transient receptor potential channel vanilloid 1 (TRPV1) agonist, has been known to stimulate the process of thermogenesis. In this study, the effects of capsaicin were assessed on two murine cellular models by quantifying the dynamic of lipid droplets (LDs) and the expression of genes involved in adipocyte browning. Present findings demonstrated that treatment with norepinephrine or capsaicin combined with norepinephrine on 3T3-L1 cells and X9 cells significantly promoted the reduction of LDs area surface and size. The transcription of browning related genes such as uncoupling protein 1 (Ucp1), T-box transcription factor 1 (Tbx1), PR domain containing 16 (Prdm16), peroxisome proliferator-activated receptor γ coactivator 1α (Ppargc1a) and cell death-inducing DNA fragmentation factor A-like effector A (Cidea) was up-regulated by chronic capsaicin treatment on differentiated 3T3-L1 cells. Instead, X9 cells were significantly responsive only to the treatment with norepinephrine, used as positive control.
Highlights
In recent years, research on adipose tissue biology and obesity has recognized in browning of white adipose tissue (WAT) a potential therapeutic strategy for the treatment of obesity and related morbidities (Peschechera and Eckel, 2013; Bartelt and Heeren, 2014)
At 4 days, 3T3-L1 cells treated with NE, 0.1CPNE and 1CP showed significantly (p < 0.0001) different total lipid droplets (LDs) area surface in comparison to CTRL cells and all other treatments (Figure 2A). 1CP showed the largest LD area surface and NE the smallest
This study aims to present the effects of different capsaicin treatments on 3T3-L1 and X9 cells, two metabolically distinct murine models, which differ in their functional role and browning response (White and Tchoukalova, 2014)
Summary
Research on adipose tissue biology and obesity has recognized in browning of white adipose tissue (WAT) a potential therapeutic strategy for the treatment of obesity and related morbidities (Peschechera and Eckel, 2013; Bartelt and Heeren, 2014). Unlike fataccumulating WAT, brown adipose tissue (BAT) promotes the dissipation of energy deriving from the catabolism of fatty acids in form of heat This process is known as thermogenesis and is driven by mitochondrial proton pump uncoupling protein 1 (UCP1) (Cannon and Nedergaard, 2004). The activation of BAT and the recruitment of brite adipocytes in WAT depots is mainly driven by cold exposure, which triggers a sympathetic response that induces the release of norepinephrine (NE) from sympathetic neurons and the activation of β3 adrenoreceptors on the membrane of adipocytes. This produces a signaling cascade involving protein kinase A (PKA) and p38
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