548
F. Tourniaire et al.
showed no effect on adipogenesis. Beside these effects, there is also evidence that
some effects of provitamin A carotenoids are mediated through retinol and its metabolites production which are known to regulate adipogenesis (reviewed in Blaner
2019).
Molecules with anti-inflammatory effects are supposed to limit the risk of
obesity-associated disorders, including insulin resistance. Such anti-inflammatory
effects of β-carotene in 3T3-L1 adipocytes were suggested to arise through limitation of TNFα-mediated down-regulation of genes linked to adipocyte biology
(Kameji et al. 2010). β-carotene also counteracted oxidative stress-mediated dysregulation of adiponectin secretion, chemokines expression, and NF-κB activation in
3T3-L1 adipocytes (Cho et al. 2018). Fucoxanthin blunted TNFα-mediated induction of pro-inflammatory cytokines in adipocytes (Hosokawa et al. 2010) and in
adipocytes/macrophages coculture systems (Maeda et al. 2015). The most studied
anti-inflammatory carotenoid is lycopene (all-trans), and we demonstrated its ability
to inhibit pro-inflammatory cytokine and chemokine expression in vitro (in murine
and human adipocytes) (Gouranton et al. 2011). These data were also reproduced
ex vivo on adipose tissue explants from mice subjected to a high fat diet (characterized by low-grade inflammation). The molecular mechanism was investigated and
the involvement of NF-κB was confirmed. Similar results (i.e., inhibition of cytokine
and chemokine expression in various in vitro and ex vivo models) were obtained with
apo-10
-lycopenoic acid, a metabolite of lycopene (Gouranton et al. 2011). Lycopene
also attenuated LPS-mediated induction of TNFα in macrophages via NF-κB and
JNK (Marcotorchino et al. 2012), as well as macrophage migration in vitro. Consequently, lycopene decreased macrophage-induced cytokine, acute phase protein and
chemokine mRNA in adipocytes. Interestingly, all-trans and 5-cis lycopene, the two
main isoforms of lycopene found in vivo, displayed similar effect in terms of inflammation control and glucose uptake in adipocytes (Fenni et al. 2019). A few studies
have shown that retinoids, similar to carotenoids, have positive effects by decreasing
the expression of adipocyte-derived inflammatory mediators such as adipsin (Antras
et al. 1991) and resistin (Felipe et al. 2004). Our group has also shown that ATRA
blunts TNF-α mediated cytokine expression in 3T3-L1 cells (Gouranton et al. 2011).
More recently, we demonstrated that ATRA limits the expression of a large range
of chemokines in vivo and in vitro. Such anti-inflammatory effect of ATRA was
associated with a reduction in the phosphorylation levels of IκB and p65, probably
mediated by PGC1α expression (Karkeni et al. 2017).
The browning process of white adipose tissue has been proposed as a putative
mechanism controlling energy homeostasis and insulin sensitivity (Chondronikola
et al. 2014). Recently an AMPK1-mediated effect on adipocyte browning and mitochondrial biogenesis has been demonstrated for zeaxanthin (Liu et al. 2019). We
reported similar mitochondrial biogenesis, induction of OXPHOS, and adipocyte
browning in adipocytes incubated with ATRA (Tourniaire et al. 2016), whereas
fucoxanthin and its metabolite fucoxanthinol were inefficient to induce adipocyte
browning (Rebello et al. 2017).
F. Tourniaire et al.
showed no effect on adipogenesis. Beside these effects, there is also evidence that
some effects of provitamin A carotenoids are mediated through retinol and its metabolites production which are known to regulate adipogenesis (reviewed in Blaner
2019).
Molecules with anti-inflammatory effects are supposed to limit the risk of
obesity-associated disorders, including insulin resistance. Such anti-inflammatory
effects of β-carotene in 3T3-L1 adipocytes were suggested to arise through limitation of TNFα-mediated down-regulation of genes linked to adipocyte biology
(Kameji et al. 2010). β-carotene also counteracted oxidative stress-mediated dysregulation of adiponectin secretion, chemokines expression, and NF-κB activation in
3T3-L1 adipocytes (Cho et al. 2018). Fucoxanthin blunted TNFα-mediated induction of pro-inflammatory cytokines in adipocytes (Hosokawa et al. 2010) and in
adipocytes/macrophages coculture systems (Maeda et al. 2015). The most studied
anti-inflammatory carotenoid is lycopene (all-trans), and we demonstrated its ability
to inhibit pro-inflammatory cytokine and chemokine expression in vitro (in murine
and human adipocytes) (Gouranton et al. 2011). These data were also reproduced
ex vivo on adipose tissue explants from mice subjected to a high fat diet (characterized by low-grade inflammation). The molecular mechanism was investigated and
the involvement of NF-κB was confirmed. Similar results (i.e., inhibition of cytokine
and chemokine expression in various in vitro and ex vivo models) were obtained with
apo-10
-lycopenoic acid, a metabolite of lycopene (Gouranton et al. 2011). Lycopene
also attenuated LPS-mediated induction of TNFα in macrophages via NF-κB and
JNK (Marcotorchino et al. 2012), as well as macrophage migration in vitro. Consequently, lycopene decreased macrophage-induced cytokine, acute phase protein and
chemokine mRNA in adipocytes. Interestingly, all-trans and 5-cis lycopene, the two
main isoforms of lycopene found in vivo, displayed similar effect in terms of inflammation control and glucose uptake in adipocytes (Fenni et al. 2019). A few studies
have shown that retinoids, similar to carotenoids, have positive effects by decreasing
the expression of adipocyte-derived inflammatory mediators such as adipsin (Antras
et al. 1991) and resistin (Felipe et al. 2004). Our group has also shown that ATRA
blunts TNF-α mediated cytokine expression in 3T3-L1 cells (Gouranton et al. 2011).
More recently, we demonstrated that ATRA limits the expression of a large range
of chemokines in vivo and in vitro. Such anti-inflammatory effect of ATRA was
associated with a reduction in the phosphorylation levels of IκB and p65, probably
mediated by PGC1α expression (Karkeni et al. 2017).
The browning process of white adipose tissue has been proposed as a putative
mechanism controlling energy homeostasis and insulin sensitivity (Chondronikola
et al. 2014). Recently an AMPK1-mediated effect on adipocyte browning and mitochondrial biogenesis has been demonstrated for zeaxanthin (Liu et al. 2019). We
reported similar mitochondrial biogenesis, induction of OXPHOS, and adipocyte
browning in adipocytes incubated with ATRA (Tourniaire et al. 2016), whereas
fucoxanthin and its metabolite fucoxanthinol were inefficient to induce adipocyte
browning (Rebello et al. 2017).