21 Carotenoids as Anti-obesity Supplements
549
21.5 Carotenoids and/or Metabolites Are Involved in Body
Weight Management and Limitation of Obesity
Comorbidities
Significant research has been dedicated to the study of the impact of β-carotene
on energy metabolism and consequences on obesity (Coronel et al. 2019). Its antiobesity effect has subsequently been demonstrated to be linked to the provitaminic
A effect (Amengual et al. 2011; van Helden et al. 2011) since BCMO1
−/− mice did
not display adipose tissue weight modification. This effect was found to be linked
to decreased expression of PPARγ in adipose tissue and the involvement of RAR
signaling in this regulation (Lobo et al. 2010).
Astaxanthin prevented obesity in mice fed with a high fat diet (Ikeuchi et al. 2007),
via the limitation of adipose tissue expansion. Similar anti-obesity effects have been
documented in mice subjected to a high fat and high fructose diet (Arunkumar et al.
2012) where insulin sensitivity and inflammation were also improved by astaxanthin. Preventive effect of astaxanthin regarding hepatic steatosis (Ni et al. 2015) and
inflammation and fibrosis in the liver in a NASH and DIO mice model (Kim et al.
2017).
Anti-adiposity properties have also been reported for β-cryptoxanthin
(Takayanagi et al. 2011), but the mechanism has not been unveiled. In addition,
β-cryptoxanthin reversed liver steatosis and insulin resistance in DIO mice; such
effect may be related to the anti-inflammatory effect of this carotenoid in the liver
(Ni et al. 2015). The potentiality of fucoxanthin in weight management has been
extensively studied (for review (Maeda 2015). This carotenoid limited weight gain,
hyperglycemia, and inhibited the expression of several pro-inflammatory cytokines
in adipose tissue of KK-a(y) mice (Hosokawa et al. 2010). Similar effects have
been depicted in DIO mice, not only through modulation of lipogenesis, adiponectin
production, and inflammation in adipose tissue (Grasa-Lopez et al. 2016), but also
via browning of white adipose tissue (Maeda 2015).
Zeaxanthin inhibited obesity in high fat fed mice, presumably by inducing AMPK
activation, and inhibition on lipogenesis in adipose tissue (Liu et al. 2017).
The anti-obesity effect of lycopene was demonstrated in mice submitted to high fat
diet, where adiposity was reduced after supplementation. Several comorbidities were
consequently reduced such as glucose tolerance insulin sensitivity steatosis (Singh
et al. 2016). We and others confirmed this beneficial effect of lycopene and/or tomato
powder rich in lycopene in DIO mice model, on adiposity, glucose homeostasis,
adipose tissue, and liver inflammation and steatosis (Fenni et al. 2017; Li et al. 2018;
Wang et al. 2019).
It is also obvious that part of the effects of carotenoids (provitamin A or not)
are due to the vitamin A effect and are mediated by RAR. Such effects have been
extensively reviewed elsewhere (Bonet et al. 2015; Coronel et al. 2019; Blaner 2019)
and will not be detailed in the present review.
549
21.5 Carotenoids and/or Metabolites Are Involved in Body
Weight Management and Limitation of Obesity
Comorbidities
Significant research has been dedicated to the study of the impact of β-carotene
on energy metabolism and consequences on obesity (Coronel et al. 2019). Its antiobesity effect has subsequently been demonstrated to be linked to the provitaminic
A effect (Amengual et al. 2011; van Helden et al. 2011) since BCMO1
−/− mice did
not display adipose tissue weight modification. This effect was found to be linked
to decreased expression of PPARγ in adipose tissue and the involvement of RAR
signaling in this regulation (Lobo et al. 2010).
Astaxanthin prevented obesity in mice fed with a high fat diet (Ikeuchi et al. 2007),
via the limitation of adipose tissue expansion. Similar anti-obesity effects have been
documented in mice subjected to a high fat and high fructose diet (Arunkumar et al.
2012) where insulin sensitivity and inflammation were also improved by astaxanthin. Preventive effect of astaxanthin regarding hepatic steatosis (Ni et al. 2015) and
inflammation and fibrosis in the liver in a NASH and DIO mice model (Kim et al.
2017).
Anti-adiposity properties have also been reported for β-cryptoxanthin
(Takayanagi et al. 2011), but the mechanism has not been unveiled. In addition,
β-cryptoxanthin reversed liver steatosis and insulin resistance in DIO mice; such
effect may be related to the anti-inflammatory effect of this carotenoid in the liver
(Ni et al. 2015). The potentiality of fucoxanthin in weight management has been
extensively studied (for review (Maeda 2015). This carotenoid limited weight gain,
hyperglycemia, and inhibited the expression of several pro-inflammatory cytokines
in adipose tissue of KK-a(y) mice (Hosokawa et al. 2010). Similar effects have
been depicted in DIO mice, not only through modulation of lipogenesis, adiponectin
production, and inflammation in adipose tissue (Grasa-Lopez et al. 2016), but also
via browning of white adipose tissue (Maeda 2015).
Zeaxanthin inhibited obesity in high fat fed mice, presumably by inducing AMPK
activation, and inhibition on lipogenesis in adipose tissue (Liu et al. 2017).
The anti-obesity effect of lycopene was demonstrated in mice submitted to high fat
diet, where adiposity was reduced after supplementation. Several comorbidities were
consequently reduced such as glucose tolerance insulin sensitivity steatosis (Singh
et al. 2016). We and others confirmed this beneficial effect of lycopene and/or tomato
powder rich in lycopene in DIO mice model, on adiposity, glucose homeostasis,
adipose tissue, and liver inflammation and steatosis (Fenni et al. 2017; Li et al. 2018;
Wang et al. 2019).
It is also obvious that part of the effects of carotenoids (provitamin A or not)
are due to the vitamin A effect and are mediated by RAR. Such effects have been
extensively reviewed elsewhere (Bonet et al. 2015; Coronel et al. 2019; Blaner 2019)
and will not be detailed in the present review.