550
F. Tourniaire et al.
21.6 The Impact of the Carotenoids on the Control
of Energy Homeostasis by Brain
As mentioned above, carotenoids can affect the biology of the adipose tissue and then
modulate the production of leptin as well as the inflammatory cytokines (Landrier
et al. 2012), and consequently may have an indirect effect on brain function. However,
several food compounds including carotenoids could reach directly the hypothalamus
(Aragones et al. 2016), where they regulate leptin signaling pathway. More precisely,
they could either cross the blood brain barrier or pass through fenestrated capillaries
of circumventricular organs and target the arcuate nucleus neurons. In the context
of the central control of feeding behavior, it is important to notice that other structures as hippocampus plays an important role and that they could be targeted by the
carotenoids as indicated below.
It is presently not clear if carotenoids act indirectly via adipose tissue or directly on
brain, nevertheless, several studies suggested an involvement of brain in body weight
management under carotenoids effect. Indeed, the continuous intake of lycopene-rich
food as well as the intraperitoneal administration of lycopene increased neuronal
activity within the paraventricular and ventromedial nuclei as shown by c-Fos, a
marker of neuronal activity, immunoreactivity (Takayama et al. 2013). This study
suggested that lycopene may have some influence on feeding behavior. In accordance with this hypothesis, a nice work of the group of Dr. Bishnoi showed that
lycopene prevented weight and adiposity in mice in a HFD model (Singh et al. 2016).
Interestingly, this effect was associated with a modulation of hypothalamic anorexigenic and orexigenic genes expression. To date, the direct effect of lycopene on
neuronal activity is unclear and more studies are necessary to thoroughly understand
this mechanism. As evoked above, lycopene can impact brain function by limiting
peripheral inflammation. In accordance with this hypothesis, Kuhad et al. showed
that chronic treatment with lycopene significantly and dose-dependently attenuated
cognitive deficit associated with inflammation in diabetic rats (Kuhad et al. 2008).
Interestingly, recent work by Zhao et al. suggest that fucoxanthin may modulate
neuro-inflammation (Zhao et al. 2017). In this work, fucoxanthin increased Nrf2 activation in LPS-activated microglia. This interesting observation needs to be
studied in in vivo model and especially in brain structures (i.e., hypothalamus or
hippocampus) involved in feeding behavior. In accordance with this idea, a recent
paper indicated that fucoxanthin treatment reversed LPS-induced defect in body
weight and food intake in mice (Jiang et al. 2019). The authors also showed that
fucoxanthin inhibited LPS-induced overexpression of pro-inflammatory cytokines
(IL-1β, IL-6, and TNF-α) in the hippocampus and hypothalamus, via the modulation
of AMPK- NF-κB signaling pathway. Interestingly, current studies have shown that
the activation of AMPK pathway is essential to maintain energy homeostasis, as they
are involved in the anorexigenic effect of leptin (Hardie 2014).
F. Tourniaire et al.
21.6 The Impact of the Carotenoids on the Control
of Energy Homeostasis by Brain
As mentioned above, carotenoids can affect the biology of the adipose tissue and then
modulate the production of leptin as well as the inflammatory cytokines (Landrier
et al. 2012), and consequently may have an indirect effect on brain function. However,
several food compounds including carotenoids could reach directly the hypothalamus
(Aragones et al. 2016), where they regulate leptin signaling pathway. More precisely,
they could either cross the blood brain barrier or pass through fenestrated capillaries
of circumventricular organs and target the arcuate nucleus neurons. In the context
of the central control of feeding behavior, it is important to notice that other structures as hippocampus plays an important role and that they could be targeted by the
carotenoids as indicated below.
It is presently not clear if carotenoids act indirectly via adipose tissue or directly on
brain, nevertheless, several studies suggested an involvement of brain in body weight
management under carotenoids effect. Indeed, the continuous intake of lycopene-rich
food as well as the intraperitoneal administration of lycopene increased neuronal
activity within the paraventricular and ventromedial nuclei as shown by c-Fos, a
marker of neuronal activity, immunoreactivity (Takayama et al. 2013). This study
suggested that lycopene may have some influence on feeding behavior. In accordance with this hypothesis, a nice work of the group of Dr. Bishnoi showed that
lycopene prevented weight and adiposity in mice in a HFD model (Singh et al. 2016).
Interestingly, this effect was associated with a modulation of hypothalamic anorexigenic and orexigenic genes expression. To date, the direct effect of lycopene on
neuronal activity is unclear and more studies are necessary to thoroughly understand
this mechanism. As evoked above, lycopene can impact brain function by limiting
peripheral inflammation. In accordance with this hypothesis, Kuhad et al. showed
that chronic treatment with lycopene significantly and dose-dependently attenuated
cognitive deficit associated with inflammation in diabetic rats (Kuhad et al. 2008).
Interestingly, recent work by Zhao et al. suggest that fucoxanthin may modulate
neuro-inflammation (Zhao et al. 2017). In this work, fucoxanthin increased Nrf2 activation in LPS-activated microglia. This interesting observation needs to be
studied in in vivo model and especially in brain structures (i.e., hypothalamus or
hippocampus) involved in feeding behavior. In accordance with this idea, a recent
paper indicated that fucoxanthin treatment reversed LPS-induced defect in body
weight and food intake in mice (Jiang et al. 2019). The authors also showed that
fucoxanthin inhibited LPS-induced overexpression of pro-inflammatory cytokines
(IL-1β, IL-6, and TNF-α) in the hippocampus and hypothalamus, via the modulation
of AMPK- NF-κB signaling pathway. Interestingly, current studies have shown that
the activation of AMPK pathway is essential to maintain energy homeostasis, as they
are involved in the anorexigenic effect of leptin (Hardie 2014).