In mammals, the amount of fat reserves depends on the interplay between several interconnected processes, including the control of feeding behavior, energy expenditure, the gut environment,
partitioning of nutrients among tissues and anabolic versus catabolic pathways, as well as ongoing processes within fat depots
determining adipocyte number (e.g., preadipocyte proliferation,
adipocyte differentiation, and apoptosis) [1, 6]. Each of these
processes involves many signals, receptors, signal transduction cascades, and downstream targets including metabolic enzymes, transport proteins, and regulatory factors. Alterations in key molecular
elements of this complex system can favor a positive energy balance,
which can ultimately lead to obesity. Such alterations may be inherited or due to environmental exposures, and can at times be very
subtle. In addition, multiple sociocultural, socioeconomic, and
behavioral factors —often interrelated and many of them still
unknown or poorly understood— appear to contribute to the
establishment and perpetuation of obese phenotypes.
In order to tackle obesity, a common approach is the use of
dietary interventions based on altering diet macronutrient composition or promoting the supplementation with bioactive ingredients
which can ultimately target key processes and molecular elements
controlling body fat content. In recent years, a novel perspective is
emerging in regard to the biological activity of carotenoids and
carotenoid-derived metabolites —including, but not restricted to,
the vitamin A retinoids— that connects these compounds to the
control of body fat reserves, with implications for the management
of obesity and obesity-related metabolic disturbances. Evidence for
the antiobesity action of specific carotenoids and their derived
metabolic products comes so far mainly from cell, animal, and
human epidemiological studies. There have been only few human
intervention studies in the field to date, but the scenario they depict
is encouraging, since beneficial effects have been observed on the
accrual of body fat, abdominal fat and related risk parameters
following carotenoids consumption. Interestingly, in the case of
beta-carotene, these effects have been achieved under mild supplementation, at doses lower than the ones that have caused concern
and controversy in large intervention trials in the past (reviewed in
[7, 8]). Antiobesity and beneficial metabolic effects of carotenoids
can relate to their direct or indirect action on different tissues,
including the liver and adipose tissues —which constitute the
main reservoirs for carotenoids and vitamin A and whose lipid
metabolism is indeed known to be affected by retinoids— as well
as on the gut microbiota. At the molecular level, mechanisms of
action are emerging that include physical and/or functional interaction of the carotenoid molecules and/or their derivatives with
transcription factors of the nuclear receptor superfamily and with
proinflammatory and antioxidant cellular signaling pathways.
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Joan Ribot et al.
partitioning of nutrients among tissues and anabolic versus catabolic pathways, as well as ongoing processes within fat depots
determining adipocyte number (e.g., preadipocyte proliferation,
adipocyte differentiation, and apoptosis) [1, 6]. Each of these
processes involves many signals, receptors, signal transduction cascades, and downstream targets including metabolic enzymes, transport proteins, and regulatory factors. Alterations in key molecular
elements of this complex system can favor a positive energy balance,
which can ultimately lead to obesity. Such alterations may be inherited or due to environmental exposures, and can at times be very
subtle. In addition, multiple sociocultural, socioeconomic, and
behavioral factors —often interrelated and many of them still
unknown or poorly understood— appear to contribute to the
establishment and perpetuation of obese phenotypes.
In order to tackle obesity, a common approach is the use of
dietary interventions based on altering diet macronutrient composition or promoting the supplementation with bioactive ingredients
which can ultimately target key processes and molecular elements
controlling body fat content. In recent years, a novel perspective is
emerging in regard to the biological activity of carotenoids and
carotenoid-derived metabolites —including, but not restricted to,
the vitamin A retinoids— that connects these compounds to the
control of body fat reserves, with implications for the management
of obesity and obesity-related metabolic disturbances. Evidence for
the antiobesity action of specific carotenoids and their derived
metabolic products comes so far mainly from cell, animal, and
human epidemiological studies. There have been only few human
intervention studies in the field to date, but the scenario they depict
is encouraging, since beneficial effects have been observed on the
accrual of body fat, abdominal fat and related risk parameters
following carotenoids consumption. Interestingly, in the case of
beta-carotene, these effects have been achieved under mild supplementation, at doses lower than the ones that have caused concern
and controversy in large intervention trials in the past (reviewed in
[7, 8]). Antiobesity and beneficial metabolic effects of carotenoids
can relate to their direct or indirect action on different tissues,
including the liver and adipose tissues —which constitute the
main reservoirs for carotenoids and vitamin A and whose lipid
metabolism is indeed known to be affected by retinoids— as well
as on the gut microbiota. At the molecular level, mechanisms of
action are emerging that include physical and/or functional interaction of the carotenoid molecules and/or their derivatives with
transcription factors of the nuclear receptor superfamily and with
proinflammatory and antioxidant cellular signaling pathways.
404
Joan Ribot et al.