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LA PLACE DES LIPIDES DANS L’ALIMENTATION
Central lipid detection and the regulation
Abstract: The modern abundance of energy-rich foods combined with a shift to more
sedentary lifestyles has led to a thermodynamic imbalance in which excessive caloricintake and reduced energy expenditure account for the prevalence of obesity. In
particular, exposure to lipid-rich diet is thought to promote metabolic alteration in
peripheral tissue associated with obesity-related diseases. The regulation of energy
balance depends on the ability of the brain to provide an adaptive response to change in
circulating factors of hunger and satiety. The hypothalamus is particularly regarded as
key integrative structure but, aside from hypothalamic-mediated homeostatic control,
feeding behavior is also modulated by sensory inputs, such as tastes and odors, as well as
by affective or emotional states. The reinforcing and motivational aspects of food areclosely tied to the release of the neurotransmitter dopamine by the mesolimbic system,
which is stimulated by calorie-dense foods as well as by most other objects of desire.
Therefore feeding behavior is regulated by homeostatic as well as non-homeostatic
inputs from the hypothalamus and the mesolimbic region. Interestingly, these structures
expresses several enzymes involved in the processing of triglyceride and fatty acid and the
recent literature provide growing evidence that fatty acid metabolism within discrete
brain regions can function as sensor of nutrient availability directly control the hedonic
4 rue Marie-Andree Lagroua Weill-Halle,
and the homeostatic aspect of feeding.
Key words: Free fatty acid, triglycerides, lipoprotein lipase, mesolimbic system, reward,
piece 512A,Case courrier 7126,75205 Paris Cedex 13,France
restriction) invariably result in a rapid
return to ‘‘set point’’ when normal
this, circulating peripheral factors such as
hormones (e.g., insulin, leptin, ghrelin)
sedentary lifestyles has led to a thermo-
and nutrients (e.g., glucose, lipids) acti-
vate discrete neural circuits in the brain
fact that globally, there has been both an
bolic rate and/or feeding behaviour.
that are high in fat, salt and a decrease in
rodent models. Therefore it is crucial to
understand the mechanism that insuresthe proper equilibrium between energyintake and expenditure.
Several observations led to the identifi-
To cite this article: Cansell C, Luquet S. Central lipid detection and the regulation of feeding behavior. OCL 2013; 20(2): 93-101. doi :
cle. They are called ‘‘first order neurons’’
factors like insulin, ghrelin or leptin.
circulating factors of hunger and satiety
Blood Barrier (BBB) is less developed.
inputs, such as tastes and odors, as well
High fat feeding and in general lipid &
receptors. ARC neurons project to ‘sec-
other brain areas, essential for the long-
like Nucleus of the Solitary Tract (NTS).
were also link to the establishment of an
other objects of desire (e.g., sex, drugs)
cortin system leads to obesity andhyperphagia in both human and rodent
In particular, the projection of midbrain
feeding and in obese state could directly
brain regions is a crucial neural substrate
effect; and thus this projection is often
referred to as the brain ‘‘reward circuit’’.
poorly studied for long time, as they were
data attest that cerebral lipids come from
be pointed that structure and function of
the BBB within hypothalamus – especial-
cular organs (CVO) – is quite different
are characterized by their small size, high
nuclei involved in food intake, including
that do not cross BBB in other part of the
both free fatty acid and triglyceride rich
particles (TG). Elevated circulating levels
dence that ‘‘central lipid sensing sens-
ing’’ is involved in the control of feeding
areas playing a critical role in the control
(FAS) or the Carnitine Palmitoyltransfer-
ase 1 (CPT-1) leads to a decrease in food
cally relevant satiety signal acting in the
sufficiently for survival, whereas restora-
tion of DA in the Nacc is not sufficient to
nists of DA receptor), sufficient to render
ful determinant of food intake. Ingestion
ulenin – another inhibitor of FAS – alter
particularly if the food is rich in sugar or
the expression profiles of feeding-related
comfort in depression or stressful states
contributes to weight loss. In vitro and in
vivo studies demonstrate that at least part
processes were termed ‘‘liking’’ and
‘‘wanting’’, respectively. With regard
5’-AMP kinase activator, rapidly lowers
(ACC), an established target of AMPK.
Collectively, these data suggest a role for
activate intracellular signaling pathways
Solitarius (NTS), the parabrachial nucle-
tially. Other circulating parameters like
firing rate of VTA DA neurons and i.c.v.
directly affect feeding behavior. In fact,
potential role of insulin in dopaminergic
greater desire for high-calorie foods.
over, i.c.v. leptin and insulin infusion or
dopamine cells and their projections into
regions involve in the rewarding aspect of
late DA neuron activity. The role of these
tions in brain circuits, other than those
regulate hunger and satiety, are involved
Leptin, insulin and ghrelin receptors are
while increasing level of ghrelin; each of
(i.c.v.) insulin administration increased
and eating behavior, thus it is premature
in response to an intravenous infusion of
tion (20 days) significantly increased D2
feeding behavior and leading to obesity.
typically a function of its fat and sugar
particularly lipids, could act directly on
tine/i.p. bromocriptine injection) partly
consistent with the fact that electrically
in mice that are inherent resistant to the
dently of weight gain, at the early stage
tion. In fact, animals consuming high fat
alter mesolimbic insulin action. In fact,
access to cafeteria diet decreased striatal
insulin-activated signaling kinase (Akt).
activation of striatal DA target regions in
suppose that nutritional lipids present in
(stimulated with pictures of high-calorie
striatal activation in response to palat-
rewarding and hedonic value of food.
associated with behavioral defaults like a
lipid levels and cognitive function is still
impaired acquisition in several cognitive
of food are closely tied to the release of
fore relay the action of TG-rich particle,
paradigms in normal body weight mice.
as well as by most other objects of desire
seen in obesity such as food reward lever
sory reward of fat is bypassed with i.p.
(NAc) and other limbic brain regions is a
of the author at the 2012 Journee of thegroup lipid nutrition. This work was
morphine) exert their effect; and thus this
projection is often referred to as the brain
‘‘reward circuit’’. Strong evidence indi-
‘‘Agence Nationale de la Recherche’’
neurons of the brain reward circuit which
effects of palatable food. Interestingly,
underlie key aspects of the addictive state
obesity prone rats still at normal weight
days of access to HF diet) had levels ofTG consistently higher in response to
tail both ‘‘homeostatic’’ inputs, arising
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SBCMS PRIMER ON BIOTERRORISM San Bernardino County Medical Society http://www.sbcms.org/bioterrorism/primer.htm Chemical Agents Reference Chart CHEMICAL SYMPTOMS TREATMENT S alivation. Atropine – initial dose 2 mg. Additional doses until symptoms resolved (will not reverse miosis). L acrimation. Pralidoxime Chloride – 1 gram IV over 20–30 minutes. U rination. Be
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