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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 Abbott NJ, Ronnback L, Hansson E. Astrocyte- endothelial interactions at the blood-brain ute to the failure of obesity-prone rats to barrier. Nat Rev Neurosci 2006; 7: 41-53.
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