High-fat diet alters the dopamine and opioid systems: effects across development
The risk for obesity is significantly increased when a person eats a calorically dense, high-fat diet. The negative health consequences of obesity are well described, and include increased risk for diabetes, cardiovascular disease, dyslipidemia, high blood pres- sure, and joint and sleep problems. More recently, adverse effects on the brain and behavior have been documented, which will be the focus of the present review, specifically how consumption of a high-fat diet during different developmental time periods can affect the function of the reward system in the central nervous system (CNS).
The mesocorticolimbic reward circuitry refers to a series of interconnected brain regions that is activated by rewarding stimuli, including both natural rewards such as palatable foods or social interaction, as well as by drugs of abuse, such as cocaine or heroin. Typically, this circuitry refers to cells located within the midbrain structure of the ventral tegmental area, which project to forebrain structures, including the ventral striatum (nucleus accumbens) and the prefrontal cortex, with important contribu- tions from the amygdala and certain hypothalamic structures as well (for example, orexin in the lateral hypothalamus). Dopamine (DA) is present in concentrated cell groups in the midbrain and to a lesser extent in the hypothalamus and olfactory bulbs. There are four primary DA pathways: the mesolimbic, mesocortical, nigros- triatal and tuberoinfundibular pathways. DA projections from the ventral tegmental area to prefrontal cortex (mesocortical) and nucleus accumbens and amygdala (mesolimbic) projections have been implicated in reward and incentive motivation by natural and pharmacological reinforcers,1,2 novelty-seeking behavior3 and locomotor activity.4 Hypothalamic DA has an important role in neuroendocrine functions, particularly prolactin secretion,5 and is known to regulate food intake.6,7 The nigrostriatal pathway (damaged in Parkinson’s disease) is critical for the generation of movement. There are currently five known DA receptors, all of
which are G-protein-coupled receptors. The D1-like family includes D1 and D5, which are coupled to Gas and are considered stimulatory receptors. The D2-like family, D2, D3 and D4, is coupled to Gai, with D2 acting both presynaptically as an autoreceptor and postsynaptically. The primary site of expression of D1 and D2 receptors is the striatum,8 but both receptor subtypes have also been localized to the hypothalamus and prefrontal cortex.9 DA uptake is facilitated by two transporters: vesicular monoamine transporter and, more specifically, the DA transporter (DAT), which clears DA from the synapse. Other important molecules related to dopaminergic function include DA- and cyclic AMP-regulated phosphoprotein (DARPP-32), a signaling molecule that acts downstream of both D1 and D2 receptors, and catechol-O-methyl transferase, an enzyme found in the synaptic cleft that degrades DA.
In addition to the DA system, opioids are also critical for encoding the rewarding properties of a stimulus.10,11 The opioid system has three endogenous ligands, encoded by precursors such as preproenkephalin (PENK), prodynorphin and pro-opiome- lanocortin. Similarly, there are three endogenous opioid receptors, delta, kappa and mu. With regard to consumption of a high-fat diet, PENK and m-opioid receptor (MOR) have been implicated as critical factors. Direct stimulation of the MOR by an agonist, such as PENK, specifically stimulates the consumption of high-fat food.
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