Abstract
BackgroundBrain glucose sensing may contribute to energy homeostasis control. The prefrontal cortex (PFC) participates in the hedonic component of feeding control. As high-fat diets may disrupt energy homeostasis, we evaluated in male Wistar rats whether intake of high-fat fish-oil diet modified cortical glucose extracellular levels and the feeding induced by intracerebroventricular glucose or PFC glucoprivation.MethodsGlucose levels in PFC microdialysates were measured before and after a 30-min meal. Food intake was measured in animals receiving intracerebroventricular glucose followed, 30-min. later, by 2-deoxy-D-glucose injected into the PFC.ResultsThe fish-oil group showed normal body weight and serum insulin while fat pads weight and glucose levels were increased. Baseline PFC glucose and 30-min. carbohydrates intake were similar between the groups. Feeding-induced PFC glucose levels increased earlier and more pronouncedly in fish-oil than in control rats. Intracerebroventricular glucose inhibited feeding consistently in the control but not in the fish-oil group. Local PFC glucoprivation with 2-DG attenuated glucose-induced hypophagia.ConclusionsThe present experiments have shown that, following food intake, more glucose reached the prefrontal cortex of the rats fed the high-fat fish-oil diet than of the rats fed the control diet. However, when administered directly into the lateral cerebral ventricle, glucose was able to consistently inhibit feeding only in the control rats. The findings indicate that, an impairment of glucose transport into the brain does not contribute to the disturbances induced by the high-fat fish-oil feeding.
Highlights
Brain glucose sensing may contribute to energy homeostasis control
White fat mass and fasting serum glucose and insulin No significant difference was observed between the groups on body weight (p = 0.3838) while white fat mass was higher in the fish-oil group than in the control group (p = 0.0005)
The levels of glucose were significantly higher in fish-oil than in control rats (p = 0.016) while insulin levels were similar between the groups (Table 1)
Summary
Brain glucose sensing may contribute to energy homeostasis control. The prefrontal cortex (PFC) participates in the hedonic component of feeding control. The homeostatic control of energy homeostasis operates through peripheral signals integrated at the central nervous system (CNS), which modulates the activity of hypothalamic anabolic and catabolic neurons [1]. Glucose has been shown to modify the activity of both glucose-excited and glucose-inhibited neurons, whose existence has been demonstrated in the hypothalamus and mesocorticolimbic structures [13,14]. Glucose signaling at these areas has been attributed a potential role as an acute satiety factor and as a long-term feeding regulator [15]
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