Avaliação por microdiálise do efeito da ingestão de óleo de peixe sobre o teor de glicose no córtex pré-frontal de ratos
Data
2013
Autores
Sousa, Isy Faria de 
Orientadores
Ribeiro, Eliane Beraldi
Tipo
Dissertação de mestrado
Título da Revista
ISSN da Revista
Título de Volume
Resumo
A deteccao da glicose por neuronios do SNC contribui para a regulacao da homeostase energetica e do metabolismo. O cortex pre-frontal (PFC) participa do componente hedonico do controle da inGestão alimentar. Como o consumo de dietas hiperlipidicas pode prejudicar o balanco energetico, avaliamos neste estudo se o consumo de dieta enriquecida com oleo de peixe (fonte de acidos graxos poliinsaturados n-3) altera o teor extracelular de glicose no PFC bem como a resposta alimentar desencadeada pela injecao intracerebroventricular (i.c.v.) de glicose ou glicoprivacao no PFC. Apos 2 meses recebendo dieta controle ou hiperlipidica, ratos Wistar machos foram implantados com probe de microdialise no PFC. Coletaram-se 3 amostras basais de microdialisato e alimento foi oferecido por 30 min.; entao 8 amostras subsequentes foram coletadas. Outros grupos de animais controle e peixe foram implantados com duas canulas-guias, uma no PFC e outra no ventriculo cerebral lateral (VL). Injetou-se glicose (20 μg) i.c.v. ou veiculo e, 30 minutos depois, 2-desoxi-D-glicose (2-DG; 100 μg) ou veiculo no PFC. A inGestão de alimento foi medida apos 2, 12 e 24 horas. O peso corporal e dos depositos de gordura, assim como a insulinemia de jejum nao foram afetadas pela inGestão cronica de dieta hiperlipidica; no entanto houve elevacao da glicemia no grupo peixe. Os niveis basais de glicose nos microdialisatos do PFC foram similares entre os animais controles (207 ± 37 ng/10μl) e peixe (149 ± 26 ng/10 μl, p = 0.25), assim como a inGestão durante 30 minutos no experimento de microdialise (controle: 2.82 ± 0.37g; peixe: 3.20 ± 0.68g). A inGestão de alimento promoveu elevacao significante nos niveis de glicose no PFC, variando entre 26 a 34% acima dos valores basais no grupo controle e entre 36 a 64% no grupo peixe. O aumento foi mais proeminente e precoce nos animais alimentados com dieta peixe. A glicose injetada i.c.v. bem como a glicoprivacao no PFC inibiram a inGestão alimentar nos animais controle, mas nao nos animais do grupo peixe. Resumidamente, nossos resultados mostram que, apos a inGestão de alimento, maior quantidade de glicose alcanca o PFC de ratos alimentados com dieta hiperlipidica enriquecida com oleo de peixe. No entanto, quando administrada diretamente no VL, a glicose inibiu a inGestão apenas nos animais controles, assim como a glicoprivacao no PFC. Esses resultados indicam que, apesar do transporte de glicose para o SNC estar elevado no grupo peixe, um defeito na sinalizacao da glicose pode ser um disturbio relevante induzido pela inGestão cronica de dieta hiperlipidica enriquecida com oleo de peixe
It is suggested that glucose sensing in CNS areas may contribute to the regulation of energy homeostasis and metabolism. The prefrontal cortex (PFC) participates in the hedonic component of feeding control. As hyperlipidic diets may cause disturbances in energy homeostasis, we evaluated whether the consumption of highfat diet enriched with fish oil (source of n3 PUFAs) modified PFC glucose extracellular levels as well as the feeding response to intracerebroventricular glucose or to PFC glucoprivation. After 2 months on control or highfat diet, male Wistar rats were implanted with a microdialysis probe aimed at the PFC. After collection of 3 baseline microdialysate samples, a 30min meal was offered and 8 additional samples were collected. Other control and highfat animals were implanted with two guide cannulas aimed at the lateral cerebral ventricle and the PFC. Glucose (20 μg) was injected i.c.v., followed, 30min. later, by the injection of either 2deoxyDglucose (2DG, 100 μg) or vehicle into the PFC. Food intake was measured 2, 12, and 24 hours later. Body and fat pads weights as well as insulinemia were not affected while glycemia was elevated by the fish diet. Baseline levels of glucose in PFC microdialysates were similar between control (207 ± 37 ng/10μl) and fish rats (149 ± 26 ng/10 μl, p = 0.25) as were the acute 30min. intakes (control: 2.82 ± 0.37g; fish: 3.20 ± 0.68g). Food intake caused significant elevations of PFC glucose, of 26 to 34% above baseline in the control group and of 36 to 64% in the fish group. The increments occurred earlier after feeding initiation and were significantly more pronounced in the fish than in the control group. I.c.v. glucose induced significant feeding inhibition in the control but not in the fish group. Moreover, local PFC glucoprivation significantly reduced intake only in the control group. In summary, the present experiments have shown that, following food intake, more glucose reached the prefrontal cortex of the rats fed the hyperlipidic fish diet than of the rats fed the control diet. However, when administered directly into the lateral cerebral ventricle, glucose was able to inhibit feeding only in the control rats. Glucoprivation in the PFC inhibited feeding in the control but not in the fish group. The findings indicate that, rather than impairment of glucose transport into the CNS, a defect in glucose signaling may be a relevant disturbance induced by the fish diet.
It is suggested that glucose sensing in CNS areas may contribute to the regulation of energy homeostasis and metabolism. The prefrontal cortex (PFC) participates in the hedonic component of feeding control. As hyperlipidic diets may cause disturbances in energy homeostasis, we evaluated whether the consumption of highfat diet enriched with fish oil (source of n3 PUFAs) modified PFC glucose extracellular levels as well as the feeding response to intracerebroventricular glucose or to PFC glucoprivation. After 2 months on control or highfat diet, male Wistar rats were implanted with a microdialysis probe aimed at the PFC. After collection of 3 baseline microdialysate samples, a 30min meal was offered and 8 additional samples were collected. Other control and highfat animals were implanted with two guide cannulas aimed at the lateral cerebral ventricle and the PFC. Glucose (20 μg) was injected i.c.v., followed, 30min. later, by the injection of either 2deoxyDglucose (2DG, 100 μg) or vehicle into the PFC. Food intake was measured 2, 12, and 24 hours later. Body and fat pads weights as well as insulinemia were not affected while glycemia was elevated by the fish diet. Baseline levels of glucose in PFC microdialysates were similar between control (207 ± 37 ng/10μl) and fish rats (149 ± 26 ng/10 μl, p = 0.25) as were the acute 30min. intakes (control: 2.82 ± 0.37g; fish: 3.20 ± 0.68g). Food intake caused significant elevations of PFC glucose, of 26 to 34% above baseline in the control group and of 36 to 64% in the fish group. The increments occurred earlier after feeding initiation and were significantly more pronounced in the fish than in the control group. I.c.v. glucose induced significant feeding inhibition in the control but not in the fish group. Moreover, local PFC glucoprivation significantly reduced intake only in the control group. In summary, the present experiments have shown that, following food intake, more glucose reached the prefrontal cortex of the rats fed the hyperlipidic fish diet than of the rats fed the control diet. However, when administered directly into the lateral cerebral ventricle, glucose was able to inhibit feeding only in the control rats. Glucoprivation in the PFC inhibited feeding in the control but not in the fish group. The findings indicate that, rather than impairment of glucose transport into the CNS, a defect in glucose signaling may be a relevant disturbance induced by the fish diet.
Descrição
Citação
SOUSA, Isy Faria de. Avaliação por microdiálise do efeito da ingestão de óleo de peixe sobre o teor de glicose no córtex pré-frontal de ratos. 2013. 68 f. Dissertação (Mestrado em Nutrição) – Escola Paulista de Medicina, Universidade Federal de São Paulo. São Paulo, 2013.