Respostas metabólicas à suplementação com frutose em exercício de força de membros inferiores Metabolic responses to fructose supplementation in strength exercise of lower limbs

A frutose, por seu metabolismo independente da insulina, realiza significativas alterações no metabolismo hepático, promovendo um entorno metabólico favorável ao metabolismo tanto da glicose como dos lipídios, durante o exercício. Essa condição tem sido bastante estudada em exercício de endurance; no entanto, nenhum estudo sobre a suplementação com frutose no exercício de força (EF) foi encontrado. O objetivo do presente estudo foi avaliar os efeitos agudos da adição de frutose a um suplemento de glicose sobre o metabolismo de lipídios em EF. Vinte homens treinados ingeriram suplemento de glicose (G) ou glicose mais frutose (G+F), 15 minutos antes de realizar exercício de força (10 séries de 10 repetições). Os sujeitos foram testados em ordem randômica em um desenho cruzado e com uma semana de intervalo em duas condições experimentais: EF+(G) e EF+(G+F). A análise dos resultados mostrou que os valores de triglicérides durante o exercício foram maiores (p < 0,05) quando os sujeitos foram suplementados com G+F do que quando suplementados apenas com G. Ao final do exercício, os valores de ácidos graxos livres foram maiores quando os sujeitos foram suplementados G+F (p < 0,05). A glicemia foi menor durante o exercício e maior na recuperação (p < 0,05) para essa condição. O comportamento da insulina não diferiu entre os experimentos durante o exercício de força (p > 0,05), mas foi maior em G+F que em G (p < 0,05) durante a recuperação. A percepção subjetiva de esforço (PSE) foi menor (p < 0,05) para a suplementação com G+F do que com G. Em conclusão, a suplementação com G+F afeta positivamente o metabolismo de lipídios durante o exercício de força e favorece seu metabolismo imediatamente após o esforço, proporcionando condição metabólica que reflete em uma condição que afeta favoravelmente a PSE.<br>Due to its insulin-independent metabolism, fructose promotes significant changes in liver metabolism, promoting a metabolic surrounding favorable to the glucose as well as lipids metabolism during the exercise. This condition has been widely studied in endurance exercises; however, none study about fructose supplementation in strength exercise (SE) was found. This study aimed to assess the acute effects of the fructose addition to a glucose supplement on lipid metabolism in strength exercise. Twenty trained male subjects ingested a glucose (G) or glucose plus fuctose (G+F) supplement, 15 minutes before practicing a strength exercise (10 sets of 10 repetitions). The subjects were tested randomly in a crossover design and with a week of pause in two experimental conditions: SE+(G) and SE+(G+F). The analysis of the results showed that values of triglycerides during the exercise were higher (p < 0.05) when the subjects were supplemented with G+F than when they were supplemented only with G. By the end of the exercise the values of free fatty acid were higher when in G+F (p < 0.05). Glycemia was lower during the exercise and higher in the recovery (p < 0.05) in this condition. Insulin values did not differ among the experiments during strength exercises (p > 0.05), but they were higher in G+F than in G (p < 0.05) during recovery. Perceived exertion (PE) was lower (p < 0.05) in G+F than in G. It can be concluded that the G+F supplementation positively affects the lipid metabolism during the strength exercise and favors its metabolism immediately after the effort, promoting a metabolic condition that reflects on a condition that favorably affects the PE

Mouse hypothalamic GT1-7 cells demonstrate AMPK-dependent intrinsic glucose-sensing behaviour

Aims/hypothesis: Hypothalamic glucose-excited (GE) neurons contribute to whole-body glucose homeostasis and participate in the detection of hypoglycaemia. This system appears defective in type 1 diabetes, in which hypoglycaemia commonly occurs. Unfortunately, it is at present unclear which molecular components required for glucose sensing are produced in individual neurons and how these are functionally linked. We used the GT1-7 mouse hypothalamic cell line to address these issues. Methods: Electrophysiological recordings, coupled with measurements of gene expression and protein levels and activity, were made from unmodified GT1-7 cells and cells in which AMP-activated protein kinase (AMPK) catalytic subunit gene expression and activity were reduced. Results: Hypothalamic GT1-7 neurons express the genes encoding glucokinase and ATP-sensitive K+ channel (KATP) subunits K ir 6.2 and Sur1 and exhibit GE-type glucose-sensing behaviour. Lowered extracellular glucose concentration hyperpolarised the cells in a concentration-dependent manner, an outcome that was reversed by tolbutamide. Inhibition of glucose uptake or metabolism hyperpolarised cells, showing that energy metabolism is required to maintain their resting membrane potential. Short hairpin (sh)RNA directed to Ampk&alpha;2 (also known as Prkaa2) reduced GT1-7 cell AMPK&alpha;2, but not AMPK&alpha;1, activity and lowered the threshold for hypoglycaemia-induced hyperpolarisation. shAmpk&alpha;1 (also known as Prkaa1) had no effect on glucose-sensing or AMPK&alpha;2 activity. Decreased uncoupling protein 2 (Ucp2) mRNA was detected in AMPK&alpha;2-reduced cells, suggesting that AMPK&alpha;2 regulates UCP2 levels. Conclusions/interpretation: We have demonstrated that GT1-7 cells closely mimic GE neuron glucose-sensing behaviour, and reducing AMPK&alpha;2 blunts their responsiveness to hypoglycaemic challenge, possibly by altering UCP2 activity. These results show that suppression of AMPK&alpha;2 activity inhibits normal glucose-sensing behaviour and may contribute to defective detection of hypoglycaemia