Gina Borghetti

Low fish oil intake improves insulin sensitivity, lipid profile and muscle metabolism on insulin resistant MSG-obese rats

BackgroundObesity is commonly associated with diabetes, cardiovascular diseases and cancer. The purpose of this study was to determinate the effect of a lower dose of fish oil supplementation on insulin sensitivity, lipid profile, and muscle metabolism in obese rats.MethodsMonosodium glutamate (MSG) (4 mg/g body weight) was injected in neonatal Wistar male rats. Three-month-old rats were divided in normal-weight control group (C), coconut fat-treated normal weight group (CO), fish oil-treated normal weight group (FO), obese control group (Ob), coconut fat-treated obese group (ObCO) and fish oil-treated obese group (ObFO). Obese insulin-resistant rats were supplemented with fish oil or coconut fat (1 g/kg/day) for 4 weeks. Insulin sensitivity, fasting blood biochemicals parameters, and skeletal muscle glucose metabolism were analyzed.ResultsObese animals (Ob) presented higher Index Lee and 2.5 fold epididymal and retroperitoneal adipose tissue than C. Insulin sensitivity test (Kitt) showed that fish oil supplementation was able to maintain insulin sensitivity of obese rats (ObFO) similar to C. There were no changes in glucose and HDL-cholesterol levels amongst groups. Yet, ObFO revealed lower levels of total cholesterol (TC; 30%) and triacylglycerol (TG; 33%) compared to Ob. Finally, since exposed to insulin, ObFO skeletal muscle revealed an increase of 10% in lactate production, 38% in glycogen synthesis and 39% in oxidation of glucose compared to Ob.ConclusionsLow dose of fish oil supplementation (1 g/kg/day) was able to reduce TC and TG levels, in addition to improved systemic and muscle insulin sensitivity. These results lend credence to the benefits of n-3 fatty acids upon the deleterious effects of insulin resistance mechanisms.

Interval training attenuates the metabolic disturbances in type 1 diabetes rat model

OBJECTIVE This study investigated the effect of interval training on blood biochemistry and immune parameters in type 1 diabetic rats. MATERIALS AND METHODS Male Wistar rats were divided into four groups: sedentary (SE, n = 15), interval training (IT, n = 17), diabetic sedentary (DSE, n = 17), diabetic interval training (DIT, n = 17). Diabetes was induced by i.v. injection of streptozotocin (60 mg/kg). Swimming Interval Training consisted of 30-s exercise with 30-s rest, for 30 minutes, during 6 weeks, four times a week, with an overload of 15% of body mass. Plasma glucose, lactate, triacylglycerol and total cholesterol concentrations, phagocytic capacity, cationic vesicle content, and superoxide anion and hydrogen peroxide production by blood neutrophils and peritoneal macrophages were evaluated. Proliferation of mesenteric lymphocytes was also estimated. RESULTS Interval training resulted in attenuation of the resting hyperglycemic state and decreased blood lipids in the DIT group. Diabetes increased the functionality of blood neutrophils and peritoneal macrophages in the DSE group. Interval training increased all functionality parameters of peritoneal macrophages in the IT group. Interval training also led to a twofold increase in the proliferation of mesenteric lymphocytes after 6 weeks of exercise in the DIT group. CONCLUSION Low-volume high-intensity physical exercise attenuates hyperglycemia and dislipidemia induced by type 1 diabetes, and induces changes in the functionality of innate and acquired immunity.

α-Linolenic Fatty Acid Supplementation Decreases Tumor Growth and Cachexia Parameters in Walker 256 Tumor-Bearing Rats

Fish oil (FO) has been shown to affect cancer cachexia, tumor mass, and immunity cell. n-3 PUFA, specifically α-linolenic fatty acid (ALA), has controversial effects. We investigated this in nontumor-bearing Wistar rats fed regular chow (C), fed regular chow and supplemented with FO or Oro Inca oil (OI), and Walker 256 tumor-bearing rats fed regular chow (W), fed regular chow and supplemented with FO (WFO) or OI (WOI). Rats were supplemented (1g/kg body weight/day) during 4 wk and then the groups tumor-bearing were inoculated with Walker 256 tumor cells suspension and 14 days later the animals were killed. WFO increased EPA fivefold and DHA 1.5-fold in the tumor tissue compared to W (P < 0.05). OI supplementation increased of threefold of ALA when compared to W (P < 0.05). Tumor mass in WFO and OI was of 2.3-fold lower, as well as tumor cell proliferation of 3.0-fold tumor tissue lipoperoxidation increased of 76.6% and cox-2 expression was 20% lower. Cachexia parameters were attenuate, blood glucose (25% higher), Triacylglycerolemia (50% lower), and plasma TNF-α (65% lower; P < 0.05) and IL-6 (62.5% lower). OI, rich in ALA, caused the same effect on cancer as those seen in FO.

Does Oil Rich in Alpha-Linolenic Fatty Acid Cause the Same Immune Modulation as Fish Oil in Walker 256 Tumor-Bearing Rats?

ABSTRACT Objective: Polyunsaturated fatty acids n-3 (PUFA n-3) have shown effects in reducing tumor growth, in particular eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) abundantly present in fish oil (FO). When these fatty acids are provided in the diet, they alter the functions of the cells, particularly in tumor and immune cells. However, the effects of α-linolenic fatty acid (ALA), which is the precursor of EPA and DHA, are controversial. Thus, our objective was to test the effect of this parental fatty acid. Methods: Non-tumor-bearing and tumor-bearing Wistar rats (70 days) were supplemented with 1 g/kg body weight of FO or Oro Inca® (OI) oil (rich in ALA). Immune cells function, proliferation, cytokine production, and subpopulation profile were evaluated. Results: We have shown that innate immune cells enhanced phagocytosis capacity, and increased processing and elimination of antigens. Moreover, there was a decrease in production of pro-inflammatory cytokines (tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6)) by macrophages. Lymphocytes showed decreased proliferation capacity, increased cluster of differentiation 8 (CD8+) subpopulation, and increased TNF-α production. Conclusions: Oil rich in ALA caused similar immune modulation in cancer when compared with FO.

Tumor growth reduction is regulated at the gene level in Walker 256 tumor-bearing rats supplemented with fish oil rich in EPA and DHA

We investigated the effect of fish oil (FO) supplementation on tumor growth, cyclooxygenase 2 (COX-2), peroxisome proliferator-activated receptor gamma (PPARγ), and RelA gene and protein expression in Walker 256 tumor-bearing rats. Male Wistar rats (70 days old) were fed with regular chow (group W) or chow supplemented with 1 g/kg body weight FO daily (group WFO) until they reached 100 days of age. Both groups were then inoculated with a suspension of Walker 256 ascitic tumor cells (3×107 cells/mL). After 14 days the rats were killed, total RNA was isolated from the tumor tissue, and relative mRNA expression was measured using the 2-ΔΔCT method. FO significantly decreased tumor growth (W=13.18±1.58 vs WFO=5.40±0.88 g, P<0.05). FO supplementation also resulted in a significant decrease in COX-2 (W=100.1±1.62 vs WFO=59.39±5.53, P<0.001) and PPARγ (W=100.4±1.04 vs WFO=88.22±1.46, P<0.05) protein expression. Relative mRNA expression was W=1.06±0.022 vs WFO=0.31±0.04 (P<0.001) for COX-2, W=1.08±0.02 vs WFO=0.52±0.08 (P<0.001) for PPARγ, and W=1.04±0.02 vs WFO=0.82±0.04 (P<0.05) for RelA. FO reduced tumor growth by attenuating inflammatory gene expression associated with carcinogenesis.

Exercício de força associado a óleo de peixe reduzem massa tumoral e caquexia em ratos

Objective: To investigate the effect of jump training associated with fish oil (FO) supplementation (1g/Kg bodyweight/day) on biochemical parameters of cachexia and tumor growth in Walker 256 tumor-bearing rats. Methods: Eighty rats were divided into sedentary nonand tumor-bearing (S and SW), exercised (EX and EXW), FO supplemented (SO and SWO), and both supplemented and exercised (EXW and EXWO). Jump training sessions consisted of 10 series of 30 seconds each, followed by 1 minute of rest. After six weeks of jump training, ascitic cells from Walker 256 tumor bearing-rat were inoculated, and after 15 days, all the animals were sacrificed. Results: The tumor mass in the SW group was 25.32 g, p<0.05 vs the SWO, EXW and EXWO groups (~11 g). The SW group presented hypoglycemia, hyperlactacidemia and hypertriacylglycerolemia and a reduction in body weight (-7.52 ± 3.19g), characterizing a state of cachexia. Supplementation with fish oil (SWO), exercise (EXW) and both (EXWO) prevented the onset of cachexia and promoted weight gain (p<0.05 vs SW), but less than that of the supplementation alone (p<0.05 vs SWO). In vitro cell proliferation of the tumor cells was lower in the SWO group (p<0.05 vs SW) and exercise reduced still further (p<0.05 vs. SW and SWO), with no increase when both therapies were applied together. Lipoperoxidation (p<0.05) was higher in the SWO, EXW, EXWO groups vs. S. Bcl-2 expression was also lower in these groups vs. SW. Conclusions: Jump training and fish oil supplementation alone were able to effectively prevent cachexia and reduce tumor growth, tumor cell proliferation, and Bcl-2 expression, but the combination of both did not promote any additive effect.OBJETIVO: Investigar o efeito do treinamento de salto associado a suplementacao com oleo de peixe (1g/kg peso corporal/dia) em ratos portadores do tumor de Walker 256, sobre parâmetros bioquimicos de caquexia e crescimento tumoral.METODOS: Oitenta Ratos foram divididos em sedentario sem ou com tumor (S ou SW), exercitado (EX ou EXW), suplementado com oleo de peixe (SO ou SWO) e suplementado e exercitado (EXO ou EXWO). Sessoes de treinamento de salto consistiram de 10 series com duracao de 30 segundos e intervalo de 1 minuto entre cada serie. Apos seis semanas de treinamento, celulas do tumor de Walker 256 foram inoculadas e apos 15 dias os animais foram mortos.RESULTADOS: O peso medio do tumor no grupo SW foi de 25,32 g, p<0,05 vs. ao dos SWO, EXW e EXWO (~11 g). O grupo SW apresentou hipoglicemia, hiperlactatemia, hipertriacilglicerolemia e perda de peso (-7,52±3,19g), caracterizando estado caquetico. Suplementacao com oleo de peixe (SWO), exercicio (EXW) e associacao de ambos (EXWO) impediram a instalacao da caquexia (p<0,05 vs. SW). No grupo SWO, EXW e suas associacoes (EXWO) promoveram ganho de peso (p<0,05 vs. SW), mas inferior ao da suplementacao isolada (p<0,05 vs. SWO). A proliferacao celular in vitro das celulas tumorais foi menor no grupo SWO (p<0,05 vs. SW) e o exercicio reduziu ainda mais (p<0,05 vs. SW e SWO), nao havendo incremento quando se associaram ambas as terapias. Lipoperoxidacao (p<0,05) foi maior nos SWO, EXW, EXWO vs. S. A expressao de Bcl-2 foi menor tambem nestes grupos vs. SW.CONCLUSOES: O treinamento de forca e a suplementacao com oleo de peixe foram eficazes em evitar a caquexia e induzir a reducao do crescimento tumoral, da proliferacao tumoral e expressao de Bcl-2, mas a associacao de ambos nao promoveu efeito aditivo.

Resistance exercise and fish oil reduce tumor mass and cachexia in rats

Objective: To investigate the effect of jump training associated with fish oil (FO) supplementation (1g/Kg bodyweight/day) on biochemical parameters of cachexia and tumor growth in Walker 256 tumor-bearing rats. Methods: Eighty rats were divided into sedentary nonand tumor-bearing (S and SW), exercised (EX and EXW), FO supplemented (SO and SWO), and both supplemented and exercised (EXW and EXWO). Jump training sessions consisted of 10 series of 30 seconds each, followed by 1 minute of rest. After six weeks of jump training, ascitic cells from Walker 256 tumor bearing-rat were inoculated, and after 15 days, all the animals were sacrificed. Results: The tumor mass in the SW group was 25.32 g, p<0.05 vs the SWO, EXW and EXWO groups (~11 g). The SW group presented hypoglycemia, hyperlactacidemia and hypertriacylglycerolemia and a reduction in body weight (-7.52 ± 3.19g), characterizing a state of cachexia. Supplementation with fish oil (SWO), exercise (EXW) and both (EXWO) prevented the onset of cachexia and promoted weight gain (p<0.05 vs SW), but less than that of the supplementation alone (p<0.05 vs SWO). In vitro cell proliferation of the tumor cells was lower in the SWO group (p<0.05 vs SW) and exercise reduced still further (p<0.05 vs. SW and SWO), with no increase when both therapies were applied together. Lipoperoxidation (p<0.05) was higher in the SWO, EXW, EXWO groups vs. S. Bcl-2 expression was also lower in these groups vs. SW. Conclusions: Jump training and fish oil supplementation alone were able to effectively prevent cachexia and reduce tumor growth, tumor cell proliferation, and Bcl-2 expression, but the combination of both did not promote any additive effect.OBJETIVO: Investigar o efeito do treinamento de salto associado a suplementacao com oleo de peixe (1g/kg peso corporal/dia) em ratos portadores do tumor de Walker 256, sobre parâmetros bioquimicos de caquexia e crescimento tumoral.METODOS: Oitenta Ratos foram divididos em sedentario sem ou com tumor (S ou SW), exercitado (EX ou EXW), suplementado com oleo de peixe (SO ou SWO) e suplementado e exercitado (EXO ou EXWO). Sessoes de treinamento de salto consistiram de 10 series com duracao de 30 segundos e intervalo de 1 minuto entre cada serie. Apos seis semanas de treinamento, celulas do tumor de Walker 256 foram inoculadas e apos 15 dias os animais foram mortos.RESULTADOS: O peso medio do tumor no grupo SW foi de 25,32 g, p<0,05 vs. ao dos SWO, EXW e EXWO (~11 g). O grupo SW apresentou hipoglicemia, hiperlactatemia, hipertriacilglicerolemia e perda de peso (-7,52±3,19g), caracterizando estado caquetico. Suplementacao com oleo de peixe (SWO), exercicio (EXW) e associacao de ambos (EXWO) impediram a instalacao da caquexia (p<0,05 vs. SW). No grupo SWO, EXW e suas associacoes (EXWO) promoveram ganho de peso (p<0,05 vs. SW), mas inferior ao da suplementacao isolada (p<0,05 vs. SWO). A proliferacao celular in vitro das celulas tumorais foi menor no grupo SWO (p<0,05 vs. SW) e o exercicio reduziu ainda mais (p<0,05 vs. SW e SWO), nao havendo incremento quando se associaram ambas as terapias. Lipoperoxidacao (p<0,05) foi maior nos SWO, EXW, EXWO vs. S. A expressao de Bcl-2 foi menor tambem nestes grupos vs. SW.CONCLUSOES: O treinamento de forca e a suplementacao com oleo de peixe foram eficazes em evitar a caquexia e induzir a reducao do crescimento tumoral, da proliferacao tumoral e expressao de Bcl-2, mas a associacao de ambos nao promoveu efeito aditivo.

Ejercicio de fuerza asociado a aceite de pescado reduce la masa tumoral y la caquexia en ratas

Objective: To investigate the effect of jump training associated with fish oil (FO) supplementation (1g/Kg bodyweight/day) on biochemical parameters of cachexia and tumor growth in Walker 256 tumor-bearing rats. Methods: Eighty rats were divided into sedentary nonand tumor-bearing (S and SW), exercised (EX and EXW), FO supplemented (SO and SWO), and both supplemented and exercised (EXW and EXWO). Jump training sessions consisted of 10 series of 30 seconds each, followed by 1 minute of rest. After six weeks of jump training, ascitic cells from Walker 256 tumor bearing-rat were inoculated, and after 15 days, all the animals were sacrificed. Results: The tumor mass in the SW group was 25.32 g, p<0.05 vs the SWO, EXW and EXWO groups (~11 g). The SW group presented hypoglycemia, hyperlactacidemia and hypertriacylglycerolemia and a reduction in body weight (-7.52 ± 3.19g), characterizing a state of cachexia. Supplementation with fish oil (SWO), exercise (EXW) and both (EXWO) prevented the onset of cachexia and promoted weight gain (p<0.05 vs SW), but less than that of the supplementation alone (p<0.05 vs SWO). In vitro cell proliferation of the tumor cells was lower in the SWO group (p<0.05 vs SW) and exercise reduced still further (p<0.05 vs. SW and SWO), with no increase when both therapies were applied together. Lipoperoxidation (p<0.05) was higher in the SWO, EXW, EXWO groups vs. S. Bcl-2 expression was also lower in these groups vs. SW. Conclusions: Jump training and fish oil supplementation alone were able to effectively prevent cachexia and reduce tumor growth, tumor cell proliferation, and Bcl-2 expression, but the combination of both did not promote any additive effect.OBJETIVO: Investigar o efeito do treinamento de salto associado a suplementacao com oleo de peixe (1g/kg peso corporal/dia) em ratos portadores do tumor de Walker 256, sobre parâmetros bioquimicos de caquexia e crescimento tumoral.METODOS: Oitenta Ratos foram divididos em sedentario sem ou com tumor (S ou SW), exercitado (EX ou EXW), suplementado com oleo de peixe (SO ou SWO) e suplementado e exercitado (EXO ou EXWO). Sessoes de treinamento de salto consistiram de 10 series com duracao de 30 segundos e intervalo de 1 minuto entre cada serie. Apos seis semanas de treinamento, celulas do tumor de Walker 256 foram inoculadas e apos 15 dias os animais foram mortos.RESULTADOS: O peso medio do tumor no grupo SW foi de 25,32 g, p<0,05 vs. ao dos SWO, EXW e EXWO (~11 g). O grupo SW apresentou hipoglicemia, hiperlactatemia, hipertriacilglicerolemia e perda de peso (-7,52±3,19g), caracterizando estado caquetico. Suplementacao com oleo de peixe (SWO), exercicio (EXW) e associacao de ambos (EXWO) impediram a instalacao da caquexia (p<0,05 vs. SW). No grupo SWO, EXW e suas associacoes (EXWO) promoveram ganho de peso (p<0,05 vs. SW), mas inferior ao da suplementacao isolada (p<0,05 vs. SWO). A proliferacao celular in vitro das celulas tumorais foi menor no grupo SWO (p<0,05 vs. SW) e o exercicio reduziu ainda mais (p<0,05 vs. SW e SWO), nao havendo incremento quando se associaram ambas as terapias. Lipoperoxidacao (p<0,05) foi maior nos SWO, EXW, EXWO vs. S. A expressao de Bcl-2 foi menor tambem nestes grupos vs. SW.CONCLUSOES: O treinamento de forca e a suplementacao com oleo de peixe foram eficazes em evitar a caquexia e induzir a reducao do crescimento tumoral, da proliferacao tumoral e expressao de Bcl-2, mas a associacao de ambos nao promoveu efeito aditivo.