Effect of stabilized rice bran-added high sucrose diet on glucose control in C57BL/6 mice / 한국영양학회지

PURPOSE: Rice bran is a byproduct of the hulling of rice and contains a variety of bioactive components. Various studies have reported on the antioxidative, anticancer, immune-enhancing, and hypocholesterolemic effects of rice bran. However, few studies about the physiological activity of stabilized rice bran supplement on dietary intake of sugars is limited. The aim of this study was to investigate the effect of stabilized rice bran supplement on blood glucose in C57BL/6 mice fed a high sucrose diet. METHODS: Animals were randomly divided into three groups respectively, and were fed a normal diet (ND group), a high sucrose diet (HSD group) or a high sucrose diet containing 20% stabilized rice bran (HSD-SRB group) for 12 weeks. RESULTS: In the oral glucose tolerance test (OGTT), after seven weeks of feeding on the experimental diets, a significantly lower result was observed for HSD-SRB than for HSD at 30 and 60 minutes after oral administration in glucose solution (2 g/kg body weight). The incremental area under the curve (IAUC) of HSD-SRB was significantly lower than that of HSD. After 12 weeks, fasting blood glucose level of HSD-SRB was significantly lower than that of HSD. No significant difference in the serum insulin level was observed between HSD and HSD-SRB. However, HOMA-IR was significantly decreased in HSD-SRB compared to HSD. In addition, HOMA beta-cell was significantly increased in HSD-SRB com-pared to HSD. Triglyceride in liver of HSD-SRB was significantly lower than that of HSD. CONCLUSIONS: Feeding diets con-taining 20% rice bran improved insulin resistance and insulin secretion by decreasing triglyceride in liver. Thus, rice bran has a positive effect on glycemic control. In addition, the results are expected to be utilized as a basis for human study and development of food products with added rice bran.

Agonistas PPAR (Rosiglitazona, Bezafibrato e Fenofibrato) e alterações bioquímicas e estruturais em órgãos-alvo de camundongos C57BL/6 alimentados com dieta hiperlipídica rica em sacarose / PPAR agonists (Rosiglitazone, Bezafibrate and Fenofibrate) and biochemical and structural alterations in organs target of C57BL/6 mice fed high-fat high sucrose chow

Este trabalho teve o objetivo de estudar o efeito de medicamentos com diferentes ações agonista PPAR (rosiglitazona, fenofibrato e bezafibrato) sobre o perfil lipídico, glicídico e alterações na massa corporal e morfologia do tecido adiposo e pancreático em modelo de diabetes e sobrepeso induzido por dieta. Camundongos C57BL/6 (2 meses de idade) foram alimentados com dieta padrão (SC, n=10) ou dieta hiperlipídica rica em sacarose (HFHS, n=40) por 6 semanas. Logo após, os animais HFHS foram subdividos em: HFHS não tratado e HFHS tratado com rosiglitazona (HFHS-Ro), fenofibrato (HFHS-Fe) ou bezafibrato (HFHS-BZ) (5 semanas). Os camundongos alimentados com dieta HFHS apresentaram maior glicemia e insulina de jejum (+33% e +138%, respectivamente), intolerância à glicose, resistência à insulina, aumento da massa corporal (MC) (+20%) e adiposidade, hipertrofia de adipócitos e redução da imunocoloração para adiponectina no tecido adiposo. No pâncreas houve aumento da massa (+28%), acúmulo de gordura (+700%), hipertrofia da ilhota (+38%) e redução da imunocoloração para GLUT-2 (-60%). A rosiglitazona diminuiu a glicemia e insulina de jejum, porém induziu o ganho de MC e hipertrofia cardíaca. O fenofibrato estabilizou a MC, enquanto o bezafibrato levou a perda de MC. Apenas o bezafibrato impediu a hipertrofia da ilhota. A imunocoloração para GLUT-2 foi aumentada por todos os medicamentos, e não houve alterações na imunocoloração para o PPARalfa. Sinais morfológicos de pancreatite foram vistos no grupo HFHS-Fe, apesar dos níveis normais de amilase e lipase séricos. A rosiglitazona exacerbou a infiltração intrapancreática de gordura (+75% vs. HFHS), e o bezafibrato aumentou a imunocoloração para o PPARbeta/delta nas ilhotas pancreáticas. Em conclusão, o bezafibrato apresentou um efeito mais amplo sobre as alterações metabólicas, morfológicas e biométricas decorrentes da dieta HFHS, sugerindo que a inibição das três isoformas do PPAR seria melhor do que a inibição...

This work aimed to evaluate the effect of peroxisome proliferator-activated receptor (PPAR) agonists (rosiglitazone, fenofibrate and bezafibrate) on lipid and glucose metabolism, body mass, and adipose and pancreatic tissue morphology in a model of diet-induced type 2 diabetes and overweight in mice. Two-month-old male C57BL/6 mice were fed a standard chow (SC, n=10) or a high-fat high-sucrose chow (HFHS, n=40) for 6 weeks, and then HFHS-fed mice were subdivided by treatment: untreated HFHS and HFHS treated with rosiglitazone (HFHS-Ro), fenofibrate (HFHS-Fe), or bezafibrate (HFHS-Bz) (5 weeks on medication). HFHS-fed mice have altered fasting glucose (+33%) and insulin (+138%), GI, IR, increased body mass (+20%) and fat pad weight, adipocyte hypertrophy, and decreased adiponectin immunostain. They also presented increased pancreatic (+28%) mass, intrapancreatic fat (+700%), islet hypertrophy (+38%), and decreased GLUT-2 immunostain (-60%). Rosiglitazone reduced fasting glucose and insulin but induced weight gain and heart hypertrophy. Fenofibrate impaired body mass gain, while bezafibrate induced weight loss. Only bezafibrate impaired islet hypertrophy. GLUT-2 immunostain was improved by all treatments, and there were no alterations in PPAR-alfa stain. There were morphological signs of pancreatitis in fenofibrate-treated mice, although there was no alteration in serum amylase and lipase. Rosiglitazone exacerbated pancreatic fat infiltration (+75% vs. HFHS group), and bezafibrate increased PPAR-beta expression in pancreatic islets. In conclusion, bezafibrate showed a wider range of action on metabolic, morphologic, and biometric alterations due to HFHS intake, suggesting that inhibiting the three PPAR isoforms is better than inhititing each isoform alone. Rosiglitazone exacerbated body mass gain, pancreatic fat infiltration and induced heart hyperthophy as well, thus, precaution has to be taken in prescribing rosiglitazone to obese patients.

Differential Effects of High-carbohydrate and High-fat Diet Composition on Muscle Insulin Resistance in Rats

This study was conducted to evaluate whether the composition of carbohydrate or fat diet affects insulin resistance by measuring the muscle glucose transport rate. Both high-sucrose and high-starch diet with or without high-fat decreased insulin-stimulated glucose transport, but there were no significant differences among groups. Calorie intake in both high-sucrose and high-starch diet groups was higher than in chow group. The high-fat high-sucrose diet induced decrease in insulin-stimulated glucose transport was partially improved by supplement with fish oil. Calorie intake in high-fat high-sucrose and fish oil supplemented groups was higher than in chow group. The decreased insulin-stimulated glucose transport was accompanied by the increase in visceral fat mass, plasma triglyceride and insulin levels. These changes were improved by the supplement with fish oil. These results demonstrate that the composition of fat in diet is clearly instrumental in the induction of muscle insulin resistance. However, in high carbohydrate diet, it is likely that the amount of calorie intake may be a more important factor in causing insulin resistance than the composition of carbohydrate. Thus, the compositions of carbohydrate and fat in diet differentially affect on muscle insulin resistance.

Combination of high fat-hgih sucrose diet and chronic stress promotes insulin resistance in rats / 中国药科大学学报

Aim: To observe the influence of high fat-high sucrose diet and chronic stress on insulin resistance. Methods: Male rats were divided into four groups: control, high fat-high sucrose diet( HFSD), chronic stress( CS), high fat-high sucrose diet plus chronic stress( HFSD + CS). After feeding the animals for 10 weeks, fat, glucose and insulin concentrations in blood and PPAR-α mRNA expression in liver were examined, and glu-cose infusion rate was detected by a hyperinsulinemic euglycemic clamp experiment. Results: Insulin resistance was observed in all three treated groups, showing the highest in the HFSD + CS group. Dyslipidemia, hypergly-cosemia, hyperinsulinism and the decrease of PPAR-α mRNA expression in liver were also shown in all treated groups. There was an obvious interaction of insulin resistance, hyperglycosemia and high FFA between high fat-high sucrose diet and chronic stress. Conclusion: Combination of high fat-high sucrose diet and chronic stress could promote the development of insulin resistance, which is likely due to the high level of serum FFA.

Functional Studies of Acyl-CoA Synthetase 4 in the Rat Liver

Acyl-CoA synthetase 4 (ACS4) is an arachidonate-preferring enzyme abundant in steroidogenic tissues. We examined ACS4 in rat liver, which contains a variety of pathways that use acyl-CoAs, in order to determine subcellular locations. We demonstrate that ACS4 protein was present most abundantly in the mitochondria and to a much lesser extent in the peroxisomes and microsomes. To determined the dietary effects on the level of ACS4 mRNA, northern blotting was carried out using total RNA from the livers of adult male rats fed various diets. Fasting, high fat diet, and fat-free high sucrose diet increased the hepatic level of ACS4 mRNA approximately 2-fold. Furthermore, the levels of ACS4 mRNA were induced by DEHP[Di- (2-ethylhexyl) phthalate]. These data suggest that ACS4 expression in the liver is regulated with a variety of pathways, including beta-oxidation, hormone, and insulin.