Long-term sucrose and glucose consumption decreases the δ-aminolevulinate dehydratase activity in mice

Brito, Verônica Bidinotto; Folmer, Vanderlei; Soares, Júlio César Mendes; Silveira, Ilson Dias da; Rocha, João Batista Teixeira da

doi:10.1016/j.nut.2007.08.002

Cited by 28 publications

(25 citation statements)

References 72 publications

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“…Thus, we believe that ALA-D activity increased due to its relation to oxidative stress, such as observed in this study. In addition, the alteration in the activity of ALA-D may interfere in hematopoiesis, since this enzyme participates in the synthesis of porphobilinogen, that catalysis two delta-aminolevulinate molecules, i.e., a precursor of heme group [6]. The hypothesis may corroborated to the hemolytic anemia observed during intoxication by aflatoxins, where a decreased in erythrocytes counts, hemoglobin content, leucopenia and bone marrow hyperplasia was evidenced [33].…”

Section: Discussionmentioning

confidence: 99%

The Protective Effects of an Adsorbent against Oxidative Stress in Quails Fed Aflatoxin-Contaminated Diet

Migliorini

Silva

Santúrio

et al. 2017

Acta Scientiae. Vet.

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Background: Contamination of crops with aflatoxin is considered a serious global threat to food safety, since potent carcinogenic, teratogenic, mutagenic and immunosuppressive effects of aflatoxins are well recognized. Recently, the use of adsorbents has been linked with protective effects against oxidative stress in several diseases. Thus, the aim of this study was to assess the occurrence of oxidative stress in quails (Coturnix coturnix) fed with aflatoxin-contaminated diet, as well as the protective effect of an adsorbent. Materials, Methods & Results: Twenty-eight quails were divided into four groups (n = 7): diet without additives (control; the group A), diet and adsorbent containing aluminosilicates (the group B), aflatoxin-contaminated diet (200 ppb) (the group C), and aflatoxin-contaminated diet (200 ppb) and adsorbent containing aluminosilicates (the group D). The composition of the adsorbent containing aluminosilicates was 0.3% based on yeast cell wall, silymarin, and bentonite. The animals received feed and water ad libitum during 20 days. At the end of the experimental period, total blood was collected by cardiac puncture in tubes without anticoagulant to obtain serum (centrifuged at 3500 g during 10 min) for later determination of biochemical parameters. The liver was placed in a solution of Tris-HCl 10 mM, pH 7.4 for TBARS (Thiobarbituric acid reactive substances), ROS (Reactive oxygen species), SOD (Superoxide dismutase) and CAT (Catalase) analysis. The hepatic tissue was gently homogenized in a glass potter in specific buffer, homogenated, and centrifuged at 10.000 g at 4ºC for 10 min to yield a supernatant (S1) used for analyses. Homogenate aliquots were stored at -80°C until utilization. Fragments of liver and intestine (5 cm) were collected for histopathological analyses. Between days 15 to 20 of the experiment, group C quails showed clinical signs, such as apathy, creepy feathers and reduced feed intake. At day 20 of experiment, macroscopically, the liver of quails belonging to the group C showed greenish yellow color differently from the other groups. Microscopically, no alterations were observed in the liver of animals in groups A and B. Severe diffuse microvacuolar degeneration (hydropic) of hepatocytes and small foci of necrosis in the liver were observed in the group C, as observed in the group D, but in a more moderate degree to microvacuolar degeneration. Seric total protein, albumin, globulin and uric acid levels decreased in the group C and D. The levels of alanine aminotransferase (ALT) increased in the group C, and the treatment with adsorbent was able to avoid this increment. Seric and hepatic reactive oxygen species and TBARS increased in the group C, and the treatment with adsorbent reduced theses parameters in the group D. Catalase (CAT) activity decreased, while ALA-D increased in the group C. The treatment with adsorbent was able to prevent CAT activity decrease, but it did not prevent the increase in ALA-D activity. Discussion: Aflatoxins are considered one of the mo...

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Section: Discussionmentioning

confidence: 99%

The Protective Effects of an Adsorbent against Oxidative Stress in Quails Fed Aflatoxin-Contaminated Diet

Migliorini

Silva

Santúrio

et al. 2017

Acta Scientiae. Vet.

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“…For example, these studies showed that high glucose consumption causes an increase in body weight and abdominal fat associated with an increased protein oxidation induced by hyperglycemia, and that carbohydrate-induced obesity is not dependent on the sweet taste of carbohydrates. 6,21,22 Another important mechanism through which the intake of carbohydrates and particularly a glucose intake may be regulated is through a modulation of the intestinal serotonergic system. Indeed, previous studies have indicated that intestinal 5-HT3R might be involved in the detection and control of carbohydrate intake, such as glucose.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, Spitzer and Rodin 5 found food intake to be increased in humans after a preload with glucose solution, whereas fructose solution had no such effect. Furthermore, Brito et al, 6 Lindqvist et al 7 and our own group 8 found that a chronic intake of glucose-sweetened drinking water, results in a significant increase in total caloric intake, body weight and abdominal fat index in rodents. Sclafani 9 reported a body weight gain, increased total caloric intake and a reduced chow intake in rats fed a 32% glucose solution in comparison with rats fed 32% glucose powder.…”

Section: Introductionmentioning

confidence: 85%

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

et al. 2009

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Objective: Sugar consumption has increased markedly over the last few decades and parallels the dramatic increase in overweight and obesity. Data obtained from animal studies suggest that the intestinal serotonergic system and herein particularly the serotonin receptor 3 (5-HT3R) may be involved in sugar detection and short-term control of food intake. Using a mouse model, we tested the hypothesis that blocking 5-HT3R prevents the development of sugar-induced obesity. Design: For 8 weeks, C57BL/J6 mice were offered either water containing 30% glucose or plain water in addition to normal chow. The effect of oral treatment with the 5-HT3R antagonist, tropisetron (0.2 mg kg À1 body weight), on body weight and caloric intake was studied. Results: Total caloric intake and weight gain were significantly increased in mice fed glucose compared with the control group. Tropisetron treatment reduced intestinal motility and almost completely blocked weight gain associated with glucose feeding; however, total caloric intake was not affected. The effect of tropisetron was not associated with a decreased expression of the intestinal and hepatic glucose transporters, SGLT1 (sodium-dependent glucose cotransporter) and Glut2 (glucose transporter 2); instead, the expression of these transporters was slightly increased by the 5-HT3R antagonist. However, expressions of carbohydrate responsive element binding protein and fatty acid synthase, as well as triglyceride levels in the liver were only enhanced in mice fed glucose, but remained unchanged at the level of the control group when mice were treated concomitantly with tropisetron. At the same time, b-hydroxybutyrate dehydrogenase mRNA expression and plasma levels of ketone bodies were significantly increased. Conclusion: Our results suggest that 5-HT3R is a new target for the modulation of hepatic glucose metabolism and for the prevention of obesity.

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“…The treatments were administered ad libitum in drinking water. The initial concentration dose of sucrose was based on Brito et al (2007) who induced hyperglycemia in mice by treating them with 10% sucrose for 60 days. We treated the animals for 60 days at this dose without any noticeable increases in the glucose level.…”

Section: Ethical Aspects Animals and Treatmentsmentioning

confidence: 99%

High consumption of sucrose induces DNA damage in male Wistar rats

Franke

Molz

Mai

et al. 2017

An. Acad. Bras. Ciênc.

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The purpose of this study was to determine the effects of the high consumption of sucrose on the levels of DNA damage in blood, hippocampus and bone marrow of rats. Male Wistar rats were treated for 4 months with sucrose (10% for 60 initial days and 34% for the following 60 days) in drinking water, and then, glycemia and glycated hemoglobin (A1C) were measured. Levels of DNA damage in blood and hippocampus were evaluated by the comet assay. The micronucleus test was used to evaluate chromosomal damages in the bone marrow. The sucrose treatment significantly increased (p<0.01) the serum glucose levels (~20%) and A1C (~60%). The level of primary DNA damage was significantly increased (p<0.05) in hippocampal cells (~60%) but not in peripheral blood leukocytes (p>0.05). Additionally, it was observed a significative increase (p<0.05) in the markers of chromosomal breaks/losses in bone marrow, as indicated by the micronucleus test. This is the first study that evaluated DNA damage induced by high sucrose concentration in the hippocampus and bone marrow of rats. Sucrose-induced DNA damage was observed in both tissues. However, the mechanism of sucrose toxicity on DNA remains unknown.

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Long-term sucrose and glucose consumption decreases the δ-aminolevulinate dehydratase activity in mice

Cited by 28 publications

References 72 publications

The Protective Effects of an Adsorbent against Oxidative Stress in Quails Fed Aflatoxin-Contaminated Diet

The Protective Effects of an Adsorbent against Oxidative Stress in Quails Fed Aflatoxin-Contaminated Diet

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

High consumption of sucrose induces DNA damage in male Wistar rats

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