Metabolic and Histopathological Effects of Fructose Intake During Pregestation, Gestation and Lactation in Rats and their Offspring

AbstractCyanobacteria are important members of lake plankton, but they have the ability to form blooms and produce cyanotoxins and thus cause a number of adverse effects. Freshwater ecosystems around the world have been investigated for the distribution of cyanobacteria and their toxins and the effects they have on the ecosystems. Similar research was performed on the Fehérvárcsurgó reservoir in Hungary during 2018. Cyanobacteria were present and blooming, and the highest abundance was recorded in July (2,822,000 cells/mL). The species present were Aphanizomenon flos-aquae, Microcystis flos-aquae, Microcystis wesenbergii, Cuspidothrix issatschenkoi, Dolichospermum flos-aquae, and Snowella litoralis. In July and September, the microcystin encoding gene mcyE and the saxitoxin encoding gene sxtG were amplified in the biomass samples. While a low concentration of microcystin-RR was found in one water sample from July, analyses of Abramis brama and Carassius gibelio caught from the reservoir did not show the presence of the investigated microcystins in the fish tissue. However, several histopathological changes, predominantly in gills and kidneys, were observed in the fish, and the damage was more severe during May and especially July, which coincides with the increase in cyanobacterial biomass during the summer months. Cyanobacteria may thus have adverse effects in this ecosystem.

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Fructose reprogrammes glutamine-dependent oxidative metabolism to support LPS-induced inflammation

Nature Communications ◽

10.1038/s41467-021-21461-4 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Nicholas Jones ◽

Julianna Blagih ◽

Fabio Zani ◽

April Rees ◽

David G. Hill ◽

...

Keyword(s):

Oxidative Metabolism ◽

Mononuclear Phagocytes ◽

Alcoholic Fatty Liver ◽

Lps Challenge ◽

Fructose Intake ◽

Mouse Macrophages ◽

Dietary Fructose ◽

Monocytes And Macrophages ◽

Developed World

AbstractFructose intake has increased substantially throughout the developed world and is associated with obesity, type 2 diabetes and non-alcoholic fatty liver disease. Currently, our understanding of the metabolic and mechanistic implications for immune cells, such as monocytes and macrophages, exposed to elevated levels of dietary fructose is limited. Here, we show that fructose reprograms cellular metabolic pathways to favour glutaminolysis and oxidative metabolism, which are required to support increased inflammatory cytokine production in both LPS-treated human monocytes and mouse macrophages. A fructose-dependent increase in mTORC1 activity drives translation of pro-inflammatory cytokines in response to LPS. LPS-stimulated monocytes treated with fructose rely heavily on oxidative metabolism and have reduced flexibility in response to both glycolytic and mitochondrial inhibition, suggesting glycolysis and oxidative metabolism are inextricably coupled in these cells. The physiological implications of fructose exposure are demonstrated in a model of LPS-induced systemic inflammation, with mice exposed to fructose having increased levels of circulating IL-1β after LPS challenge. Taken together, our work underpins a pro-inflammatory role for dietary fructose in LPS-stimulated mononuclear phagocytes which occurs at the expense of metabolic flexibility.

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Biochemical and histopathological effects of low dose vanadium in the healing of acetic acid-induced colitis in male wistar rats

Journal of Basic and Clinical Physiology and Pharmacology ◽

10.1515/jbcpp-2020-0246 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Tosan Peter Omayone ◽

Samuel Babafemi Olaleye

Keyword(s):

Acetic Acid ◽

Untreated Control ◽

Wistar Rats ◽

Low Dose ◽

Healing Process ◽

Beneficial Effects ◽

Male Wistar Rats ◽

Haematological Changes ◽

Therapeutic Properties ◽

Histopathological Effects

Abstract Objectives Vanadium has been reported to possess relevant therapeutic properties such as anti-diabetic and anti-tumoral. This study aimed at determining the effects of vanadium on experimentally induced colitis in rats. Methods Forty-five male Wistar rats (103 ± 3.90 g, n=15) were used for this study and were divided into three groups. Group 1 (Untreated control) had nothing added to their drinking, while groups 2 and 3 received sodium metavanadate at a dose of 50 and 200 mg/L respectively in their drinking water for 10 weeks. Colitis was thereafter induced by intra colonic administration of 1.50 mL of 6% acetic acid. Animals were sacrificed on day 0 (pre-induction), three- and seven-days post induction. Blood samples were collected for haematological variables and the distal 8 cm of the colon was collected for macroscopic, histological and biochemical (malondialdehyde-MDA, superoxide dismutase-SOD, catalase-CAT, glutathione peroxidase- GPx and nitrite concentration- NO) assessment. Results Low dose vanadium proved beneficial in ameliorating acetic acid-induced colitis by improving both histopathological and haematological changes. Gross observation showed a faster healing rate in vanadium treated groups (50 and 200 mg/L) compared with untreated control at day 3 (40 and 26.20 vs. 2.50%) and day 7 (80 and 66.70 vs. 42%) respectively. Vanadium also appears to exert its beneficial effects on acetic acid-induced colitis via up regulation of antioxidant enzymes (SOD, CAT, GPx) and NO while decreasing the over production of MDA. Conclusions Vanadium at small concentration functions as an essential trace element and may be able to promote healing process during ulcerative colitis.

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Morpho-molecular identification of Heterophyes heterophyes encysted metacercariae and its immunological and histopathological effects on farmed Mugil cephalus in Egypt

Aquaculture International ◽

10.1007/s10499-021-00708-3 ◽

2021 ◽

Author(s):

Marwa M. Attia ◽

Mamdouh Y. Elgendy ◽

Mohamed Abdelsalam ◽

Azza Hassan ◽

Abdelbary Prince ◽

...

Keyword(s):

Molecular Identification ◽

Mugil Cephalus ◽

Histopathological Effects

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High-Fructose Diet Increases Inflammatory Cytokines and Alters Gut Microbiota Composition in Rats

Mediators of Inflammation ◽

10.1155/2020/6672636 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Yong Wang ◽

Wentao Qi ◽

Ge Song ◽

Shaojie Pang ◽

Zhenzhen Peng ◽

...

Keyword(s):

Uric Acid ◽

Inflammatory Response ◽

Gut Microbiota ◽

Inflammatory Cytokines ◽

Proinflammatory Cytokines ◽

Lipid Accumulation ◽

Fasting Blood Glucose ◽

High Fructose Diet ◽

Fructose Intake ◽

High Fructose

High-fructose diet induced changes in gut microbiota structure and function, which have been linked to inflammatory response. However, the effect of small or appropriate doses of fructose on gut microbiota and inflammatory cytokines is not fully understood. Hence, the abundance changes of gut microbiota in fructose-treated Sprague-Dawley rats were analyzed by 16S rRNA sequencing. The effects of fructose diet on metabolic disorders were evaluated by blood biochemical parameter test, histological analysis, short-chain fatty acid (SCFA) analysis, ELISA analysis, and Western blot. Rats were intragastrically administered with pure fructose at the dose of 0 (Con), 2.6 (Fru-L), 5.3 (Fru-M), and 10.5 g/kg/day (Fru-H) for 20 weeks. The results showed that there were 36.5% increase of uric acid level in the Fru-H group when compared with the Con group. The serum proinflammatory cytokines (IL-6, TNF-α, and MIP-2) were significantly increased ( P < 0.05 ), and the anti-inflammatory cytokine IL-10 was significantly decreased ( P < 0.05 ) with fructose treatment. A higher fructose intake induced lipid accumulation in the liver and inflammatory cell infiltration in the pancreas and colon and increased the abundances of Lachnospira, Parasutterella, Marvinbryantia, and Blantia in colonic contents. Fructose intake increased the expressions of lipid accumulation proteins including perilipin-1, ADRP, and Tip-47 in the colon. Moreover, the higher level intake of fructose impaired intestinal barrier function due to the decrease of the expression of tight junction proteins (ZO-1 and occludin). In summary, there were no negative effects on body weight, fasting blood glucose, gut microbiota, and SCFAs in colonic contents of rats when fructose intake is in small or appropriate doses. High intake of fructose can increase uric acid, proinflammatory cytokines, intestinal permeability, and lipid accumulation in the liver and induce inflammatory response in the pancreas and colon.

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