Histological Changes on Liver Glycogen Storage in Mice (<i>Mus musculus</i>) Caused by Unbalanced Diets

Ulusoy, Esma; Eren, Banu

doi:10.4137/cpath.s505

Cited by 8 publications

(6 citation statements)

References 31 publications

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“…For hepatic glycogen staining, samples were fixed in 4% paraformaldehyde for 24−48 h, then embedded in paraffin, and sectioned into 6 mm slices. Hepatic glycogen was stained with the periodic acid/leucofuchsin method (PAS) [22] . Prunosus particles were observed in the cytoplasm following staining.…”

Section: Rat Experimentsmentioning

confidence: 99%

Astragalus polysaccharides alleviates glucose toxicity and restores glucose homeostasis in diabetic states via activation of AMPK

et al. 2009

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Aim: To establish the mechanism underlying the improvement of glucose toxicity by Astragalus polysaccharide (APS), which occurred via an AMP activated protein kinase (AMPK)-dependent pathway. Methods: In vivo and in vitro effects of APS on glucose homeostasis were examined in a type 2 diabetes mellitus (T2DM) rat model. The T2DM rat model was duplicated by a high-fat diet (58% fat, 25.6% carbohydrate, and 16.4% protein) and a small dose of streptozotocin (STZ, 25 mg/kg, ip). After APS therapy (700 mg·kg -1 ·d -1, ig) for 8 weeks, blood glucose, glycosylated hemoglobin, and serum insulin were measured. Insulin sensitivity was evaluated by the comprehensive analysis of oral glucose tolerance tests (OGTT) and HOMA IR index. Hepatic glycogen was observed by the PAS staining method. The expression and activity of skeletal muscle AMPKα and acetyl-CoA carboxylase (ACC), and the phosphorylation of hepatic glycogen synthase (GS), the glycogen synthase (GS),were measured by Western blotting. Glucose uptake was measured with the 2-deoxy-[3 H]-D-glucose method in C2C12 cells. Results: The hyperglycemia status, insulin sensitivity, glucose uptake, and activation level of AMPK in diabetic rats were improved in response to APS administration. APS could also alleviate glucose toxicity in cultured mouse cells by the activation of AMPK. Conclusion: APS can alleviate glucose toxicity by increasing liver glycogen synthesis and skeletal muscle glucose translocation in the T2DM rat model, via activation of AMPK.

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Section: Rat Experimentsmentioning

confidence: 99%

Astragalus polysaccharides alleviates glucose toxicity and restores glucose homeostasis in diabetic states via activation of AMPK

et al. 2009

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“…Generally, hepatocyte nuclear vacuolation is considered benign, and in humans, is associated with non-alcohol-related fatty liver disease, 34 or simply due to changes in food intake. 35…”

Section: Resultsmentioning

confidence: 99%

Biocompatibility of Multi-Imaging Engineered Mesoporous Silica Nanoparticles: In Vitro and Adult and Fetal In Vivo Studies

Sweeney¹,

Adamcakova‐Dodd²,

Thorne³

et al. 2017

j biomed nanotechnol

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Despite potentially serious adverse effects of engineered nanoparticles on maternal health and fetal development, little is known about their transport across the placenta. Human and animal studies are primarily limited to ex vivo approaches; the lack of a real-time, minimally invasive tool to study transplacental transport is clear. We have developed functionalized mesoporous silica nanoparticles (MSN) for use in magnetic resonance, ultrasound, and fluorescent imaging. This material is designed as a model for, or a carrier of, environmental toxicants, allowing for in vivo evaluation. To establish a baseline of biocompatibility, we present data describing MSN tolerance using in vitro and in vivo models. In cultured cells, MSN were tolerated to a dose of 125 µg/mL with minimal effect on viability and doubling time. For the 42 day duration of the study, none of the mice exhibited behaviors usually indicative of distress (lethargy, anemia, loss of appetite, etc.). In gravid mice, the body and organ weights of MSN-exposed dams were equivalent to those of control dams. Embryos exposed to MSN during early gestation were underweight by a small degree, while embryos exposed during late gestation were of a slightly larger weight. The rate of spontaneous fetal resorptions were equivalent in exposed and control mice. Maternal livers and sera were screened for a complement of cytokines/chemokines and reactive oxygen/nitrogen species (ROS/RNS). Only granulocyte-colony stimulating factor was elevated in mice exposed to MSN during late gestation, while ROS/RNS levels were elevated in mice exposed during early/mid gestation. These findings may usher future experiments investigating environmental toxicants using real-time assessment of transport across the placenta.

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“…Although glycogen naturally accumulates after milk consumption within 18 h of last supplementation 36 , long-time glycogen deposit and hydropic degeneration are compatible with subacute liver injury 37,38 .…”

Section: Discussionmentioning

confidence: 99%

Galectin-3 in the Gut-liver axis Regulates Autistic-like Behaviors by Mechanism Associated with Cerebral Shank-3+ cell Niches in BALB/c Mice

Lemos¹,

Prins²,

Carpi-Santos³

et al. 2021

Preprint

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Galectin-3 stabilizes cell-cell junctions and regulates inflammatory pathways in the gut-liver axis. Galectin-3 knockout (Lgals3−/−) mice have atypical behaviors by obscure mechanisms. Given that BALB/c mice naturally develop low-sociability, stereotypies and restrict interest, they have been included as autism experimental model. Our major aims were to investigate whether galectin-3 in the gut-liver axis interferes with autistic-like behaviors analyzing BALB/c Lgals3−/− mice or under partial inhibition of galectin-3 oral intake of cow’s milk for 7 days. Behavioral patterns were assessed using a three-chambers test, open field, and self-grooming. Histological analysis and immunohistochemistry (Galectin-3, NOS-2, Iba-1, Ki-67, Dll-4, Shank-3, Synaptophysin and Drebrin) were performed in gut, liver, and/or brain. Lgals3−/− mice amplified stereotypies, social retraction and restrict interest associated with reduction of cerebral Shank-3+ cells. In Lgals3+/+ mice, cow’s milk intake also amplified atypical behaviors, reduced galectin-3 in enterocytes and Kupffer cells, and disturbed niches of intestinal KI67+ and Dll-4+ cells and hepatic NOS2+ cells. In the brain of milk-treated mice, Iba-1+ microglial cells and NOS2+ Purkinje cells were increased whereas Shank-3+ and Drebrin+Synaptophysin+ cells were reduced suggesting, for the first time, that galectin-3 interferes with autistic behavior. Perhaps, a perspective to new therapies in genetically predisposed individuals to atypical behaviors.

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Histological Changes on Liver Glycogen Storage in Mice (Mus musculus) Caused by Unbalanced Diets

Cited by 8 publications

References 31 publications

Astragalus polysaccharides alleviates glucose toxicity and restores glucose homeostasis in diabetic states via activation of AMPK

Astragalus polysaccharides alleviates glucose toxicity and restores glucose homeostasis in diabetic states via activation of AMPK

Biocompatibility of Multi-Imaging Engineered Mesoporous Silica Nanoparticles: In Vitro and Adult and Fetal In Vivo Studies

Galectin-3 in the Gut-liver axis Regulates Autistic-like Behaviors by Mechanism Associated with Cerebral Shank-3+ cell Niches in BALB/c Mice

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