scholarly journals Tegretol (Carbamazepine) Effect on the Morphometric Assay of Liver in Female White Mice (Mus musculus)

2018 ◽  
Vol 31 (3) ◽  
pp. 1
Author(s):  
Nawar R. Jaber ◽  
Nahla A. Al-Bakri

Carbamazepine (CBZ) is one of many anticonvulsants used to treat trigeminal neuralgia and epilepsy. Antiepileptic drugs (AED`s) are the second most important class of medications that lead to hepatotoxicity and induced liver injury, this study was conducted to evaluate the effects of CBZ on the liver. A total of 40 female mice were taken and divided into four groups (A/treated for 14 days, B/ control, C/ treated for 30 days, D/ control), the drug was given as an oral suspension formula 100mg/5ml at dose 20 mg/kg/mouse via gastric gavage daily for 14 and 30 days. Statistical analysis revealed that there were no significant differences in the white female mice body weight (P>0.05) in the treated group for 14 days as well as the treated group for 30 days, but there were significant differences between the treated groups studied. Statistical analyses result of liver weight, hepatocytes diameter, central vein and portal vein diameters showed significant differences in the treated group for 14 days (P<0.05) as well as the treated group for 30 days, and there were significant differences between all treated groups studied. The study concluded that carbamazepine (CBZ) can had no effect on body weight but it can induce several hepatic changes if it used on a short or long terms, therefore, it was advised to take cautions when describing this drug.

Author(s):  
Sarah Ibrahim Al Othman, Faten khalif Alanazi, Ghada Jaber S

Monosodium glutamate (MSG) is widely used as a food additive. Excessive consumption of monosodium glutamate has also been shown to affect the liver and kidneys, causing damage to these tissues because of oxidative stress leading to increased production of reactive oxygen species (ROS). The purpose of the study described in this paper was to find out how the liver and kidney toxicity caused by monosodium glutamate can be mitigated using pectin. To this end, 30 albino mice females were divided into four groups. The animals were distributed in special cages. 12-15 weeks with an average body weight of 60 grams. The animals were divided into four groups: the experimental control group (1) comprising 5 female mice were given normal drinking water and the treated group (2) comprising 10 female mice were given monosodium glutamate at a dose of 3 g/kg body weight in drinking water. For three weeks, the treatment group (3) comprising 10 female mice was given pectin at a dose of 300 mg/70 kg body weight in drinking water immediately after the monosodium glutamate dose for three weeks and the pectin group (4) comprising 5 female mice were given Pectin at a dose of 300 mg/70 kg body weight in drinking water for three weeks. The mice were then anesthetized, dissected, and liver and kidney samples were taken from female mice and kept in a 10% neutral formalin solution to make tissue segments. The results showed many histological changes in the liver, such as congestion of the central vein, widening of the sinuses, and the appearance of signs of the death of most hepatocytes, infiltration of the central vein and an invasion of inflammatory cells around the central vein with the emergence of several gaps within the cells. Many of them cavity with the death of most of the tubule cells, the closure of some of them and the expansion and infiltration in others and bleeding inside the tissue. Pectin therapy has led to the disappearance of most of these changes and the emergence of a clear improvement in hepatic and renal tissue.


2020 ◽  
Vol 319 (1) ◽  
pp. E146-E162 ◽  
Author(s):  
Stefanie Y. Tan ◽  
Xia Lei ◽  
Hannah C. Little ◽  
Susana Rodriguez ◽  
Dylan C. Sarver ◽  
...  

Secreted hormones facilitate tissue cross talk to maintain energy balance. We previously described C1q/TNF-related protein 12 (CTRP12) as a novel metabolic hormone. Gain-of-function and partial-deficiency mouse models have highlighted important roles for this fat-derived adipokine in modulating systemic metabolism. Whether CTRP12 is essential and required for metabolic homeostasis is unknown. We show here that homozygous deletion of Ctrp12 gene results in sexually dimorphic phenotypes. Under basal conditions, complete loss of CTRP12 had little impact on male mice, whereas it decreased body weight (driven by reduced lean mass and liver weight) and improved insulin sensitivity in female mice. When challenged with a high-fat diet, Ctrp12 knockout (KO) male mice had decreased energy expenditure, increased weight gain and adiposity, elevated serum TNFα level, and reduced insulin sensitivity. In contrast, female KO mice had reduced weight gain and liver weight. The expression of lipid synthesis and catabolism genes, as well as profibrotic, endoplasmic reticulum stress, and oxidative stress genes were largely unaffected in the adipose tissue of Ctrp12 KO male mice. Despite greater adiposity and insulin resistance, Ctrp12 KO male mice fed an obesogenic diet had lower circulating triglyceride and free fatty acid levels. In contrast, lipid profiles of the leaner female KO mice were not different from those of WT controls. These data suggest that CTRP12 contributes to whole body energy metabolism in genotype-, diet-, and sex-dependent manners, underscoring complex gene-environment interactions influencing metabolic outcomes.


2020 ◽  
Vol 21 (2) ◽  
pp. 81
Author(s):  
Charles Venirius Lisnahan ◽  
Oktavianus Rafael Nahak

The aim of this experiment was to identify the internal organs weight of 6-weeks old native chickens after treatment feed with l-threonine and l-tryptophan supplement. This experimental research used 128 native chickens aged one-week-old in a Completely Randomized Design with four treatments and four replications. The dietary treatments were T0 (control feed), T1 (T0 + 0.35% l-threonine + 0.10% l-tryptophan), T2 (T0 + 0.68% l-threonine + 0.17% l-tryptophan), and T3 (T0 + 1.00% l-threonine + 0.25% l-tryptophan). The variables measured included body weight, liver weight, pancreas weight, gizzard weight, and intestinal length. Statistical analysis showed that l-threonine and l-tryptophan significantly affected body weight, liver weight, pancreas weight, gizzard weight and intestinal length. Supplementing 1.00% l-threonine and 0.25% l- tryptophan to feed contributed to the highest body weight and internal organs weight of native chickens.


Author(s):  
El-Khedr Mohamed Mostafa El-gamal

Nitrosamine compounds are known hepatic carcinogens. This study was designed to study the efficacy of dietary supplementation with blueberries (BB) on diethylnitrosamine (DEN)-initiated hepatocarcinogenesis in male wistar rats. Rats were divided into three groups. The first group served as normal control group, the second group received DEN at a dose of 10 mg/kg body weight five times a week for 15 weeks. The third one received DEN as in DEN-treated group simultaneously with 4% BB-supplemented diet. The results showed that BB caused significant decrease in the elevated serum levels of α-fetoprotein (AFP), homocysteine (Hcy) along with levels of glutathione(GSH), deoxyribonucleic acid (DNA), ribonucleic acid (RNA)and activity of glutathione reductase (GR) in liver. Normalization of elevated 2-macroglobulin (2M) and total antioxidant capacity (TAC) levels in serum, hepatic Glutathione-S-transferase (GST), glutathione peroxidase (GPx) activities and liver weight was achieved whereas body weight was significantly decreased. Moreover, no significant change was observed in elevated relative liver weight, hepatic glucose-6-P-dehydrogenase (G6PD), lactate dehydrogenase (LDH) along with serum aminotransferases, alkaline phosphatase (ALP) and ɤ -glutamyltransferase (ɤ-GT) activities. Significant increase in reduced hepatic activity of xanthine oxidase (XO) was achieved and histopathological damage was minimized in BB-treated group. It is suggested that BB suppress DEN-induced hepatocarcinogenesis and could be developed as a promising chemoprotective natural supplement for liver cancer.


2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Peter Dornbos ◽  
Amanda Jurgelewicz ◽  
Kelly A. Fader ◽  
Kurt Williams ◽  
Timothy R. Zacharewski ◽  
...  

Abstract The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor. The prototypical ligand of the AHR is an environmental contaminant called 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD exposure is associated with many adverse health outcomes in humans including non-alcoholic fatty liver disease (NAFLD). Previous studies suggest that AHR ligands alter cholesterol homeostasis in mice through repression of genes involved in cholesterol biosynthesis, such as Hmgcr, which encodes the rate-limiting enzyme of cholesterol biosynthesis called 3-hydroxy-3-methyl-glutaryl coenzyme A reductase (HMGCR). In this study, we sought to characterize the impact of HMGCR repression in TCDD-induced liver injury. C57BL/6 mice were exposed to TCDD in the presence or absence of simvastatin, a competitive inhibitor of HMGCR. Simvastatin exposure decreased TCDD-induced hepatic lipid accumulation in both sexes, but was most prominent in females. Simvastatin and TCDD (S + T) co-treatment increased hepatic AHR-battery gene expression and liver injury in male, but not female, mice. In addition, the S + T co-treatment led to an increase in hepatic glycogen content that coincides with heavier liver in female mice. Results from this study suggest that statins, which are amongst the most prescribed pharmaceuticals, may protect from AHR-mediated steatosis, but alter glycogen metabolism and increase the risk of TCDD-elicited liver damage in a sex-specific manner.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 682-682 ◽  
Author(s):  
Kayla Dillard ◽  
Morgan Coffin ◽  
Gabriella Hernandez ◽  
Victoria Smith ◽  
Catherine Johnson ◽  
...  

Abstract Objectives Non-alcoholic fatty liver disease (NAFLD) represents the major cause of pediatric chronic liver pathology in the United States. The objective of this study was to compare the relative effect of inclusion of isocaloric amounts of saturated medium-chain fatty acids (hydrogenated coconut oil), saturated long-chain fatty acids (lard) and unsaturated long-chain fatty acids (olive oil) on endpoints of NAFLD and insulin resistance. Methods Thirty-eight 15-d-old Iberian pigs were fed 1 of 4 diets containing (g/kg body weight × d) 1) control (CON; n = 8): 0 g fructose, 10.5 g fat, and 187 kcal metabolizable energy (ME), 2) lard (LAR; n = 10): 21.6 g fructose, 17.1 g fat (100% lard) and 299 kcal ME, 3) hydrogenated coconut oil (COCO; n = 10): 21.6 g fructose, 16.9 g fat (42.5% lard and 57.5% coconut oil) and 299 kcal ME, and 4) olive oil (OLV, n = 10): 21.6 g fructose, 17.1 g fat (43.5% lard and 56.5% olive oil) and 299 kcal ME, for 9 consecutive weeks. Body weight was recorded every 3 d. Serum markers of liver injury and dyslipidemia were measured on d 60 at 2 h post feeding, with all other serum measures assessed on d 70. Liver tissue was collected on d 70 for histology, triacylglyceride (TG) quantification, and metabolomics analysis. Results Tissue histology indicated the presence of steatosis in LAR, COCO and OLV compared with CON (P ≤ 0.001), with a further increase in in non-alcoholic steatohepatitis (NASH) in OLV and COCO compared with LAR (P ≤ 0.01). Alanine and aspartate aminotransferases were higher in COCO and OLV (P ≤ 0.01) than CON. All treatment groups had lower liver concentrations of methyl donor's choline and betaine versus CON, while bile acids were differentially changed (P ≤ 0.05). COCO had higher levels of TGs with less carbons (Total carbons &lt; 52) than all other groups (P ≤ 0.05). Several long-chain acylcarnitines involved in fat oxidation were higher in OLV versus all other groups (P ≤ 0.05). Conclusions Inclusion of fats enriched in medium-chain saturated and long-chain unsaturated fatty acids in a high-fructose high-fat diet increased liver injury, compared with fats with a long-chain saturated fatty acid profile. Further research is required to investigate the mechanisms causing this difference in physiological response to these dietary fat sources. Funding Sources ARI, AcornSeekers.


Molecules ◽  
2021 ◽  
Vol 26 (2) ◽  
pp. 302
Author(s):  
Ahtesham Hussain ◽  
Jin Sook Cho ◽  
Jong-Seok Kim ◽  
Young Ik Lee

Background: Currently, obesity is a global health challenge due to its increasing prevalence and associated health risk. It is associated with various metabolic diseases, including diabetes, hypertension, cardiovascular disease, stroke, certain forms of cancer, and non-alcoholic liver diseases (NAFLD). Objective: The aim of this study to evaluate the effects of polyphenol enriched herbal complex (Rubus crataegifolius/ellagic acid, Crataegus pinnatifida Bunge/vitexin, chlorogenic acid, Cinnamomum cassiaa/cinnamic acid) on obesity and obesity induced NAFLD in the high-fat diet (HFD)-induced obese mouse model. Methods: Obesity was induced in male C57BL/6 mice using HFD. After 8 weeks, the mice were treated with HFD+ plants extract for 8 weeks. Body weight, food intake weekly, and blood sugar level were measured. After sacrifice, changes in the treated group’s liver weight, fat weight, serum biochemical parameters, hormone levels, and enzyme levels were measured. For histological analysis, tissues were stained with hematoxylin-eosin (H&E) and Oil Red-O. Results: Our results showed that the herbal complex ameliorated body weight and liver weight gain, and decreased total body fat in HFD-fed animals. Post prandial blood glucose (PBG) and fasting blood glucose (FBG) were lower in the herbal complex-treated group than in the HFD control group. Additionally, herbal formulation treatment significantly increased HDL levels in serum and decreased TC, TG, AST, ALT, deposition of fat droplets in the liver, and intima media thickness (IMT) in the aorta. Herbal complex increased serum adiponectin and decreased serum leptin. Herbal complex also increased carnitine palmityl transferase (CPT) activity and significantly decreased enzyme activity of beta-hydroxy beta methyl glutamyl-CoA (HMG-CoA) reductase, and fatty acid synthase (FAS). Conclusions: The results of this study demonstrated that the herbal complex is an effective herbal formulation in the attenuation of obesity and obesity-induced metabolic dysfunction including NAFLD in HFD-induced mouse model.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Thunnicha Ondee ◽  
Krit Pongpirul ◽  
Peerapat Visitchanakun ◽  
Wilasinee Saisorn ◽  
Suthicha Kanacharoen ◽  
...  

AbstractObesity, a major healthcare problem worldwide, induces metabolic endotoxemia through the gut translocation of lipopolysaccharides (LPS), a major cell wall component of Gram-negative bacteria, causing a chronic inflammatory state. A combination of several probiotics including Lactobacillus acidophilus 5 (LA5), a potent lactic acid-producing bacterium, has previously been shown to attenuate obesity. However, data on the correlation between a single administration of LA5 versus microbiota alteration might be helpful for the probiotic adjustment. LA5 was administered daily together with a high-fat diet (HFD) for 8 weeks in mice. Furthermore, the condition media of LA5 was also tested in a hepatocyte cell-line (HepG2 cells). Accordingly, LA5 attenuated obesity in mice as demonstrated by weight reduction, regional fat accumulation, lipidemia, liver injury (liver weight, lipid compositions, and liver enzyme), gut permeability defect, endotoxemia, and serum cytokines. Unsurprisingly, LA5 improved these parameters and acidified fecal pH leads to the attenuation of fecal dysbiosis. The fecal microbiome analysis in obese mice with or without LA5 indicated; (i) decreased Bacteroidetes (Gram-negative anaerobes that predominate in non-healthy conditions), (ii) reduced total fecal Gram-negative bacterial burdens (the sources of gut LPS), (iii) enhanced Firmicutes (Gram-positive bacteria with potential benefits) and (iv) increased Verrucomycobia, especially Akkermansia muciniphila, a bacterium with the anti-obesity property. With LA5 administration, A. muciniphila in the colon were more than 2,000 folds higher than the regular diet mice as determined by 16S rRNA. Besides, LA5 produced anti-inflammatory molecules with a similar molecular weight to LPS that reduced cytokine production in LPS-activated HepG2 cells. In conclusion, LA5 attenuated obesity through (i) gut dysbiosis attenuation, partly through the promotion of A. muciniphila (probiotics with the difficulty in preparation processes), (ii) reduced endotoxemia, and (iii) possibly decreased liver injury by producing the anti-inflammatory molecules.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1477
Author(s):  
Emanuela Pannia ◽  
Rola Hammoud ◽  
Ruslan Kubant ◽  
Jong Yup Sa ◽  
Rebecca Simonian ◽  
...  

Supplementation with [6S]-5-methyltetrahydrofolic acid (MTHF) is recommended as an alternative to folic acid (FA) in prenatal supplements. This study compared equimolar gestational FA and MTHF diets on energy regulation of female offspring. Wistar rats were fed an AIN-93G diet with recommended (2 mg/kg diet) or 5-fold (5X) intakes of MTHF or FA. At weaning, female offspring were fed a 45% fat diet until 19 weeks. The 5X-MTHF offspring had higher body weight (>15%), food intake (8%), light-cycle energy expenditure, and lower activity compared to 5X-FA offspring (p < 0.05). Both the 5X offspring had higher plasma levels of the anorectic hormone leptin at birth (60%) and at 19 weeks (40%), and lower liver weight and total liver lipids compared to the 1X offspring (p < 0.05). Hypothalamic mRNA expression of leptin receptor (ObRb) was lower, and of suppressor of cytokine signaling-3 (Socs3) was higher in the 5X-MTHF offspring (p < 0.05), suggesting central leptin dysregulation. In contrast, the 5X-FA offspring had higher expression of genes encoding for dopamine and GABA- neurotransmitter receptors (p < 0.01), consistent with their phenotype and reduced food intake. When fed folate diets at the requirement level, no differences were found due to form in the offspring. We conclude that MTHF compared to FA consumed at high levels in the gestational diets program central and peripheral mechanisms to favour increased weight gain in the offspring. These pre-clinical findings caution against high gestational intakes of folates of either form and encourage clinical trials examining their long-term health effects when consumed during pregnancy.


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