High fat diet on animal induce huperlipidemia primer or secondary

In conclusion, we demonstrated that maternal HF diet induced overweight, increased adiposity, dyslipidemia, over expression of the ECS and impairment of the antioxidant capacity in liver of adult offspring, with male rats more affected.

However, we did not observe significant difference in the body weights among those groups of rats, consistent with previous reports in this model of rats[ 1314 ]. Table 1 Components of Bofu-tsusho-san BO. Furthermore, IL treatment resulted in a dose-dependent reduction in the abundance of Escherichia coli, which in turn correlated with the decrease in serum endotoxin levels.

In obese women, CB2 mRNA levels in liver correlates positively with hepatic Acetyl-coenzyme A carboxylase 1 ACC1 gene expression, a key lipogenic enzyme of the de novo synthesis of fatty acids Therefore, the approaches to treatment of type 2 diabetes mellitus become to be an important issue.

Colonna R. The present study investigated the liver tumorigenic effects of dietary fat in a carcinogen-initiated HCC mouse model by replacing dietary fat with refined carbohydrates digestible saccharides without altering other dietary components.

For this reason, it is important to further investigate the influence of high-fat and high-carbohydrate diets on brain function at different points during lifespan, especially in mature and aging animals.

High Fat and High Sucrose (Western) Diet Induce Steatohepatitis that is Dependent on Fructokinase

Moreover, we noticed diminished O-glycans in the glycocalyx, which is the carbohydrate-rich zone found at the apical epithelial surface, consisting of glycoproteins including cell surface mucins that project into the intestinal lumen Fig.

However, of note, the present study focused on the regulation of the protein content of ECS components instead of transcript levels.

Wrote the paper: Triglyceride levels were then determined using the automated chemistry analyzer VetACEthen were normalized for protein concentration as measured by the BCA protein assay Pierce.

Differently, maternal HF diet decreased the activity of the antioxidant enzymes glutathione peroxidase, superoxide dismutase and catalase, and increased oxidative stress markers in both sexes. In older adults, daily fructose consumption was associated with increased hepatic inflammation and hepatocyte ballooning 8.

Actually, the influence of iron on the development of NAFLD has been the object of many experimental and clinical studies, where the dysregulation of iron overload could appear crucial in a progressive disease phenotype [26] — [28].

Bofu-tsusho-san, AMP-activated protein kinase phosphorylation, glucose transporter 4 1. The major macromolecular component of this barrier is the mucin glycoprotein, Muc2, produced by intestinal goblet cells 1. While no major changes were observed in the colon weight or length ratio shown in Supplementary Fig.

Obesity is associated with endocannabinoid system ECS over activation and oxidative stress. Consistent with this pro-inflammatory response to the HFD, epidemiological studies have implicated high dietary fat intake with an increased risk of IBD Results showed that HCD-fed mice had a comparable degree of hepatic tumorigenesis tumor number and volume as HFD-fed mice, despite having significantly reduced body weights.

Variants of high fat, or high-fat and high-carbohydrate HFCD diet are experimental tools often used to model the effects of energy dense food.

KG and MK analyzed the data.

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Furthermore, dietary control or combined with ATO treatment mitigated the HFD-induced hepatic steatosis, which was associated with the improvement of liver and systemic lipid profiles and function, leading to reduction in the severity of hyperlipidemia in NAFLD rats.

High level of NO may influence synaptic plasticity and induce cell death, leading to neuronal degeneration Brown and Bal-Price We also studied nNOS-positive cell abundance in the hippocampus and motor cortex M1 area. Briefly, total lipids in liver tissues were extracted with chloroform-methanol 2: KJ and ZS provided oversight.

To this end, we used an in-vitro model of intestinal goblet cells, the human colonic LST cells that contain secretory cells predominantly producing MUC2 9. Figure 8: Taken together with other results that question this simplistic view, we posit that a complex interplay of dietary composition, total caloric intake, the quality and type of fat consumed, as well as interactions with other life-changing phenomena like stress, age, and physical activity should be considered as potential factors influencing the relationship between obesity and cognitive decline.

Nat Rev Neurosci 8 1: HFD feeding is known to increase pro-inflammatory cytokines in the intestine and to lead to increased intestinal permeability 10111239 Physiol Behav 1: In the present study, we show that HFD-feeding leads to spontaneous goblet cell dysfunction, impaired mucosal barrier function and inflammation, and exacerbates the development of pathology in mice predisposed to ER stress-induced colitis.

Collectively, these data suggest that non-esterified fatty acid-induced cellular stress and intestinal inflammation with chronic high fat feeding leads to a diminished mucosal barrier and shifts in microbial populations that can be reversed by IL treatment.

At birth, the litters were adjusted to three male and three female pups per each dam, a number that maximizes lactation performance. · Diets high in fat and/or sugar have been shown to induce low-grade intestinal inflammation in mice 10,11,12,13,14, and are also linked to changes in the composition of the gut microbiota 13,15,16,17, which can be reversed by using intestinal anti-inflammatory agents such as 5-aminosalicylic acid Cited by: (A) Rats given the medium and high-fat diets gained significantly more body weight than regular-diet controls.

There was no difference in weight gain between the medium and high-fat diet groups. (B) Serum leptin was elevated in animals fed either a medium or high-fat diet compared to Cited by:  · We have shown that maternal high-fat (HF) diet during gestation and lactation induces obesity in the offspring associated with thyroid and adrenal dysfunction, hyperleptinemia with Author: Rosiane Aparecida Miranda, Mariana Macedo De Almeida, Camilla Pereira Dias Da Rocha, Larissa de Brit.

· High-fat diet, purchased from Laboratorio Dottori Piccioni (Gessate, Milan, Italy), had 58,1% of energy derived from fat, 16% from protein, and % from carbohydrates. The composition of high fat diet has been previously described by Surwit et al. [29].Cited by:  · Abstract.

Maternal obesity is a worldwide problem associated with increased risk of metabolic diseases in the offspring. Genetic deletion of the gastric inhibitory polypeptide (GIP) receptor (GIPR) prevents high-fat diet (HFD)–induced obesity in mice due to specific changes in energy and fat Cited by: 3.

High Fat Diet Induces Liver Steatosis and Early Dysregulation of Iron Metabolism in Rats

High-fat (HF) diets induce obesity, hyperglycemia, insulin resistance, and fatty liver in C57BL/6J mice. HF diet is well-known to increase body weight, body fat and induce insulin resistance and elevated levels of triglycerides [ 21 ].Cited by: 8.

High fat diet on animal induce huperlipidemia primer or secondary
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