Interleukin mechanism in high fat diet obesity

Diet-induced obesity model

The quantity and quality of purified DNA was assessed using the E. Intestinal permeability and plasma LPS were increased together with phosphorylation of myosin light chain and localization of occludin in the cytoplasm of epithelial cells.

Inflammatory bowel disease exhibited a higher level of pathogenic bacteria interaction with PPs and a higher level of translocation through M cell monolayers.

The specific fatty foods used in the diets vary across studies, ranging from Crisco to lard to palm oil.

There was a problem providing the content you requested

Reuter Table 1. Some research shows that nightly eating, low eating frequency, and large meal size may contribute to diet-induced obesity. Barcodes that allow sample multiplexing during pyrosequencing were incorporated between the adaptor and the forward primer. Other illnesses[ edit ] Multiple mental and physical illnesses, along with some of the medications that treat such illnesses can increase someone's risk of obesity.

Falmouth, MA according to manufacturer's protocol. Phosphorylated myosin light chain p-MLC expression was measured by Western blot of ileum as previously described PPs continuously take up gut luminal antigens through M cells, including both beneficial and antigens.

Conventionalization of germ-free mice with microbiota from lean mice or from genetically or diet-induced obese mice results in recapitulation of the original phenotype 5.

However, recent studies have demonstrated that a variety of cytokines and inflammatory mediators, as well as increased oxidative stress as reflected in increased reactive oxygen species, could accelerate the development of metabolic syndrome [4][5].

Cycling conditions were as follows: Limulus amoebocyte lysate assay Plasma and fecal endotoxin contents were determined by using the Diazo-coupled limulus amoebocyte lysate LAL assays Cape Cod Inc. Blood glucose was assayed using commercial kits Jingmei BioTech Co.

In studies with A. Macroscopic assessment of the disease grade was scored according to a previously reported scoring system 0, no ulcer and no inflammation; 1, ulceration and local hyperemia; 2, ulceration without hyperemia; 3, ulceration and inflammation at one site only; 4, two or more sites of ulceration and inflammation; 5, ulceration extending more than 2 cm [20] and the colon tissue was used for ELISA and immunoblotting according to the methods described by Joh and Kim [21].

However, the variation in the results of those models has caused the difficulties to interpret and find the relation to human case. These observations add to growing evidence linking hypothalamic inflammation to obesity pathogenesis.

The data showed that consumption of a HF diet induces changes in gut microbiota, but it is the development of inflammation in response to these changes that is associated with the appearance of hyperphagia and an obese phenotype.

It also has a pro-inflammatory effect in promoting bacterial load and organ failure during septic peritonitis [6]. Conclusions HFD induces inflammation by increasing endotoxin levels in the intestinal lumen as well as in the plasma by altering the gut microbiota composition and increasing its intestinal permeability through the induction of TLR4, thereby accelerating obesity.

After 8 or 12 wk, tissue was removed to determine adiposity and gut epithelial function and to analyze the gut microbiota using PCR. DIO-P vs. HFD induced the growth of Enterobecteriaceae and the production of endotoxin in vitro.

For example, mice were put on a high-fat diet, but given either tap water, green tea, or Goishi tea to drink. Similar effects were seen in mice who were slowly introduced to propolis while on the high-fat diet. We analyzed whether adipose tissues express these two receptors. A fusion gene between IL and Ig ameliorates experimental autoimmune myocarditis in rats [8].

In the present study, the hypothesis to be tested was that ingestion of a HF diet alters the gut microbiota, induces gut inflammation and elevated LPS, and that this only occurs in obese-prone rats.

Abstract In peripheral tissues, the link between obesity and insulin resistance involves low-grade inflammation induced by macrophage activation and proinflammatory cytokine signaling. Absorbance was read at nm at 5 min Plasma measurement Plasma lipid [total plasma cholesterol TC and triglyceride TG ] and glucose concentrations were determined using enzymatic kits Asan, Daijon, Korea.

Stereotaxic Surgery All rats underwent surgical implantation of an indwelling stainless steel cannula into the third cerebral ventricle 3V under isoflurane anesthesia, as described previously Measurement of bacterial 16S rRNA showed a decrease in total bacterial density and an increase in the relative proportion of Bacteroidales and Clostridiales orders in high-fat-fed rats regardless of phenotype; an increase in Enterobacteriales was seen in the microbiota of DIO-P rats only.

The increased number of fat cells persists even after the diet becomes lower in fat. All samples were analysed in duplicate. After 25 weeks, 30 mice in HFD were classified by body weight gain range from Charles, MO. Quantitative assessment of gut microbiota order abundance by sequence analysis of the microbial 16S rRNA gene.

Gastrointestinal and Liver Physiology website. The adipose tissue was weighted and frozen in liquid nitrogen for RNA extraction. The amplification, sequencing, and basic analysis were performed according to the methods described by Chun et al.

To study the effects of the fungusscientists injected it into mice while they were on an unrestricted high-fat diet.Changes in Gut Microbiota Control Metabolic Endotoxemia-Induced Inflammation in High-Fat Diet–Induced Obesity and Diabetes in Mice Patrice D.

Cani,1,2 Rodrigo Bibiloni,3 Claude Knauf,2 Aure´lie Waget,2 Audrey M. Neyrinck,1. · Consumption of diets high in fat and calories leads to hyperphagia and obesity, which is associated with chronic “low-grade” systemic by:  · Introduction.

Metabolic syndrome, a group of inter-related metabolic abnormalities that include hyperglycemia, insulin resistance, dyslipidemia, hypertension, and obesity, is exacerbated by environmental factors, such as a fat-enriched diet, a sedentary life style, and perhaps by by: The diet-induced obesity model (DIO model) is an animal model used to study obesity using animals that have obesity caused by being fed high-fat or high-density diets.

It is intended to mimic the most common cause of obesity in humans. Typically mice, rats, dogs, or non-human primates are used in these models.

In summary, indigenous opportunistic bacteria on the interior of PPs was significantly different among control diet mice, high-fat diet induced obesity-prone mice, and obiestiy-resistant mice. By cohabiting within the organized PPs, these bacteria affect the development and maturation of the host mucosal immune system.

Further, the PP-inhabiting, commensal microbiota are an additional element that Cited by: In contrast, high‐fat diets in patients with high BMI elevate TNF‐α production.

In addition, obese patients may have multiple pulmonary abnormalities (7). These include reduction of functional residual capacity, ventilation/perfusion mismatch, and by:

Interleukin mechanism in high fat diet obesity
Rated 5/5 based on 43 review