Interleukin mechanism in high fat diet obesity

Mean triplicate numbers of 16S amplicons per microliter effluent detected greater than or equal log-fold above background noise control were considered signal using MJ Opticon Monitor Analysis Software, version 3. The film was analyzed by Imagequant version 5.

Measurement of plasma LPS. Histological analysis indicated that the tumors were well-differentiated liposarcomas with infiltration of inflammatory cells.

This observation provides an interesting and potentially useful model in which to investigate the role of the gut in generating the obese phenotype in response to a HF diet and potentially gain insight into whether changes in the gut microbiota are driven by the HF diet or by the ensuing obesity.

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 aging.

One-way ANOVA with diet as variable was used to analyze data, and differences among group means were analyzed using a multiple-comparison procedure Tukey's method. Analyzed the data: The researchers found that Goishi tea prevented the growth of adipocytes and prevented changes caused by tumor necrosis factor alpha and interleukin 6 when the mice were on a high fat diet.

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

Ltd, Shenzhen, China and estimated by the glucose oxidase method. In this study, an animal model of a high-fat diet-induced OP or OR phenotype was used to test the hypothesis that the changes of indigenous opportunistic bacteria on the interior of the PPs are associated with obesity induced by high-fat diet.

The mice who drank Goishi tea gained less weight and had less sugar in their blood than the mice who drank tap water and green tea. However, the IL transgenic mice developed spontaneous liposarcomas in adipose tissue after long-term feeding with high fat diet, indicating that diet may interact with inflammation changes associated with IL overexpression in tumorigenesis in adipose tissue.

It was reported that IL can promote cell growth and survival in HepG2 cells by activating STAT3 and inducing expression of a variety of anti-apoptotic and mitogenic proteins [11]. Together, PPs are a major inductive and regulatory site for mucosal immunity.

The objective of the present study was to elucidate the mechanism for a link between HFD and obesity, particularly the effects of endotoxin-induced inflammation via TLR4 signaling pathway in response to a HFD. One potential mechanism to explain this effect links inflammation in hypothalamic areas central to energy homeostasis, such as the arcuate nucleus, with resistance to input from key afferent signals, including the hormones insulin and leptin 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 Plasma measurement Plasma lipid [total plasma cholesterol TC and triglyceride TG ] and glucose concentrations were determined using enzymatic kits Asan, Daijon, Korea.

Therefore Bacteroidales, Clostridiales, and Enterobacteriales were chosen for the current study.

For example, mice were put on a high-fat diet, but given either tap water, green tea, or Goishi tea to drink. Wrote the paper: Moreover, the sources of fat were diverse from butter, beef tallowand lardto vegetable and fish oils. Results HFD induced macrophage infiltration and inflammation in the adipose tissue, as well as an increase in the circulating proinflammatory cytokines.

Weight put on during the high-fat diet also tends to persist. We generated a transgenic mouse model with overexpression of IL specifically in adipose tissue.

The human gut contains at least microorganisms, collectively referred to as the microbiota [13]. Assay of myeloperoxidase activity Myeloperoxidase MPO activity in colon was assayed as previously described [21] and expressed in unit per milligram protein.

To generate transgenic mice, the transgenic cassette was excised from the plasmid and used in microinjection into the pronuclei of fertilized oocytes of the ICR strain of mice. For instance, the age at which mice begin the high-fat diet greatly impacts the metabolic effects.

Diet-induced obesity model

All the mice used in this study were of ICR background. The specific fatty foods used in the diets vary across studies, ranging from Crisco to lard to palm oil.

Cycling conditions were as follows:High Fat Diet Induces Formation of Spontaneous Liposarcoma in Mouse Adipose Tissue with Overexpression of Interleukin 22 Zheng Wang, # 1 Ling Yang, # 1 Yuhui Jiang, 1 Zhi-Qiang Ling, 2 Zhigang Li, 1 Yuan Cheng, 1 Heng Huang, 1 Lingdi Wang, 1 Yi Pan, 1 Zhenzhen Wang, 1 Xiaoqiang Yan, 3 and Yan Chen 1, *Cited by: Thus, these data suggest that high fat diets and obesity can influence AT-TNF bioactivity and secretion but in an apparent fat pad-specific manner.

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(Endocrinology  · Consumption of diets high in fat and calories leads to hyperphagia and obesity, which is associated with chronic “low-grade” systemic by:  · Consumption of dietary fat is one of the key factors leading to obesity.

High-fat diet (HFD)-induced obesity is characterized by induction of inflammation in the hypothalamus; however, the 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: Moreover, mice lacking endogenous ST2, a member of the Toll-interleukin 1 receptor (TIR) superfamily that does not activate NFκB, had increased body weight and fat mass and impaired insulin secretion and glucose regulation when fed a high-fat diet.

Therefore, akin to IL, IL may have a protective role in the development of adipose tissue inflammation during by:

Interleukin mechanism in high fat diet obesity
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