Interleukin mechanism in high fat diet obesity

Study Protocols Experiment 1: We addressed this hypothesis by perturbing the inflammatory milieu of the hypothalamus in adult male Wistar rats using intracerebroventricular icv administration of interleukin-4 IL-4a Th2 cytokine that promotes alternative activation M2 of macrophages and microglia.

Often, the experiment aims to see how obesity affects some other physiological or behavioral outcome, so other measures may be taken. Gastrointestinal and Liver Physiology website. Therefore Bacteroidales, Clostridiales, and Enterobacteriales were chosen for the current study.

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After 25 weeks, mice in high-fat diet exhibit either an obesity-prone OP or an obesity-resistant OR phenotype. One such side effect is that the body gains more fat cells.

Tissue inflammation during high-fat HF feeding results from the recruitment and activation of macrophages, which can cause insulin resistance through local or systemic release of proinflammatory cytokines 121925 It also has a pro-inflammatory effect in promoting bacterial load and organ failure during septic peritonitis [6].

Although adipose tissue is an undeniable source of inflammation in the development of obesity, emerging evidence suggests that a HFD promotes inflammation in the gastrointestinal tract which is considered as another potential source of inflammation associated with HFD-induced obesity [12].

Addition of reagents led to formation of a magenta derivative that absorbs light at nm. Moreover, conventionalization of adult GF mice with a normal microbiota harvested from conventionally raised animals CONV produced an increase in body fat [14].

This article has been cited by other articles in PMC. Some research shows that nightly eating, low eating frequency, and large meal size may contribute to diet-induced obesity. Materials and Methods Animal experiments The animal experiment was performed in compliance with the fundamental guidelines for proper conduct of animal experiments and related activities in academic research institutions under the jurisdiction of the Ministry of Education of China and approved by the Jiangnan University Institutional Animal Care and Use Committee.

HFD reduced the expression of tight junction-associated proteins claudin-1 and occludin in the colon. Additionally, obesity remains in both species for long periods of time after it has initially set in.

Mice without lymphotoxin alphalymphotoxin betaor a lymphotoxin beta receptor gained less weight on a high-fat diet than wild type mice did, even after remaining on a high-fat diet for a prolonged period of time.

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.

For instance, the age at which mice begin the high-fat diet greatly impacts the metabolic effects. All experiments were performed in accordance with protocols reviewed and approved by the Institutional Animal Care and Use Committee, University of California Davis.

The IL transgenic mice had no apparent changes in obesity and insulin resistance after feeding with high fat diet HFD. Rodents are nocturnal and are mostly feeding at night, in their natural habitat. In this study, we further investigated the potential function of IL on adipose tissue by generation of a transgenic mouse model with adipose-specific expression of IL Epididymal, mesenteric, and retroperitoneal fat tissues were dissected and weighed, and adiposity index was determined.

Weight put on during the high-fat diet also tends to persist. The adipose tissue was weighted and frozen in liquid nitrogen for RNA extraction. · 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.

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.

(Endocrinology Recent evidence that HF feeding increases the expression of proinflammatory cytokines, including TNFα, interleukin (IL)-1β, and IL-6, in the hypothalamus as well as in peripheral tissues has raised the possibility that hypothalamic inflammation contributes to the pathogenesis of diet-induced obesity (DIO).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:

Diet-induced obesity model
Interleukin mechanism in high fat diet obesity
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