Adipose tissue metabolism and inflammation are differently affected by weight loss in obese mice due to either a high-fat diet restriction or change to a low-fat diet

Although recognized as an important endocrine organ, little is known about the mechanisms through which adipose tissue can regulate inflammatory responses in distant tissues, such as lung, that are affected by obesity. To explore potential mechanisms, male C57BL/6J mice were provided either high-fat diet, low-fat diet, or were provided a high-fat diet then switched to the low-fat diet to promote weight loss. Visceral adipocytes were then cultured in vitro to generate conditioned media (CM) that was used to treat both primary (MTEC) and immortalized (MTCC) airway epithelial cells. Adiponectin levels were greatly depressed in the CM from both obese and diet-switched adipocytes relative to mice continually fed the low-fat diet. MTEC from obese mice secreted higher baseline levels of inflammatory cytokines than MTEC from lean or diet-switched mice. MTEC treated with obese adipocyte CM increased their secretion of these cytokines compared to MTEC treated with lean CM. Diet-switched CM modestly decreased the production of cytokines compared to obese CM, and these effects were recapitulated when the CM was used to treat MTCC. Adipose stromal vascular cells from obese mice expressed genes consistent with an M1 macrophage phenotype and decreased eosinophil abundance compared to lean SVF, a profile that persisted in the lean diet-switched mice despite substantial weight loss. Soluble factors secreted from obese adipocytes exert a pro-inflammatory effect on airway epithelial cells, and these alterations are attenuated by diet-induced weight loss, which could have implications for the airway dysfunction related to obese asthma and its mitigation by weight loss.

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Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00363.2015 ◽

2016 ◽

Vol 310 (11) ◽

pp. E886-E899 ◽

Cited By ~ 25

Author(s):

Pia Kiilerich ◽

Lene Secher Myrmel ◽

Even Fjære ◽

Qin Hao ◽

Floor Hugenholtz ◽

...

Keyword(s):

Gene Expression ◽

Adipose Tissue ◽

Gut Microbiota ◽

Dietary Fat ◽

High Fat Diet ◽

High Fat ◽

Low Fat ◽

Low Fat Diet ◽

Low Protein

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.

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Altered Gut Microbiota Is a Novel Mechanism for the Adverse Effects Induced by Foodborne Titanium Dioxide Nanoparticles in Obese and Non-obese Mice (P21-021-19)

Current Developments in Nutrition ◽

10.1093/cdn/nzz041.p21-021-19 ◽

2019 ◽

Vol 3 (Supplement_1) ◽

Author(s):

Hengjun Du ◽

Xiaoqiong Cao ◽

Yanhui Han ◽

Min Gu ◽

Hang Xiao

Keyword(s):

Titanium Dioxide ◽

Adverse Effects ◽

Gut Microbiota ◽

High Fat Diet ◽

Obese Mice ◽

High Fat ◽

Low Fat ◽

Colonic Inflammation ◽

Tio2 Nps ◽

Low Fat Diet

Abstract Objectives Many food products contain inorganic nanoparticles (NPs), such as titanium dioxide (TiO2) NPs. There is increasing concern about the potential unintended health risks associated with foodborne TiO2 NPs in certain populations, such as the obese. The purpose of this study was to determine the adverse effects of TiO2 NPs in obese individuals, the molecular mechanism involved and the potential role of gut microbiota in mediating the adverse effects. Methods Two types of TiO2 (30 nm and E171-Food grade TiO2) were mixed with mouse diet at 0.1 wt% and fed to two populations of mice (high-fat diet-fed obese mice and non-obese mice). Meanwhile, fecal samples from the above groups of mice were collected weekly for transplanting to four groups of mice fed a low-fat diet for 10 weeks. 16 s rRNA gene amplicon sequencing, histological analysis, immunohistochemistry, ELISA and SCFAs analysis were utilized to characterize the composition of the microbiota, inflammation status, and the effects of altered gut microbiota on the inflammation status of the mouse colon. Results TiO2 NPs significantly altered the composition of gut microbiota with stronger alterations in the high-fat diet-fed obese mice than the low-fat diet-fed non-obese mice. The abundance of inflammation-related cytokines (e.g., IL-10, IL-12p70, and IL-17) and myeloperoxidase (MPO) in the mouse colonic mucosa were significantly altered by TiO2 NPs to produce an inflammatory state. TiO2 NPs decreased the cecal levels of SCFAs such as butyrate. Moreover, the magnitude of the above alteration was higher in the obese mice than in the non-obese mice. After 10 weeks of microbial transplant, microbiota from the mice consuming a high-fat diet with TiO2 NPs led to an increase of pro-inflammatory cytokines, loss of healthy colonic morphology, and infiltration of immune cells in the colon of the low-fat diet-fed recipient mice, indicating a significant colonic inflammation. Conclusions TiO2 NPs altered gut microbiota in both obese and non-obese mice, with stronger effects in the obese mice, and the alteration of gut microbiota led to colonic inflammation in the mice. Overall, these findings provided a valuable new perspective on the potential adverse effects and appropriate mechanisms of foodborne TiO2 NPs among populations with different obese status. Funding Sources USDA/NIFA competitive grants to Hang Xiao.

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Adiponectin and 8-epi-PGF2α as intermediate influence factors in weight reduction after legumes consumption: a 12-week randomized controlled trial

10.21203/rs.3.rs-46032/v1 ◽

2020 ◽

Author(s):

Youngmin Han ◽

Jong Ho Lee ◽

Minjoo Kim

Keyword(s):

Weight Loss ◽

High Fat Diet ◽

Diet Group ◽

Controlled Study ◽

High Fat ◽

Low Fat ◽

Carbohydrate Source ◽

Randomized Controlled ◽

Low Fat Diet ◽

Obese Subjects

Abstract Background and Aims: The current nutritional intervention study was designed to determine the effect of legume on body weight in obese subjects. Methods Randomized controlled study of 12 weeks with 383 participants (body mass index ≥ 25 kg/m2) was enrolled for the study. The intervention program consisted of replacing 1/3 refined rice intake with legumes three times per day as a carbohydrate source in high fat diet group. In contrast, low fat diet group was recommended to eat as their usual diet. Results In high fat diet group, intake of energy and carbohydrate were lower, while the intake of fat and protein were higher. Mean weight loss at 12 weeks was 2.87 ± 0.21 kg and 0.17 ± 0.11 kg in the high fat diet group and low fat diet group, respectively, and was significantly different between groups (P < 0.001). HDL-cholesterol and adiponectin were increased, while glucose, insulin, triglyceride, HOMA-IR index, and 8-epi-PGF2α were decreased at 12 weeks in the high fat diet group compared with baseline. Conclusions The conclusion is that the consumption of legumes may accelerate weight loss accompanied by regulation of adiponectin and 8-epi-PGF2α in obese subjects. Also, increases in plasma adiponectin induced by a larger amount of weight loss may relate to greater activation of insulin resistance. Trial registrations: NCT04392882 (Registered 19 May 2020 - Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT04392882?cond=NCT04392882&draw=2&rank=1)

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