Chronic intake of moderate fat-enriched diet induces fatty liver and low-grade inflammation without obesity in rabbits

Sigrist-Flores, Santiago Cristobal; Ponciano-Gómez, Alberto; Pedroza-González, Alexander; Gallardo‐Ortíz, Itzell A.; Villalobos‐Molina, Rafael; Pardo-Vázquez, Juan Pablo; Saucedo-Campos, Alberto Daniel; Jiménez-Flores, Rafael; Méndez-Cruz, Adolfo René

doi:10.1016/j.cbi.2019.01.004

Cited by 12 publications

(9 citation statements)

References 36 publications

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“…In our study, the downstream mediator of NLRP3, IL-18 but not IL-1, was particularly increased. In mice on a high-fat diet, IL-18 has previously been identified among the intermediate markers of hepatic steatosis [ 24 ] and similar findings have been obtained in early steatosis in rabbits [ 25 ]. In humans, elevated serum IL-18 concentration correlated with ALT as a marker of hepatocyte injury in obese children [ 26 ].…”

Section: Discussionsupporting

confidence: 62%

IL-18 But Not IL-1 Signaling Is Pivotal for the Initiation of Liver Injury in Murine Non-Alcoholic Fatty Liver Disease

Hohenester

Kanitz

Schiergens

et al. 2020

IJMS

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Non-alcoholic fatty liver disease (NAFLD) is rising in prevalence, and a better pathophysiologic understanding of the transition to its inflammatory phenotype (NASH) is key to the development of effective therapies. To evaluate the contribution of the NLRP3 inflammasome and its downstream effectors IL-1 and IL-18 in this process, we applied the true-to-life “American lifestyle-induced obesity syndrome” (ALiOS) diet mouse model. Development of obesity, fatty liver and liver damage was investigated in mice fed for 24 weeks according to the ALiOS protocol. Lipidomic changes in mouse livers were compared to human NAFLD samples. Receptor knockout mice for IL-1 and IL-18 were used to dissect the impact of downstream signals of inflammasome activity on the development of NAFLD. The ALiOS diet induced obesity and liver steatosis. The lipidomic changes closely mimicked changes in human NAFLD. A pro-inflammatory gene expression pattern in liver tissue and increased serum liver transaminases indicated early liver damage in the absence of histological evidence of NASH. Mechanistically, Il-18r−/−- but not Il-1r−/− mice were protected from early liver damage, possibly due to silencing of the pro-inflammatory gene expression pattern. Our study identified NLRP3 activation and IL-18R-dependent signaling as potential modulators of early liver damage in NAFLD, preceding development of histologic NASH.

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Section: Discussionsupporting

confidence: 62%

IL-18 But Not IL-1 Signaling Is Pivotal for the Initiation of Liver Injury in Murine Non-Alcoholic Fatty Liver Disease

Hohenester

Kanitz

Schiergens

et al. 2020

IJMS

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“…obesity and type 2 diabetes) in humans and rats (Pataky, et al , ; Guo, et al , ; Tang, et al , ; Kong, et al , ). In rabbits, low‐grade inflammation and fat deposition have been known to negatively impact growth (Sigrist‐Flores, et al , ). Interestingly, we did not observe bacteria associated with the metabolism of breast milk, such as Bifidobacterium , Lactobacillus , Enterococcus and Staphylococcus exhibit significant associations with weaning weight (Jost, et al , ; de Muinck and Trosvik, ).…”

Section: Discussionmentioning

confidence: 89%

Faecal microbiota and functional capacity associated with weaning weight in meat rabbits

Fang

Chen

Zhou

et al. 2019

Microbial Biotechnology

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Summary Weaning weight is an important economic trait in the meat rabbit industry. Evidence has linked the gut microbiota to health and production performance in rabbits. However, the effect of gut microbiota on meat rabbit weaning weight remains unclear. In this study, we performed 16S rRNA gene sequencing analysis of 135 faecal samples from commercial Ira rabbits. We detected 50 OTUs significantly associated with weaning weight. OTUs that showed positive associations with weaning weight were mostly members of the family Ruminococcaceae which are important in degrading dietary fibres and producing butyrate. On the contrary, OTUs annotated to genera Blautia, Lachnoclostridium and Butyricicoccus correlated with fat deposition were negatively associated with weaning weight. Predicted functional capacity analysis revealed that 91 KOs and 26 KEGG pathways exhibited potential correlations with weaning weight. We found that gut microbiota involved in the metabolism of amino acids, butanoate, energy and monosaccharides affected weaning weight. Additionally, cross‐validation analysis indicated that 16.16% of the variation in weaning weight was explained by the gut microbiome. Our findings provide important information to improve weaning weight of meat rabbits by modulating their gut microbiome.

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“…Многие клинические и экспериментальные исследования позволили установить связь между висцеральным ожирением и хронической воспалительной реакцией в жировой ткани больных ожирением, ответственной за его метаболические осложнения [18][19][20][21].…”

Section: хроническое воспаление при ожиренииunclassified

“…Таким образом, низкоуровневое вялотекущее хроническое воспаление важно для защиты от развития дисфункции адипоцитов [27]. Неалкогольный жировой гепатоз тесно связан с ожирением и МС, однако у некоторых пациентов данное заболевание развивается при отcутствии ожирения [19]. В экспериментальных условиях подтверждено, что высокожировая диета в течение 6 месяцев приводила к развитию ожирения печени и хронического воспаления, характеризующегося повышением уровня TNF-α, IL-13 и IL-18.…”

Section: хроническое воспаление при ожиренииunclassified

“…После 12 месяцев данной диеты наблюдалась гиперэкспрессия IL-6, IL-10, IL-13, циклооксигеназы-2 (COX-2) и TLR. По заключению авторов, данный иммунный ответ оказывает защитный эффект, предотвращая развитие метаболических нарушений [19].…”

Section: хроническое воспаление при ожиренииunclassified

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Toll-like receptors in the pathophysiology of obesity

Kytikovа

Юрьевна²,

Новгородцева

et al. 2020

Obes. metabol.

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Obesity is a complex and relevant global medical and social problem. The adipose tissue is not only a place of deposition of energy substrates but also a source of secretion of pro-inflammatory and anti-inflammatory mediators involved in the development of the chronic latent systemic inflammatory process in the organism with obesity. The metabolic signal in obesity contributes to the polarization of macrophages in the M1 direction and triggers the Th1 immune response, causing the development of adipose tissue inflammation. A chronic inflammatory condition plays a key role in the pathophysiology of obesity-induced insulin resistance. Toll-like receptors (TLRs) may be a possible pathophysiological link in the development of insulin resistance in inflammation. At the same time, inflammation-induced lipolysis is necessary for the release of energy resources during the development of the infectious process. Thus, low-grade inflammation is important to protect against adipocyte dysfunction. These results suggest that pro-inflammatory signaling is not exclusively pathogenic in obesity. In this regard, the study of inflammatory signaling pathways involved in the modulation of chronic inflammation of adipose tissue is particularly relevant. This review summarizes current views on the structure, function of TLRs and their involvement in the pathogenesis of chronic inflammation in obesity. The possibility of using TLRs as a therapeutic target in this pathology is discussed. Obviously, further study of inflammatory signaling pathways involving TLRs initiating the development of chronic inflammation of adipose tissue will allow the development of new and effective therapeutic strategies for obesity and its metabolic complications.

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Chronic intake of moderate fat-enriched diet induces fatty liver and low-grade inflammation without obesity in rabbits

Cited by 12 publications

References 36 publications

IL-18 But Not IL-1 Signaling Is Pivotal for the Initiation of Liver Injury in Murine Non-Alcoholic Fatty Liver Disease

IL-18 But Not IL-1 Signaling Is Pivotal for the Initiation of Liver Injury in Murine Non-Alcoholic Fatty Liver Disease

Faecal microbiota and functional capacity associated with weaning weight in meat rabbits

Toll-like receptors in the pathophysiology of obesity

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