Metabolic and immunomodulatory effects of n-3 fatty acids are different in mesenteric and epididymal adipose tissue of diet-induced obese mice

Ludwig, Tobias; Worsch, Stefanie; Heikenwälder, Mathias; Daniel, Hannelore; Hauner, Hans; Bader, B.

doi:10.1152/ajpendo.00171.2012

Cited by 33 publications

(46 citation statements)

References 85 publications

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“…50 In our study, neither dietary TMAO nor fish oil had any significant influence on the mRNA expression of macrophage markers F4/80 and CD11b. 50 In our study, neither dietary TMAO nor fish oil had any significant influence on the mRNA expression of macrophage markers F4/80 and CD11b.…”

Section: Discussioncontrasting

confidence: 68%

Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice

Gao

Jiang

et al. 2015

Food Funct.

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Trimethylamine N-oxide (TMAO), a component commonly present in seafood, has been found to have a harmful impact on glucose tolerance in high-fat diet (HFD)-fed mice. However, seafood also contains fish oil (FO), which has been shown to have beneficial effects on metabolism. Here, we investigated the effect of FO on TMAO-induced impaired glucose tolerance in HFD-fed mice. Male C57BL/6 mice were randomly assigned to the high fat (HF), TMAO, and fish oil groups. The HF group was fed a diet containing 25% fat, the TMAO group was fed the HFD plus 0.2% TMAO, and the FO group was fed the HFD plus 0.2% TMAO and 2% fish oil for 12 weeks. After 10 weeks of feeding, oral glucose tolerance tests were performed. Dietary FO improved the fasting glucose level, the fasting insulin level, HOMA-IR value, QUICKI score and ameliorated TMAO-induced exacerbated impaired glucose tolerance in HFD-fed mice. These effects were associated with the expression of genes related to the insulin signalling pathway, glycogen synthesis, gluconeogenesis, and glucose transport in peripheral tissues. Dietary fish oil also decreased TMAO-aggravated adipose tissue inflammation. Our results suggested that dietary FO ameliorated TMAO-induced impaired glucose tolerance, insulin signal transduction in peripheral tissue, and adipose tissue inflammation in HFD-fed mice.

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Section: Discussioncontrasting

confidence: 68%

Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice

Gao

Jiang

et al. 2015

Food Funct.

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“…Both murine and human studies have shown that MAT mass and function is altered in mice and humans suffering from colitis, indicating an active interaction between the intestine and MAT [35e37]. Furthermore, diet has a more pronounced influence on MAT compared to other, more distant, ATdepots [38,39]. Therefore, it can be hypothesized that MATinflammation has a direct influence on the intestine, possibly influencing the enteric endocrine system.…”

Section: Discussionmentioning

confidence: 99%

Inflammatory characteristics of distinct abdominal adipose tissue depots relate differently to metabolic risk factors for cardiovascular disease

et al. 2015

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“…This led to an emerging interest in the role of mitochondria in NAFLD and nonalcoholic steatohepatitis (Guo et al, 2013;Thomas et al, 2013;Li et al, 2014;Nesteruk et al, 2014). Most of these studies investigated the development of fatty liver in mice at juvenile life stages and clearly demonstrate that fat accumulation in adolescent mice can be induced by high fat diet depending on the fat source and the duration of feeding (Satapati et al, 2012;Fontana et al, 2013;Ludwig et al, 2013;Nakamura and Terauchi, 2013). In humans, the prevalence of metabolic diseases, including NAFLD, increases with age (Sheedfar et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

“…In our effort to trace the early molecular events that facilitate the development of an imbalance in hepatic fatty acid metabolism, we aimed to delineate age-and dietrelated effects at an early stage of disease development. A previous study demonstrated that 12 weeks of feeding our control and high fat diet are sufficient to increase hepatic triglyceride content in adolescent mice (Ludwig et al, 2013). To study the effect of age on this process at an even earlier stage, we applied a fixed period of 9 weeks high fat feeding in adolescent (A), young adult (YA), and middleaged (MA) mice.…”

Section: Introductionmentioning

confidence: 99%

Reduced mitochondrial mass and function add to age-related susceptibility toward diet-induced fatty liver in C57BL/6J mice

et al. 2016

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Nonalcoholic fatty liver disease (NAFLD) is a major health burden in the aging society with an urging medical need for a better understanding of the underlying mechanisms. Mitochondrial fatty acid oxidation and mitochondrial‐derived reactive oxygen species (ROS) are considered critical in the development of hepatic steatosis, the hallmark of NAFLD. Our study addressed in C57BL/6J mice the effect of high fat diet feeding and age on liver mitochondria at an early stage of NAFLD development. We therefore analyzed functional characteristics of hepatic mitochondria and associated alterations in the mitochondrial proteome in response to high fat feeding in adolescent, young adult, and middle‐aged mice. Susceptibility to diet‐induced obesity increased with age. Young adult and middle‐aged mice developed fatty liver, but not adolescent mice. Fat accumulation was negatively correlated with an age‐related reduction in mitochondrial mass and aggravated by a reduced capacity of fatty acid oxidation in high fat‐fed mice. Irrespective of age, high fat diet increased ROS production in hepatic mitochondria associated with a balanced nuclear factor erythroid‐derived 2 like 2 (NFE2L2) dependent antioxidative response, most likely triggered by reduced tethering of NFE2L2 to mitochondrial phosphoglycerate mutase 5. Age indirectly influenced mitochondrial function by reducing mitochondrial mass, thus exacerbating diet‐induced fat accumulation. Therefore, consideration of age in metabolic studies must be emphasized.

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Metabolic and immunomodulatory effects of n-3 fatty acids are different in mesenteric and epididymal adipose tissue of diet-induced obese mice

Abstract: Ludwig T, Worsch S, Heikenwalder M, Daniel H, Hauner H, Bader BL. Metabolic and immunomodulatory effects of n-3 fatty acids are different in mesenteric and epididymal adipose tissue of diet-induced obese mice.

Cited by 33 publications

References 85 publications

Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice

Fish oil ameliorates trimethylamine N-oxide-exacerbated glucose intolerance in high-fat diet-fed mice

Inflammatory characteristics of distinct abdominal adipose tissue depots relate differently to metabolic risk factors for cardiovascular disease

Reduced mitochondrial mass and function add to age-related susceptibility toward diet-induced fatty liver in C57BL/6J mice

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