Effects of high-fat diet on plasma profiles of eicosanoid metabolites in mice

Wang, Weicang; Yang, Jun; Yang, Haixia; Sanidad, Katherine Z.; Hammock, Bruce D.; Kim, Dae-Young; Zhang, Guodong

doi:10.1016/j.prostaglandins.2016.11.003

Cited by 18 publications

(12 citation statements)

References 33 publications

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“…In addition, adverse effects as result of high-fat exposure were reported in the following areas: brain, cognition, memory, mental well-being, Alzheimer’s, autistic behaviour [ 33 , 34 , 61 – 63 ]; obesity, metabolic dysfunction, inflammation, liver damage, cardiometabolic risks’ [ 34 , 38 , 64 – 68 ]; risks of cancer [ 66 , 69 ]; osteoporosis [ 70 ]. In elegant animal models, Cani et al [ 71 ] clearly demonstrated that high fat feeding, which induces low intakes of fermentable dietary fibers, may lead to intestinal microbiota changes which are associated with an increased intestinal permeability resulting in endotoxemia and triggers for inflammation and metabolic disorders (note: the examples are only given as an illustration, not for an exhaustive picture).…”

Section: Is a Lchf Diet Healthy And Safe?mentioning

confidence: 99%

Overweight and diabetes prevention: is a low-carbohydrate–high-fat diet recommendable?

2018

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In the past, different types of diet with a generally low-carbohydrate content (< 50–< 20 g/day) have been promoted, for weight loss and diabetes, and the effectiveness of a very low dietary carbohydrate content has always been a matter of debate. A significant reduction in the amount of carbohydrates in the diet is usually accompanied by an increase in the amount of fat and to a lesser extent, also protein. Accordingly, using the term “low carb–high fat” (LCHF) diet is most appropriate. Low/very low intakes of carbohydrate food sources may impact on overall diet quality and long-term effects of such drastic diet changes remain at present unknown. This narrative review highlights recent metabolic and clinical outcomes of studies as well as practical feasibility of low LCHF diets. A few relevant observations are as follows: (1) any diet type resulting in reduced energy intake will result in weight loss and related favorable metabolic and functional changes; (2) short-term LCHF studies show both favorable and less desirable effects; (3) sustained adherence to a ketogenic LCHF diet appears to be difficult. A non-ketogenic diet supplying 100–150 g carbohydrate/day, under good control, may be more practical. (4) There is lack of data supporting long-term efficacy, safety and health benefits of LCHF diets. Any recommendation should be judged in this light. (5) Lifestyle intervention in people at high risk of developing type 2 diabetes, while maintaining a relative carbohydrate-rich diet, results in long-term prevention of progression to type 2 diabetes and is generally seen as safe.

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Section: Is a Lchf Diet Healthy And Safe?mentioning

confidence: 99%

Overweight and diabetes prevention: is a low-carbohydrate–high-fat diet recommendable?

2018

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“…As a result, C18-derived oxylipins are present in much higher amounts than would be predicted from their fatty acid levels, suggesting that they may have a greater impact on physiology. Although much less is known about the physiological effects of C18 compared with C20-and C22-derived oxylipins, they have been associated with varied effects that are either protective or harmful in a number of states, including inflammation in processes associated with atherosclerosis, mitogenic effects associated with cancer, pain sensitivity, and with obesity and the metabolic syndrome (55,56).…”

Section: Discussionmentioning

confidence: 99%

Dietary LA and sex effects on oxylipin profiles in rat kidney, liver, and serum differ from their effects on PUFAs

Leng

Winter

Aukema

2017

Journal of Lipid Research

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A vast literature on fatty acids in mammals exists, but comparable compositional data on oxylipins is lacking. Weanling Sprague-Dawley rats were therefore provided control diets or diets with higher linoleic acid (LA) or with higher LA and α-linolenic acid (LA+ALA) for 6 weeks. Kidneys, livers, and serum were analyzed for oxylipins and fatty acids. The proportion of tissue oxylipins derived from LA was greater than the relative proportion of LA itself, whereas arachidonic acid (AA) oxylipins were overrepresented in serum. Higher dietary LA increased kidney LA and AA oxylipins, despite not altering LA or AA. In liver, both LA and AA and their oxylipins were higher, whereas in serum only LA oxylipins were higher with higher dietary LA. Higher LA resulted in a higher ratio of n-6/n-3 PUFA-derived oxylipins; adding ALA to the LA diet mitigated this and many, but not all, effects of the LA diet. Approximately 40% of oxylipins detected were influenced by sex and, unlike their PUFA precursors, most (>90%) of these were higher in males. These differences in dietary LA and sex on oxylipin and fatty acid profiles further our understanding of the effects of fatty acids and may have implications for dietary LA recommendations.

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“…Chronic low-grade inflammation was reported to play a pivotal role in the pathogenesis of obesity ( Hotamisligil, 2006 ). Thus, targeting inflammation appears as an attractive strategy to counter the burden of obesity and its associated comorbidities ( Hardwick et al, 2013 ; Wang et al, 2016 ). Among potential targets, PGE2 appears of particular interest since previous works have reported their contribution to the uncontrolled inflammation observed in obese individuals ( González-Périz and Clària, 2010 ).…”

Section: Discussionmentioning

confidence: 99%

Invalidation of Microsomal Prostaglandin E Synthase-1 (mPGES-1) Reduces Diet-Induced Low-Grade Inflammation and Adiposity

et al. 2018

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Chronic low-grade inflammation is known to be linked to obesity, and to occur in the early stages of the disease. This mechanism is complex and involves numerous organs, cells, and cytokines. In this context, inflammation of white adipose tissue seems to play a key role in the development of obesity. Because of its properties, prostaglandin E2 (PGE2), an emblematic inflammatory mediator, has been proposed as an actor linking inflammation and obesity. Indeed, PGE2 is involved in mechanisms that are dysregulated in obesity such as lipolysis and adipogenesis. Microsomal prostaglandin E synthase-1 (mPGES-1) is an enzyme, which specifically catalyzes the final step of PGE2 biosynthesis. Interestingly, mPGES-1 invalidation dramatically alters the production of PGE2 during inflammation. In the present work, we sought to determine whether mPGES-1 could contribute to inflammation associated with obesity. To this end, we analyzed the energy metabolism of mPGES-1 deficient mice (mPGES-1-/-) and littermate controls, fed with a high-fat diet. Our data showed that mPGES-1-/- mice exhibited resistance to diet-induced obesity when compared to wild-type littermates. mPGES-1-/- mice fed with a high-fat diet, showed a lower body weight gain and a reduced adiposity, which were accompanied by a decrease in adipose tissues inflammation. We also observed an increase in energy expenditures in mPGES-1-/- mice fed with a high-fat diet without any changes in activity and browning process. Altogether, these data suggest that mPGES-1 inhibition may prevent diet-induced obesity.

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Effects of high-fat diet on plasma profiles of eicosanoid metabolites in mice

Cited by 18 publications

References 33 publications

Overweight and diabetes prevention: is a low-carbohydrate–high-fat diet recommendable?

Overweight and diabetes prevention: is a low-carbohydrate–high-fat diet recommendable?

Dietary LA and sex effects on oxylipin profiles in rat kidney, liver, and serum differ from their effects on PUFAs

Invalidation of Microsomal Prostaglandin E Synthase-1 (mPGES-1) Reduces Diet-Induced Low-Grade Inflammation and Adiposity

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