Arachidonic acid impairs hypothalamic leptin signaling and hepatic energy homeostasis in mice

Cheng, Licai; Yu, Yinghua; Zhang, Qingsheng; Szabo, Alexander; Wang, Hongqin; Huang, Xu‐Feng

doi:10.1016/j.mce.2015.04.025

Cited by 29 publications

(20 citation statements)

References 51 publications

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“…Mice were sacrificed at the end of week 12 and blood, liver and brain samples were collected for protein (synaptic proteins in brain) and lipid analyses. promoting obesity (Cheng et al, 2015). However, there is still a debate about the ARA influence on obesity-associated inflammation (Suitor et al, 2017).…”

Section: Arachidonic Acid In the Current Western Dietsmentioning

confidence: 99%

Dietary arachidonic acid: a Janus face actor in brain and Alzheimer’s disease?

Pinchaud

Maguin‐Gaté

Olivier

2018

OCL

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Arachidonic acid is the second polyunsaturated fatty acid in brain and the first one belonging to the ω-6 series. Dietary intakes of arachidonic are between 50 and 300 mg/day in western diets but they might be underestimated. Triglycerides from fat would provide similar amounts than phospholipids of lean meat. Alzheimer’s disease is an age-associated degenerative disease and a critical health concern worldwide. Amyloid-β peptide oligomers are presently recognized as the main and earliest agents of Alzheimer’s disease although their neurotoxicity requires the presence of tau protein. We and others established that the arachidonic-specific cytosolic phospholipase A2 is critical for the amyloid-β peptide oligomer neurotoxicity. Then, we showed that an arachidonic acid-rich diet increases the mouse sensitivity to the amyloid-β peptide oligomer deleterious effect without major increase of arachidonic acid levels in brain. This suggests that dietary arachidonic acid can exert its effects in brain through peripheral modifications. Involvement of systemic sub-inflammation and gut-brain communications are discussed based on the recent literature. The various data suggest that dietary arachidonic acid should be taken into account in the design of preventive strategies against Alzheimer’s disease.

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Section: Arachidonic Acid In the Current Western Dietsmentioning

confidence: 99%

Dietary arachidonic acid: a Janus face actor in brain and Alzheimer’s disease?

Pinchaud

Maguin‐Gaté

Olivier

2018

OCL

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“…With HFD feeding, mice accumulate a number of fatty acid species in the hypothalamus, including triacylglycerols, diacylglycerols and ceramides (34). Furthermore, acute intracerebroventricular (icv) infusion of lipids such as the saturated fatty acid palmitate and the ω-6 polyunsaturated arachidonate induces inflammatory signaling (11, 35–37), alters autophagic protection from cellular stress (38), increases the unfolded protein response in the endoplasmic reticulum (39, 40••), promotes insulin and leptin resistance (11, 41) and possibly triggers apoptosis (42). Likewise, lipid ingestion via milk fat gavage or butter-based HFD consumption increases the hypothalamic levels of saturated fatty acids and proinflammatory gene expression without evidence of systemic inflammation (15••, 17).…”

Section: Dietary and Cellular Mediators Of Hypothalamic Inflammationmentioning

confidence: 99%

Hypothalamic inflammation and gliosis in obesity

Dorfman

Thaler

2015

Current Opinion in Endocrinology, Diabetes &Amp; Obesity

120

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Structured Abstract Purpose of review Hypothalamic inflammation and gliosis are recently discovered mechanisms that may contribute to obesity pathogenesis. Current research in this area suggests that investigation of these CNS responses may provide opportunities to develop new weight loss treatments. Recent findings In rodents, hypothalamic inflammation and gliosis occur rapidly with high-fat diet consumption prior to significant weight gain. In addition, sensitivity or resistance to diet-induced obesity in rodents generally correlates with the presence or absence of hypothalamic inflammation and reactive gliosis (brain response to injury). Moreover, functional interventions that increase or decrease inflammation in neurons and glia correspondingly alter diet-associated weight gain. However, some conflicting data have recently emerged that question the contribution of hypothalamic inflammation to obesity pathogenesis. However, several studies have detected gliosis and disrupted connectivity in obese humans, highlighting the potential translational importance of this mechanism. Summary There is growing evidence that obesity is associated with brain inflammation in humans, particularly in the hypothalamus where its presence may disrupt body weight control and glucose homeostasis. More work is needed to determine whether this response is common in human obesity and to what extent it can be manipulated for therapeutic benefit.

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“…High-fat diets rich in ω-6 fatty acids, as in current Western diets, increase the risk of leptin resistance, diabetes and obesity in humans and rodents. [25][26][27] A diet high in the ω-6 to ω-3 ratio causes an increase in the endocannabinoid signalling and related mediators, which leads to an increased inflammatory state, energy homeostasis and mood. 28 In animal experiments, a high ω-6 fatty acid intake leads to decreased insulin sensitivity in muscle and promotes fat accumulation in adipose tissue.…”

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confidence: 99%