Metabolic syndrome: a brain disease

2012 ◽  
Vol 90 (9) ◽  
pp. 1171-1183 ◽  
Author(s):  
Ram B. Singh ◽  
Siddharth Gupta ◽  
Parinita Dherange ◽  
Fabien De Meester ◽  
Agnieszka Wilczynska ◽  
...  

Recent research indicates an association between brain dysfunction and the pathogenesis of metabolic syndrome. To investigate this, we created a Medline search (up to December 2011) of articles in PubMed. The results indicated that refined carbohydrates, saturated and total fat, high levels of ω-6 fatty acids, and low levels of ω-3 fatty acids and other long chain polyunsaturated fatty acids (PUFA), all in conjunction with sedentary behaviour and mental stress can predispose to inflammation. Increased sympathetic activity, with increased secretion of catecholamine, cortisol, and serotonin can cause oxidative stress, which may damage the arcuate nucleus as well as the hypothalamus and macrophages, and the liver may release pro-inflammatory cytokines. These, in conjunction with an underlying deficiency in long chain PUFA, may damage the arcuate nucleus as well as neuropeptide-Y and pro-opiomelanocortin neurons and insulin receptors in the brain, especially during fetal life, infancy, and childhood, resulting in their dysfunction. Of the fatty acids in the brain, 30%–50% are long chain PUFA, which are incorporated in the cell membrane phospholipids. Hence, ω-3 fatty acids, which are also known to enhance parasympathetic activity and increase the secretion of anti-inflammatory cytokines interleukin (IL)-4 and IL-10 as well as acetylcholine in the hippocampus, may be protective. Therefore, treatment with ω-3 fatty acids may be applied for the prevention of metabolic syndrome.

2002 ◽  
Vol 2002 ◽  
pp. 7-7 ◽  
Author(s):  
J. L. Capper ◽  
R. G. Wilkinson ◽  
L. A. Sinclair ◽  
S. E. Pattinson ◽  
A. M. Mackenzie

The long-chain polyunsaturated fatty acids (PUFA) docosahexaenoic acid (DHA) and arachidonic acid (AA) are the most abundant fatty acids in the brain and are vital for its correct development and for that of the nervous system (Huang and Craig-Schmidt, 1996). Ruminant diets are low in DHA and its precursor alpha-linolenic acid. In addition, dietary PUFAs are substantially hydrogenated in the rumen. Consequently, it may be argued that the diets of pregnant and lactating ewes may be deficient in DHA and that a response to supplementation may be observed. Studies involving the supplementation of pregnant ewes with supraoptimal levels of vitamin E have shown that lambs born to supplemented dams are more vigorous immediately after birth and have higher liveweight gains (Merrell, 1998). The objective of this experiment was to investigate the effects of dietary long-chain PUFA in combination with vitamin E supplementation of ewes on ewe and lamb performance.


1967 ◽  
Vol 45 (6) ◽  
pp. 853-861 ◽  
Author(s):  
W. Thompson

The hydrolysis of monophosphoinositide by soluble extracts from rat brain is described. Diglyceride and inositol monophosphate are liberated along with a small amount of free fatty acids. Hydrolysis of the lipid is optimal at pH 5.4 in acetate buffer. The reaction is stimulated by calcium ions or by high concentration of monovalent cations and, to a less extent, by long-chain cationic amphipathic compounds. Enzyme activity is lost on dialysis of the brain extract and can be restored by diffusible factor(s). Some differences in the conditions for hydrolysis of mono- and tri-phosphoinositides are noted.


Author(s):  
Shuangshuang Chen ◽  
Qingqing Wu ◽  
Li Zhu ◽  
Geng Zong ◽  
Huaixing Li ◽  
...  

ABSTRACT Background Animal studies have highlighted critical roles of glycerophospholipid (GP) metabolism in various metabolic syndrome (MetS)-related features such as dyslipidemia, obesity, and insulin resistance. However, human prospective studies of associations between circulating GPs and risks of MetS are scarce. Objectives We aimed to investigate whether GPs are associated with incidence of MetS in a well-established cohort. Methods A total of 1243 community-dwelling Chinese aged 50–70 y without MetS at baseline and followed up for 6 y were included in current analyses. A total of 145 plasma GPs were quantified by high-throughput targeted lipidomics. MetS was defined using the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian Americans. Results After 6 y, 429 participants developed MetS. Eleven GPs, especially those with long-chain polyunsaturated fatty acids (LCPUFAs) or very-long-chain polyunsaturated fatty acids (VLCPUFAs) at the sn-2 position, including 1 phosphatidylcholine (PC) [PC(18:0/22:6)], 9 phosphatidylethanolamines (PEs) [PE(16:0/22:6), PE(18:0/14:0), PE(18:0/18:1), PE(18:0/18:2), PE(18:0/20:3), PE(18:0/22:5), PE(18:0/22:6), PE(18:1/22:6), and PE(18:2/22:6)], and 1 phosphatidylserine (PS) [PS(18:0/18:0)], were positively associated with incident MetS (RRs: 1.16–1.30 per SD change; Bonferroni-corrected P < 0.05). In network analysis, the strongest positive association for MetS incidence was evidenced in a module mainly composed of PEs containing C22:6 and PSs [RR: 1.21; 95% CI: 1.12, 1.31 per SD change; Bonferroni-corrected P < 0.05]. This association was more pronounced in participants with lower erythrocyte total n–3 PUFA concentrations [Bonferroni-corrected Pinter(P value for the interaction)< 0.05]. Conclusions Elevated plasma concentrations of GPs, especially PEs with LCPUFAs or VLCPUFAs at the sn-2 position, are associated with higher risk of incident MetS. Future studies are merited to confirm our findings.


2020 ◽  
Vol 40 (10) ◽  
Author(s):  
Cory J. White ◽  
Jieun Lee ◽  
Joseph Choi ◽  
Tiffany Chu ◽  
Susanna Scafidi ◽  
...  

ABSTRACT The metabolic state of the brain can greatly impact neurologic function. Evidence of this includes the therapeutic benefit of a ketogenic diet in neurologic diseases, including epilepsy. However, brain lipid bioenergetics remain largely uncharacterized. The existence, capacity, and relevance of mitochondrial fatty acid β-oxidation (FAO) in the brain are highly controversial, with few genetic tools available to evaluate the question. We have provided evidence for the capacity of brain FAO using a pan-brain-specific conditional knockout (KO) mouse incapable of FAO due to the loss of carnitine palmitoyltransferase 2, the product of an obligate gene for FAO (CPT2B−/−). Loss of central nervous system (CNS) FAO did not result in gross neuroanatomical changes or systemic differences in metabolism. Loss of CPT2 in the brain did not result in robustly impaired behavior. We demonstrate by unbiased and targeted metabolomics that the mammalian brain oxidizes a substantial quantity of long-chain fatty acids in vitro and in vivo. Loss of CNS FAO results in robust accumulation of long-chain acylcarnitines in the brain, suggesting that the mammalian brain mobilizes fatty acids for their oxidation, irrespective of diet or metabolic state. Together, these data demonstrate that the mammalian brain oxidizes fatty acids under normal circumstances with little influence from or on peripheral tissues.


2019 ◽  
Vol 316 (4) ◽  
pp. R362-R375 ◽  
Author(s):  
Morag F. Dick ◽  
Christopher G. Guglielmo

The migratory flights of birds are primarily fueled by fat; however, certain fatty acids may also enhance flight performance and the capacity to oxidize fat. The natural doping hypothesis posits that n–3 long-chain polyunsaturated fatty acids (PUFA) increase membrane fluidity and aerobic and fatty acid oxidative enzymes in the flight muscles, which enables prolonged endurance flight. Support for this hypothesis is mixed, and there is no empirical evidence for increased flight performance. We fed yellow-rumped warblers ( Setophaga coronata coronata) diets enriched in either n–3 or n–6 long-chain PUFA or low in long-chain PUFA and evaluated flight muscle metabolism and endurance performance in a wind tunnel flights lasting up to 6 h. Fatty acid profiles of muscle phospholipids confirmed enrichment of the targeted dietary fatty acids, whereas less substantial differences were observed in adipose triacylglycerol. Contrary to the predictions, feeding n–3 PUFA decreased peroxisome proliferator-activated receptors-β mRNA abundance and muscle oxidative enzyme activities. However, changes in muscle metabolism were not reflected in whole animal performance. No differences were observed in flight performance among diet treatments in terms of endurance capacity, energy costs, or fuel composition. These measures of flight performance were more strongly influenced by body mass and flight duration. Overall, we found no support for the natural doping hypothesis in a songbird. Furthermore, we caution against extending changes in flight muscle metabolic enzymes or fatty acid composition to changes to migratory performance without empirical evidence.


2009 ◽  
Vol 68 (OCE3) ◽  
Author(s):  
J. Costa Leite ◽  
A. P. Hearty ◽  
A. P. Nugent ◽  
M. J. Gibney

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