scholarly journals Molecular effects of dietary fatty acids on brain insulin action and mitochondrial function

2019 ◽  
Vol 400 (8) ◽  
pp. 991-1003
Author(s):  
Chantal Chudoba ◽  
Kristina Wardelmann ◽  
André Kleinridders

Abstract The prevalence of obesity and its co-morbidities such as insulin resistance and type 2 diabetes are tightly linked to increased ingestion of palatable fat enriched food. Thus, it seems intuitive that the brain senses elevated amounts of fatty acids (FAs) and affects adaptive metabolic response, which is connected to mitochondrial function and insulin signaling. This review will address the effect of dietary FAs on brain insulin and mitochondrial function with a special emphasis on the impact of different FAs on brain function and metabolism.

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1518
Author(s):  
Mareike Schell ◽  
Chantal Chudoba ◽  
Antoine Leboucher ◽  
Eugenia Alfine ◽  
Tanina Flore ◽  
...  

Overconsumption of high-fat and cholesterol-containing diets is detrimental for metabolism and mitochondrial function, causes inflammatory responses and impairs insulin action in peripheral tissues. Dietary fatty acids can enter the brain to mediate the nutritional status, but also to influence neuronal homeostasis. Yet, it is unclear whether cholesterol-containing high-fat diets (HFDs) with different combinations of fatty acids exert metabolic stress and impact mitochondrial function in the brain. To investigate whether cholesterol in combination with different fatty acids impacts neuronal metabolism and mitochondrial function, C57BL/6J mice received different cholesterol-containing diets with either high concentrations of long-chain saturated fatty acids or soybean oil-derived poly-unsaturated fatty acids. In addition, CLU183 neurons were stimulated with combinations of palmitate, linoleic acid and cholesterol to assess their effects on metabolic stress, mitochondrial function and insulin action. The dietary interventions resulted in a molecular signature of metabolic stress in the hypothalamus with decreased expression of occludin and subunits of mitochondrial electron chain complexes, elevated protein carbonylation, as well as c-Jun N-terminal kinase (JNK) activation. Palmitate caused mitochondrial dysfunction, oxidative stress, insulin and insulin-like growth factor-1 (IGF-1) resistance, while cholesterol and linoleic acid did not cause functional alterations. Finally, we defined insulin receptor as a novel negative regulator of metabolically stress-induced JNK activation.


2010 ◽  
Vol 30 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Taha A Kumosani ◽  
Said S Moselhy

Omega-3 fatty acids were used in the treatment of psychiatric diseases such as bipolar disorder. Na +, K+-ATPase is also a well-known target for these fatty acids. In this study, we investigated the impact of cod-liver oil (CLO), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on Na+, K+-ATPase, cholinesterase activities, the levels of norepinephrine (NE) and acetylcholine in different regions of rat brain. Our results showed that DHA caused a significant depression in cerebellum Na+, K +-ATPase, whereas CLO activated it. In addition, CLO, EPA and DHA produced a significant activation in Na+, K+-ATPase activity in medulla, midbrain and hypothalamus. There were non-significant changes in the activity of cholinesterase enzyme in cerebellum and medulla, while in midbrain and hypothalamus the CLO, DHA and EPA enhanced the activity by 75%, 100% and 78%, respectively. The content of NE in hypothalamus showed slight increase in different regions of the brain of animals fed CLO, DHA or EPA. In conclusion, CLO, DHA or EPA supplementation had a beneficial effect that associated with a normalization of fatty acids incorporation into phospholipid membranes and a partial restoration of Na+, K+-ATPase activity, suggesting that CLO supplementation may improve fatty acid composition and moderately enhance Na+, K+-ATPase activity.


2013 ◽  
Vol 13 (16) ◽  
pp. 7-8
Author(s):  
M. Mosley ◽  
A. C. Carpentier

2018 ◽  
Vol 64 (1) ◽  
pp. 72-81 ◽  
Author(s):  
Piriyah Sinclair ◽  
Neil Docherty ◽  
Carel W le Roux

Abstract BACKGROUND Obesity can be defined as a chronic subcortical brain disease, as there is an important neurophysiological component to its etiology based on changes in the functioning of those areas of the brain controlling food intake and reward. Extensive metabolic changes accompany bariatric surgery-based treatment of obesity. Consequently, the term “metabolic” surgery is being increasingly adopted in relation to the beneficial effects these procedures have on chronic diseases like type 2 diabetes. CONTENT In the present review, we focus on the key biochemical and physiological changes induced by metabolic surgery and highlight the beneficial effects accrued systemically with the use of an organ-based approach. Understanding the impact on and interactions between the gut, brain, adipose tissue, liver, muscle, pancreas, and kidney is key to understanding the sum of the metabolic effects of these operations. SUMMARY Further mechanistic studies are essential to assess the true potential of metabolic surgery to treat metabolic comorbidities of obesity beyond type 2 diabetes. Approaches that may mitigate the metabolic side effects of surgery also require attention. Understanding the positive impact of metabolic surgery on metabolic health may result in a wider acceptance of this intervention as treatment for metabolic, comorbid conditions.


2008 ◽  
Vol 11 (11) ◽  
pp. 1149-1155 ◽  
Author(s):  
Nadiah Moussavi ◽  
Victor Gavino ◽  
Olivier Receveur

AbstractBackgroundAnimal studies and a few clinical trials lend credibility to the hypothesis that not all types of fatty acids carry the same potential for weight gain. Only a few epidemiological studies concerning this issue are currently available and results are conflicting.AimThe purpose of the present ecological study was to test the existence of an association between obesity prevalence and the types of fat available in 168 countries.MethodsData on the prevalence of obesity (BMI ≥ 30 kg/m2) for women over 15 years of age were obtained from the WHO Global InfoBase. Food balance sheets for the years 1998 to 2002 were obtained from the FAOSTAT database. Five-year means for energy, total fat, MUFA, PUFA, SFA and ‘other fat’ per capita were calculated, with their standard deviations, for each country. Bivariate correlations and a multiple linear regression model were used to test for the association between prevalence of obesity and types of fat available in these countries.ResultsNot surprisingly, dietary energy supply, SFA, PUFA and ‘other fat’ were positively associated with the prevalence of obesity. We also found, however, a strong negative association between MUFA availability and obesity prevalence (β= −0·68,P< 0·0001).ConclusionPopulations with a lower prevalence of obesity seem to consume a greater amount of MUFA. Considering the partial correlations between variables, our results suggest that in countries with higher obesity prevalence, it is the shift from MUFA to PUFA that particularly appears to be associated with the risk of obesity.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 861-861
Author(s):  
Jowy Seah Yi Hoong ◽  
Wee Siong Chew ◽  
Federico Torta ◽  
Chin Meng Khoo ◽  
Markus R Wenk ◽  
...  

Abstract Objectives Sphingolipid concentrations have been associated with risk of type 2 diabetes and cardiovascular diseases. Because sphingolipids can be synthesized de novo from saturated fatty acids (SFA), dietary fatty acids may affect plasma sphingolipid concentrations. We aimed to evaluate dietary fat and protein intakes in relation to circulating sphingolipid levels. Methods We used cross-sectional data from 2860 ethnic Chinese Singaporeans collected from 2004–2007. Nutrient intakes were estimated on the basis of a validated 159-item food frequency questionnaire. We quantified 79 molecularly distinct sphingolipids in a large-scale lipidomic evaluation from plasma samples. Results Higher saturated fat intake was associated with higher concentrations of 16:1; O2 sphingolipids including ceramides, monohexosylcermides, dihexosylceramides, sphingomyelins, and sphingosine 1-phosphates. Higher polyunsaturated fat intake was associated with lower plasma long-chain ceramides and long-chain monohexosylcermide concentrations. Protein intake was inversely associated with concentrations of most subclasses of sphingolipids, with the exception of sphingolipids containing a 16:1; O2 sphingoid base. Lower intake of saturated fat and higher intake of polyunsaturated fat and protein may decrease plasma concentrations of several sphingolipid classes. Conclusions These findings may represent a novel biological mechanism for the impact of nutrient intakes on cardio-metabolic health. Funding Sources This work was supported by the National Research Foundation Investigatorship grant (NRF-NRFI2015–05, to MRW), A*STAR (I1901E0040), and the National University Health System (NUHSRO/2014/085/AF-Partner/01, DRH). FT was supported by the NRF and A*STAR IAF-ICP I1901E0040.


2019 ◽  
Vol 79 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Leanne Hodson ◽  
Fredrik Rosqvist ◽  
Siôn A Parry

Non-alcoholic fatty liver disease encompasses a spectrum of conditions from hepatic steatosis through to cirrhosis; obesity is a known risk factor. The liver plays a major role in regulating fatty acid metabolism and perturbations in intrahepatic processes have potential to impact on metabolic health. It remains unclear why intra-hepatocellular fat starts to accumulate, but it likely involves an imbalance between fatty acid delivery to the liver, fatty acid synthesis and oxidation within the liver and TAG export from the liver. As man spends the majority of the day in a postprandial rather than postabsorptive state, dietary fatty acid intake should be taken into consideration when investigating why intra-hepatic fat starts to accumulate. This review will discuss the impact of the quantity and quality of dietary fatty acids on liver fat accumulation and metabolism, along with some of the potential mechanisms involved. Studies investigating the role of dietary fat in liver fat accumulation, although surprisingly limited, have clearly demonstrated that it is total energy intake, rather than fat intake per se, that is a key mediator of liver fat content; hyperenergetic diets increase liver fat whilst hypoenergetic diets decrease liver fat content irrespective of total fat content. Moreover, there is now, albeit limited evidence emerging to suggest the composition of dietary fat may also play a role in liver fat accumulation, with diets enriched in saturated fat appearing to increase liver fat content to a greater extent when compared with diets enriched in unsaturated fats.


2018 ◽  
Vol 121 (2) ◽  
pp. 130-136
Author(s):  
Véronique Chajès ◽  
Lorna J. Gibson ◽  
Carine Biessy ◽  
Nadia Slimani ◽  
Gershim Asiki ◽  
...  

AbstractNon-communicable diseases are projected to become the most common causes of death in Africa by 2030. The impact on health of epidemiological and nutritional transitions in sub-Saharan Africa remains unclear. To assess the trends of dietary fatty acids over time in Uganda, we examined fatty acids in serum collected from individuals in rural south-west Uganda, at three time points over two decades. Independent cross-sectional samples of 915 adults and children were selected from the general population cohort in 1990 (n 281), 2000 (n 283) and 2008 (n 351). Serum phospholipid fatty acids were measured by GC. Multivariate regression analyses were performed to compare the geometric means of fatty acids by time period. Serum fatty acid profiling showed high proportions of SFA, cis-MUFA and industrial trans-fatty acids (iTFA), likely to be biomarkers of high consumption of palm oil and hydrogenated fats. In contrast, proportions of n-6 and n-3 PUFA from vegetable oils and fish were low. From 1990 to 2008, serum phospholipids showed increases in absolute amounts of SFA (17·3 % increase in adults and 26·4 % in children), MUFA (16·7 % increase in adults and 16·8 % in children) and n-6:n-3 PUFA (40·1 % increase in adults and 39·8 % in children). The amount of elaidic acid, iTFA from hydrogenated fats, increased in children (60·1 % increase). In this rural Ugandan population, we show evidence of unfavourable trends over time of dietary fatty acids.


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