Comparative Serum Fatty Acid Profiles of Captive and Free-Ranging Cheetahs (Acinonyx jubatus) in Namibia
- Adrian S. W. Tordiffe ,
- Bettina Wachter,
- Sonja K. Heinrich,
- Fred Reyers,
- Lodewyk J. Mienie
- Published: December 19, 2016
- https://doi.org/10.1371/journal.pone.0167608
Abstract
Cheetahs (Acinonyx jubatus) are highly specialised large felids, currently listed as vulnerable on the IUCN red data list. In captivity, they are known to suffer from a range of chronic non-infectious diseases. Although low heterozygosity and the stress of captivity have been suggested as possible causal factors, recent studies have started to focus on the contribution of potential dietary factors in the pathogenesis of these diseases. Fatty acids are an important component of the diet, not only providing a source of metabolisable energy, but serving other important functions in hormone production, cellular signalling as well as providing structural components in biological membranes. To develop a better understanding of lipid metabolism in cheetahs, we compared the total serum fatty acid profiles of 35 captive cheetahs to those of 43 free-ranging individuals in Namibia using gas chromatography-mass spectrometry. The unsaturated fatty acid concentrations differed most remarkably between the groups, with all of the polyunsaturated and monounsaturated fatty acids, except arachidonic acid and hypogeic acid, detected at significantly lower concentrations in the serum of the free-ranging animals. The influence of age and sex on the individual fatty acid concentrations was less notable. This study represents the first evaluation of the serum fatty acids of free-ranging cheetahs, providing critical information on the normal fatty acid profiles of free-living, healthy individuals of this species. The results raise several important questions about the potential impact of dietary fatty acid composition on the health of cheetahs in captivity.
βDiet may both increase and decrease oxidative stress in the body. We compared the effects of four strictly controlled isocaloric diets with different intakes of polyunsaturated fatty acids (PUFA, 11 or 3% of energy) and vegetables and fruit (total amount of vegetables and fruit 516 or 1059 g/10 MJ) on markers associated with oxidative stress in 77 healthy volunteers (19β52 years). Plasma protein carbonyls (2-aminoadipic semialdehyde residues) and whole-body DNA and nucleotide oxidation (urinary 8- oxo-7,8-dihydro-20-deoxyguanosine excretion) tended to decrease in all treatment groups with no differences between the diets. The diets did not differ in their effects on red blood cell antioxidative enzyme activities, either. The results suggest that in healthy volunteers with adequate nutrient intakes, 6-week diets differing markedly in the amount of PUFA or vegetables and fruit do not differ in their effects on markers associated with oxidative stress.β
https://www.nature.com/articles/1602865.pdf
Intake of Ο-6 Polyunsaturated Fatty Acid-Rich Vegetable Oils and Risk of Lifestyle Diseases
Tetsumori Yamashima, Tsuguhito Ota, Eishiro Mizukoshi, Hiroyuki Nakamura, Yasuhiko Yamamoto, Mitsuru Kikuchi, Tatsuya Yamashita, Shuichi Kaneko Advances in Nutrition, Volume 11, Issue 6, November 2020, Pages 1489β1509, https://doi.org/10.1093/advances/nmaa072 Published: 04 July 2020 Article history Cite Permissions Icon Permissions Share
https://academic.oup.com/advances/article-abstract/11/6/1489/5867525
Abstract
Although excessive consumption of deep-fried foods is regarded as 1 of the most important epidemiological factors of lifestyle diseases such as Alzheimer's disease, type 2 diabetes, and obesity, the exact mechanism remains unknown. This review aims to discuss whether heated cooking oil-derived peroxidation products cause cell degeneration/death for the occurrence of lifestyle diseases. Deep-fried foods cooked in Ο-6 PUFA-rich vegetable oils such as rapeseed (canola), soybean, sunflower, and corn oils, already contain or intrinsically generate βhydroxynonenalβ by peroxidation. As demonstrated previously, hydroxynonenal promotes carbonylation of heat-shock protein 70.1 (Hsp70.1), with the resultant impaired ability of cells to recycle damaged proteins and stabilize the lysosomal membrane. Until now, the implication of lysosomal/autophagy failure due to the daily consumption of Ο-6 PUFA-rich vegetable oils in the progression of cell degeneration/death has not been reported. Since the βcalpain-cathepsin hypothesisβ was formulated as a cause of ischemic neuronal death in 1998, its relevance to Alzheimer's neuronal death has been suggested with particular attention to hydroxynonenal. However, its relevance to cell death of the hypothalamus, liver, and pancreas, especially related to appetite/energy control, is unknown. The hypothalamus senses information from both adipocyte-derived leptin and circulating free fatty acids. Concentrations of circulating fatty acid and its oxidized form, especially hydroxynonenal, are increased in obese and/or aged subjects. As overactivation of the fatty acid receptor G-protein coupled receptor 40 (GPR40) in response to excessive or oxidized fatty acids in these subjects may lead to the disruption of Ca2+ homeostasis, it should be evaluated whether GPR40 overactivation contributes to diverse cell death. Here, we describe the molecular implication of Ο-6 PUFA-rich vegetable oil-derived hydroxynonenal in lysosomal desta
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Western high-fat diet can cause chronic pain, according to new study
A typical Western high-fat diet can increase the risk of painful disorders common in people with conditions such as diabetes or obesity, according to a groundbreaking paper authored by a team led by The University of Texas Health Science Center at San Antonio, also referred to as UT Health San Antonio.
Moreover, changes in diet may significantly reduce or even reverse pain from conditions causing either inflammatory pain -- such as arthritis, trauma or surgery -- or neuropathic pain, such as diabetes. The novel finding could help treat chronic-pain patients by simply altering diet or developing drugs that block release of certain fatty acids in the body.
The paper, more than five years in the making, was published in the June edition of the journal Nature Metabolism by a collaborative team of 15 local researchers, headed by first co-authors Jacob T. Boyd, MD, PhD, and Peter M. LoCoco, PhD, of the Department of Endodontics at UT Health San Antonio.
In all, 11 of the co-authors are from UT Health San Antonio, including seven current or former students of its Graduate School of Biomedical Sciences; three represent the Department of Chemistry at the University of Texas at San Antonio; and one is from the Department of Neurology with the South Texas Veterans Health Care System.
"This study exemplifies team science at its best -- multiple scientists and clinicians with complementary expertise working together to make lives better," said Kenneth M. Hargreaves, DDS, PhD, professor and chair of the Department of Endodontics at UT Health San Antonio, and senior author of the paper.
Fatty acids and pain
Chronic pain is a major cause of disability around the world. But although fat-reduction often is advised to manage diabetes, auto-immune disorders and cardiovascular diseases, the role of dietary lipids, or fatty acids, in pain conditions has been relatively unknown.
In the new paper, Dr. Boyd and his colleagues used multiple methods in both mice and humans to study the role of polyunsaturated fatty acids in pain conditions. They found that typical Western diets high in omega-6 polyunsaturated fats served as a significant risk factor for both inflammatory and neuropathic pain.
**Omega-6 fats, mainly found in foods with vegetable oils, have their benef
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Article
Peroxidation of n-3 and n-6 polyunsaturated fatty acids in the acidic tumor environment leads to ferroptosis-mediated anticancer effects
EmelineDierge12ElenaDebock2CΓ©lineGuilbaud1CyrilCorbet1EricMignolet2LouiseMignard2EstelleBastien1ChantalDessy1YvanLarondelle23OlivierFeron134
https://doi.org/10.1016/j.cmet.2021.05.016
Highlights
β’ n-3 and n-6 PUFAs preferentially accumulate in lipid droplets of acidic cancer cells
β’ Excess LC-PUFAs undergo peroxidation and induce ferroptosis in acidic cancer cells
β’ DGAT inhibitors prevent the formation of lipid droplets and promote ferroptosis
β’ DGATi enhance the tumor growth inhibitory effects of dietary n-3 LC-PUFAs in mice
Summary
Tumor acidosis promotes disease progression through a stimulation of fatty acid (FA) metabolism in cancer cells. Instead of blocking the use of FAs by acidic cancer cells, we examined whether excess uptake of specific FAs could lead to antitumor effects. We found that n-3 but also remarkably n-6 polyunsaturated FA (PUFA) selectively induced ferroptosis in cancer cells under ambient acidosi
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