A list of puns related to "List of unsaturated fatty acids"
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.
A question more of biology than philosophy.
I know that aquatic animals such as fish are already (relatively) rich in saturated fat usually exceeding 15%, sometimes even exceeding 40% depending on the fish.
I know the reason why animals have saturated fat, particularly ruminants farmed or wild have high levels of saturated fat usually hovering around 50% of the fat composition. It is because when they ferment fiber short chain fatty acids are produced which are 100% saturated fat which they then incorporate into their own bodies, occasionally elongating these saturated fats to create other fatty acids.
But what is the ecological+biological reason that fish has so much unsaturated fatty acids monounsaturated and polyunsaturated?
The presence of a cis or trans CΞ±=CΞ² double bond in unsaturated fatty acid substrates dramatically changes the catalytic efficiency and chemo-/regioselectivity of three representative CYP152 peroxygenases including OleTJE, P450SPΞ±, and P450BSΞ², which provides new insights into their unusual catalytic mechanisms.
CYP152 peroxygenases catalyze decarboxylation and hydroxylation of fatty acids using H2O2 as cofactor. To understand the molecular basis for the chemo- and regioselectivity of these unique P450 enzymes, we analyze the activities of three CYP152 peroxygenases (OleTJE, P450SPΞ±, P450BSΞ²) towards cis- and trans-dodecenoic acids as substrate probes. The unexpected 6S-hydroxylation of the trans-isomer and 4R-hydroxylation of the cis-isomer by OleTJE, and molecular docking results suggest that the unprecedented selectivity is due to OleTJEβs preference of C2βC3 cis-configuration. In addition to the common epoxide products, undecanal is the unexpected major product of P450SPΞ± and P450BSΞ² regardless of the cis/trans-configuration of substrates. The combined H218O2 tracing experiments, MD simulations, and QM/MM calculations unravel an unusual mechanism for Compoundβ I-mediated aldehyde formation in which the active site water derived from H2O2 activation is involved in the generation of a four-membered ring lactone intermediate. These findings provide new insights into the unusual mechanisms of CYP152 peroxygenases.
https://ift.tt/3llcyl6
https://doi.org/10.3390/nu13051737
https://pubmed.ncbi.nlm.nih.gov/34065380
Fasting and postprandial hypertriglyceridemia are causal risk factors for atherosclerosis. The prevalence of hypertriglyceridemia is approximately 25-30% and most hypertriglyceridemic patients suffer from mild to moderate hypertriglyceridemia. Data regarding dietary interventions on postprandial triglyceride metabolism of mildly to moderately hypertriglyceridemic patients is, however, sparse. In a randomized controlled trial, eight mildly hypertriglyceridemic patients and five healthy, normolipidemic controls received three separate standardized fat-meals containing either saturated fatty acids (SFA), mono-unsaturated fatty acids (MUFA), or medium-chain fatty acids (MCFA) in a randomized order. Fasting and postprandial lipid parameters were determined over a 10 h period and the (incremental) area under the curve (AUC/iAUC) for plasma triglycerides and other parameters were determined. MCFA do not lead to a significant elevation of postprandial total plasma triglycerides and other triglyceride parameters, while both SFA (patients:p = 0.003, controls:p = 0.03 compared to MCFA) and MUFA (patients:p = 0.001, controls:p = 0.14 compared to MCFA) do lead to such an increase. Patients experienced a significantly more pronounced increase of plasma triglycerides than controls (SFA: patients iAUC = 1006 mgh/dL, controls iAUC = 247 mgh/dL,p = 0.02, MUFA: patients iAUC = 962 mgh/dL, controls iAUC = 248 mgh/dL,p = 0.05). Replacing SFA with MCFA may be a treatment option for mildly to moderately hypertriglyceridemic patients as it prevents postprandial hypertriglyceridemia.
------------------------------------------ Info ------------------------------------------
Open Access: True
Authors: Alexander Folwaczny - Elisa Waldmann - Julia Altenhofer - Kerstin Henze - Klaus G. Parhofer -
Additional links:
https://pubmed.ncbi.nlm.nih.gov/12848276/
Review Lipids
. 2003 Apr;38(4):317-21. doi: 10.1007/s11745-003-1066-0.
William E M Lands 1Affiliations expand
The 2002 ISSFAL Meeting arranged a special evening discussion with professional dietitians about diet-tissue-disease relationships involving essential fatty acids and eicosanoids. The balance of eicosanoid precursors in human tissues differs widely, reflecting voluntary dietary choices among different groups worldwide. An empirical quantitative diet-tissue relationship fits these diverse values as well as other research reports on essential fatty acid metabolism. Information for dietitians and nutritionists about essential fatty acids and eicosanoids is also given in two distance learning web sites, http://ods.od.nih.gov/eicosanoids/ and http:// efaeducation.nih.gov/, which facilitate dietitian education and diet counseling. These sites also have an innovative, interactive diet planning software program with the empirical equation embedded in it to help evaluate personal food choices in the context of the diet-tissue-disease relationship and other widely recommended dietary advice.
https://academic.oup.com/advances/advance-article/doi/10.1093/advances/nmab013/6164876?login=true
> > # Perspective: The Saturated FatβUnsaturated Oil Dilemma: Relations of Dietary Fatty Acids and Serum Cholesterol, Atherosclerosis, Inflammation, Cancer, and All-Cause Mortality > > Glen D Lawrence > > Advances in Nutrition, nmab013, https://doi.org/10.1093/advances/nmab013 > > Published: 09 March 2021 > > ## ABSTRACT > > PUFAs are known to regulate cholesterol synthesis and cellular uptake by multiple mechanisms that do not involve SFAs. Polymorphisms in any of the numerous proteins involved in cholesterol homeostasis, as a result of genetic variation, could lead to higher or lower serum cholesterol. PUFAs are susceptible to lipid peroxidation, which can lead to oxidative stress, inflammation, atherosclerosis, cancer, and disorders associated with inflammation, such as insulin resistance, arthritis, and numerous inflammatory syndromes. Eicosanoids from arachidonic acid are among the most powerful mediators that initiate an immune response, and a wide range of PUFA metabolites regulate numerous physiological processes. There is a misconception that dietary SFAs can cause inflammation, although endogenous palmitic acid is converted to ceramides and other cell constituents involved in an inflammatory response after it is initiated by lipid mediators derived from PUFAs. This article will discuss the many misconceptions regarding how dietary lipids regulate serum cholesterol, the fact that all-cause death rate is higher in humans with low compared with normal or moderately elevated serum total cholesterol, the numerous adverse effects of increasing dietary PUFAs or carbohydrate relative to SFAs, as well as metabolic conversion of PUFAs to SFAs and MUFAs as a protective mechanism. Consequently, dietary saturated fats seem to be less harmful than the proposed alternatives. >
Full text:
https://academic.oup.com/advances/advance-article/doi/10.1093/advances/nmab013/6164876?guestAccessKey=cddd09e8-cfae-46b4-b073-bcb41bcc7c91&fbclid=IwAR3Hbow_gigFuVG0JJO7LQT_VAIlGSijSL8iv8G9gfxkEpzS1xdVs9njz5s
If you cook a fatty pork roast for several hours in the oven, some of the fat will be rendered, ending up as liquid fat in the bottom of the pan. When the roast is done, the layer of fat on it wil be thinner, due to the partial rendering. Will the fatty acid profile now be the same for the fat that is still solid and attached to the meat, as that for the rendered liquid fat? Or will the unsaturated fat be rendered first due to a lower melting point, thus leaving you with a more saturated layer of fat on your roast, the longer it is cooked?
Mason, Paul et al. βSCD1 inhibition causes cancer cell death by depleting mono-unsaturated fatty acids.β PloS one vol. 7,3 (2012): e33823. doi:10.1371/journal.pone.0033823
https://preview.redd.it/o5w730h1tai71.png?width=1278&format=png&auto=webp&s=98a5d62b440e589576587ebe544ec730821d38f5
SCD1 inhibition kills cancer and they use a chemical called TOFA to inhibit SCD1
I see that "PUFA" spitted out in their conversations as so matter-of-factly-bad it's almost like a curse word among them. They are quite sternly advocating to stop eating seed oils and start eating lard and butter. Mono-unsaturated fatty acids such as in olive oil seem to be on neutral ground among them. But I rarely if ever see it expounded upon further as to "why?". I'd ask this in their subreddits, but unfortunately they have all permabanned me for asking questions about their diet already. :)
Give me the best research on the dangers of PUFA compared to SFA, I'm curious.
Arch Physiol Biochem. 2011 Jul;117(3):131-9. doi: 10.3109/13813455.2011.557387. Epub 2011 Mar 11.
Adipose tissues function as the primary storage compartment of fatty acids and as an endocrine organ that affects peripheral tissues. Many of adipose tissue-derived factors, often termed adipokines, have been discovered in recent years. The synthesis and secretion of these factors vary in different depots of adipose tissues. Excessive lipid accumulation in adipocytes induces inflammatory processes by up-regulating the expression and release of pro-inflammatory cytokines. In addition, activated macrophages in the obese adipose tissue release inflammatory cytokines. Adipose tissue inflammation has also been linked to an enhanced metabolism of polyunsaturated fatty acids (PUFAs). The non-enzymatic peroxidation of PUFAs and of their 12/15-lipoxygenase-derived hydroperoxy metabolites leads to the generation of the reactive aldehyde species 4-hydroxyalkenals. This review shows that 4-hydroxyalkenals, in particular 4-hydroxynonenal, play a key role in lipid storage homeostasis in normal adipocytes. Nonetheless, in the obese adipose tissue an increased production of 4-hydroxyalkenals contributes to the inflamed phenotype.
PMID: 21395403 DOI: 10.3109/13813455.2011.557387
So I was reading my book and came across these lines, " Wax is insoluble in water and made out of unsaturated fatty acids. They're chemically inert as their hydrocarbon chains don't have any double bonds ". Now, this is where they lost me, how can a fatty acid be unsaturated and the wax molecule not have double bonds at the same time?
A polyaromatic cavity: The exclusive binding of a monounsaturated fatty acid from a mixture with the corresponding saturated substrate was demonstrated by an artificial polyaromatic receptor in water. Competitive binding experiments revealed higher binding affinity of the receptor for oligoβ and polyunsaturated fatty acids (see picture). Within the receptor, the biosubstrates were stabilized against air, light, and heat owing to the polyaromatic shielding effect.
Selective recognition of natural fatty acids is intrinsically difficult owing to the long, flexible, and poorly interactive hydrocarbon chains. Inspired by biological recognition systems, we herein demonstrate the exclusive binding of a monounsaturated fatty acid by an artificial polyaromatic receptor from a mixture of the unsaturated and corresponding saturated substrates (i.e., oleic and stearic acids) in water. The selectivity stems from multiple CHβΟ/ΟβΟ interactions between the host framework and the guest in its roughly coiled conformation. Moreover, competitive binding experiments elucidate higher binding affinities of the receptor for oligoβ and polyunsaturated fatty acids (e.g., Ξ±βlinolenic acid and EPA). Within the receptor, the biosubstrates are remarkably stabilized against air, light, and heat owing to the polyaromatic shielding effect.
https://ift.tt/33CHzrq
My EK textbook says that unsaturated fatty acids have lower reduction potential than saturated fatty acids. But how? Unsaturated fatty acids have 2 fewer electrons per double bond present (compared to saturated). Doesn't less electrons mean you WANT more electrons --> increase reduction potential? Like for example, alkenes (double bonds) are more likely to get reduced (increase reduction potential) right? If alkenes are similar to unsaturated fatty acids (bc they have double bonds), aren't both more likely to get reduced, hence increase reduction potential?
Trying to figure out the best fats for Keto. I know MCTs are great and vegetable oils are a no-go.
What is the clinical relevance of saturated and mono-unsaturated fatty acids?
Please note that this site uses cookies to personalise content and adverts, to provide social media features, and to analyse web traffic. Click here for more information.