Docosahexaenoic acid (DHA), a crucial nervous system n-3 PUFA, may be obtained in the diet or synthesized in vivo from dietary a-linolenic acid (LNA). We addressed whether DHA synthesis is regulated by the availability of dietary DHA in artificially reared rat pups, during p8 to p28 development. Over 20 days, one group of rat pups was continuously fed deuterium-labeled LNA (d5-LNA) and no other n-3 PUFA (d5-LNA diet), and a second group of rat pups was fed a d5-LNA diet with unlabeled DHA (d5-LNA 1 DHA diet). The rat pups were then euthanized, and the total amount of deuterium-labeled docosahexaenoic acid (d5-DHA) (synthesized DHA) as well as other n-3 fatty acids present in various body tissues, was quantified. In the d5-LNA 1 DHA group, the presence of dietary DHA led to a marked decrease (3-to 5-fold) in the total amount of d5-DHA that accumulated in all tissues that we examined, except in adipose. Overall, DHA accretion from d5-DHA was generally diminished by availability of dietary preformed DHA, inasmuch as this was found to be the predominant source of tissue DHA. When preformed DHA was unavailable, d5-DHA and unlabeled DHA were preferentially accreted in some tissues along with a net loss of unlabeled DHA from other organs.-DeMar, Jr., J. C., C. DiMartino, A. W. Baca, W. Lefkowitz, and N. Salem, Jr. Effect of dietary docosahexaenoic acid on biosynthesis of docosahexaenoic acid from alpha-linolenic acid in young rats. J. Lipid Res. 2008Res. . 49: 1963Res. -1980 Supplementary key words essential fatty acids • lipid metabolism • early development • infant formula composition Docosahexaenoic acid (DHA; 22:6n-3) is an n-3 PUFA that is particularly enriched in the phospholipids of cells constituting the mammalian nervous system (1, 2). Functionally, DHA enhances membrane elasticity and molecular motion and thus promotes signal transduction via enhanced protein/receptor interactions (3-6). DHA is also the activating ligand for multiple transcriptional factors that control the expression of enzymes involved in fatty acid synthesis and b-oxidation (7). DHA may be directly obtained in the diet, as preformed DHA, or synthesized in vivo from other common dietary n-3 PUFAs such as a-linolenic acid (LNA, 18:3n-3), eicosapentaenoic acid (EPA, 20:5n-3), or docosapentaenoic acid (DPA, 22:5n-3) (8). All of these n-3 PUFAs may be converted in vivo to DHA through sequential steps of elongation, desaturation, and peroxisomal b-oxidation (9). Prolonged dietary deprivation of all n-3 PUFAs in rat pups, initiated prior to weaning, depletes up to 80% of their brain DHA (10-12). Such depletion of brain DHA in rodents leads to distinct impairments in brain function (11,(13)(14)(15)(16)(17). Piglets and monkeys also show impaired neural function when deprived of n-3 PUFA for an extended period during infancy (18,19). The essentiality of DHA for human infant nutrition in support of neuronal function has been shown by DHA supplementation, enhancing visual acuity and cognition-related test scores in human infants (20)(21)(2...
In the Rocky Mountains of the USA, abundances and distributions of grizzly bear Ursus arctos and gray wolf Canis lupus have increased (Bangs et al., 2001; Nicholson & Hendricks, 2018). This has led to increased predation of livestock in areas where livestock producers have not needed to implement conflict prevention methods in recent history. Lethal removal of carnivores that kill livestock remains a common source of carnivore mortalities (Woodroffe, 2001; Broekhuis, Cushman & Elliot, 2017). In the USA, the U.S. Department of Agriculture's Wildlife Services (USDA-WS) is often asked by the U.S. Fish and Wildlife Service or a State's wildlife management agency to lethally remove large carnivores that depredate livestock. Where possible, conservation practitioners favor increased use of non-lethal tools to replace lethal methods aimed at preventing depredation of livestock. Conservation groups often dispute management actions for large carnivores, sometimes resulting in lawsuits. It is often challenging to look beyond these differences and note that the ultimate goal of these diverse groups is typically some variation on the same theme: to increase coexistence by reducing conflicts between humans and carnivores. Non-lethal tools that reduce livestock depredation could facilitate coexistence; however, scientists note a distinct lack of experimental studies that adequately evaluate the efficacy of non-lethal tools (Eklund et al., 2017; van Eeden et al., 2018). A call for more research is warranted, but the time and resource requirements associated with research are often mismatched to the immediate needs of protecting livestock, large carnivores, and the livelihoods of livestock producers. One non-lethal tool available to reduce depredation of livestock by wolves is fladry. Fladry consists of strands of flags, measuring approximately 50-cm long by 10-cm wide, sewn onto nylon rope at 45-cm intervals. Fladry acts as a primary repellent by taking advantage of the fact that wolves are neophobic and relies on producing a flight response to deter them (Shivik, 2006). When the flags are hung just
Feeding mice, over 3 generations, an equicaloric diet in which α-linolenic acid, the dietary precursor of n-3 polyunsaturated fatty acids, was substituted by linoleic acid, the dietary precursor of n-6 polyunsaturated fatty acids, significantly increased body weight throughout life when compared with standard diet-fed mice. Adipogenesis observed in the low n-3 fatty acid mice was accompanied by a 6-fold upregulation of stearyl-coenzyme A desaturase 1 (Scd1), whose activity is correlated to plasma triglyceride levels. In total liver lipid and phospholipid extracts, the sum of n-3 fatty acids and the individual longer carbon chain acids, eicosapentaenoic acid (20:5n3), docosapentaenoic acid (22:5n3), and docosahexaenoic acid (22:6n3) were significantly decreased whereas arachidonic acid (20:4n6) was significantly increased. In addition, low n-3 fatty acid-fed mice had liver steatosis, heart, and kidney hypertrophy. Hence, reducing dietary α-linolenic acid, from 1.02 energy % to 0.16 energy % combined with raising linoleic acid intake resulted in obesity and had detrimental consequences on organ function.
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