Skip to main content
Download PDF

Characterization of the fatty acid profile in the ventral midbrain of mice exposed to dietary imbalance between omega-6 and omega-3 fatty acids during specific life stages

BMC Research Notes volume 15, Article number: 285 (2022) Cite this article

Abstract

Objective

Omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFAs) are essential nutrients. Dietary imbalance between these PUFAs, in particular high in n-6 PUFAs and low in n-3 PUFAs (n-6high/n-3low), is common in modern society. We have previously reported that C57BL/6 mouse male offspring derived from mothers exposed to an n-6high/n-3low diet during the gestation had an augmented ventral midbrain dopamine system in adulthood; however, the fatty acid composition in this brain region has not yet been investigated. This follow-up study aims to characterize the fatty acid profile of the ventral midbrain of mice exposed to the n-6high/n-3low diet during specific life stages.

Results

n-6 PUFAs, especially linoleic acid, were increased in the ventral midbrain of offspring exposed to the n-6high/n-3low diet during the gestation compared to those exposed to a well-balanced control diet throughout life. On the other hand, n-3 PUFAs, especially docosahexaenoic acid, were decreased in the ventral midbrain of offspring exposed to the n-6high/n-3low diet during the gestation, lactation, or postweaning period compared to those exposed to the control diet throughout life. Thus, exposure to the n-6high/n-3low diet in pregnancy increases linoleic acid and that in any life stage decreases docosahexaenoic acid in the offspring's ventral midbrain.

Introduction

Fatty acids are primary components of lipids and are mainly categorized into saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and omega-6 (n-6) and omega-3 (n-3) polyunsaturated fatty acids (PUFAs). In the brain, these fatty acids work as structural components of the cellular membrane and serve as signaling molecules [1]. Animals can biosynthesize SFAs and MUFAs, but most animals cannot synthesize n-6 or n-3 PUFAs. Thus, these PUFAs are essential nutrients that must be obtained from the diet.

Major dietary sources of n-6 and n-3 PUFAs are linoleic acid (LA) and α-linolenic acid (ALA), respectively [2, 3], but major components of n-6 and n-3 PUFAs in the brain are arachidonic acid (ARA) and docosahexaenoic acid (DHA), respectively [4]. Regarding n-6 PUFAs in the brain, a large amount of n-6 docosapentaenoic acid (n-6 DPA) is synthesized when dietary deficiency in n-3 PUFAs is prolonged [5]. Regarding the functional aspects of these PUFAs, LA, ARA, ALA, and DHA in the culture medium induce the proliferation and/or differentiation of embryonic neural stem cells [6,7,8,9], and maintaining appropriate and sufficient levels of these PUFAs in the cellular membrane is essential for proper brain development [10,11,12]. Even after birth, the supply of these PUFAs is also critical for postnatal brain growth [13, 14], and the composition of n-6 and n-3 PUFAs in the adult brain is thought to affect various behaviors [5]. The supply of ARA and DHA also appears to be involved in the prevention of the age-accelerated functional decline in the brain [4, 15]. This evidence clearly shows that n-6 and n-3 PUFAs are indispensable components of the brain in every life stage.

n-6 and n-3 PUFAs are generally competitive in various metabolic processes, and the n-6/n-3 ratios of PUFAs that compose our bodies and our diets warrant particular attention [5, 16]. Regarding recent nutritional trends leading to foods that are high in n-6 PUFAs and low in n-3 PUFAs [17, 18], life-long exposure to a diet high in n-6 and low in n-3 PUFAs (an n-6high/n-3low diet) beginning from conception to adulthood increased the levels of ARA and n-6 DPA and decreased that of DHA in the offspring’s whole brain during the embryonic, early postnatal, and adult periods compared to the offspring’s whole brain exposed to a well-balanced control diet [11, 12]. In parallel with such changes in the brain fatty acid profile, life-long exposure to the n-6high/n-3low diet resulted in increased sucrose intake in the offspring compared to the offspring exposed to the control diet [12]. As sucrose intake behavior is strongly mediated by the ventral midbrain dopamine system [19], these data indicate that increased and/or decreased levels of PUFAs in the adult brain might augment the dopamine system, which was also proposed by another study [20].

In addition to the well-accepted notion that n-6 and n-3 PUFAs that compose the adult brain control various behaviors [5], recent birth cohort studies have found that maternal dietary n-6 and n-3 PUFAs are relevant to offspring behaviors in childhood [21, 22]. In animal studies, we also found that increased levels of ARA and n-6 DPA and decreased levels of DHA in the embryonic and early postnatal whole brain of the offspring exposed to the n-6high/n-3low diet [11] were completely recovered to control levels in the adult whole brain of the offspring exposed to diets adequate in ALA from the early postnatal period to adulthood [23]; nevertheless, maternal exposure to the n-6high/n-3low diet limited to the gestation period similarly led to increased sucrose intake in the offspring [12]. Thus, it is likely that offspring in utero exposed to the n-6high/n-3low diet show increased sucrose intake without significant changes in the fatty acid profile of the adult whole brain. However, the fatty acid composition in the ventral midbrain of these mice has not yet been investigated. To further expand the findings obtained in our previous studies, we investigated the level of each fatty acid in the ventral midbrain of offspring exposed to the n-6high/n-3low diet during specific life stages.

Main text

Materials and methods

Animals

C57BL/6 J mice were obtained from Clea Japan Inc. (Tokyo, Japan) and housed at Fukushima Medical University under a standard 12-h light/12-h dark schedule. Food and water were available ad libitum. No material for environmental enrichment was used. Animal or cage location was not randomized. All mice (n = 55) were healthy throughout the experiment, and no mouse was excluded from the analyses (> 20% reduction of body weight was set as a humane endpoint).

Diets

The control and n-6high/n-3low diets [12] were manufactured by Clea Japan Inc. The control diet was based on the AIN-93G diet [24] and was formulated to contain the following components: 51.9486 g cornstarch, 1 g α-cornstarch, 10 g sucrose, 7 g soybean oil (Additional file 1: Table S1), 1.4 mg tert-butylhydroquinone, 20 g milk casein, 0.3 g L-cystine, 5 g cellulose powder, 3.5 g AIN-93G mineral mix, 1 g AIN-93 vitamin mix, and 0.25 g choline bitartrate per 100 g complete diet. The n-6high/n-3low diet was produced by replacing soybean oil in the control diet with high-linoleic safflower oil (Additional file 1: Table S1), as previously reported [10,11,12, 23]. Consequently, the n-6high/n-3low diet contained more LA (18:2n-6) and less ALA (18:3n-3) than the control diet (Table 1).

Table 1 Fatty acid composition of the diets
Full size table

Feeding paradigm

Female mice (n = 3/group) were fed either the diet from 11 weeks of age and bred with male mice at 13 weeks of age. The offspring were weaned at 3 weeks of age, and the male offspring (n = 8/group) were group-housed at 2–4 mice per cage and those in adulthood were used for the behavioral and histological experiments in the previous study [12] and for the fatty acid analysis in this follow-up study.

For life-long dietary exposure, we fed mother mice and their offspring with either the control diet or the n-6high/n-3low diet throughout gestation, lactation, and postweaning periods, which were defined as the control group or the life-long group, respectively (Fig. 1a). We also fed them with the n-6high/n-3low diet either during the gestation, lactation, or postweaning periods, and fed with the control diet during the remaining periods, which were defined as the gestation group, the lactation group, or the postweaning group (Fig. 1a).

Fig. 1
figure 1

Experimental design to examine the effects of exposure to the n-6high/n-3low diet during specific life stages on the fatty acid profile in the ventral midbrain in adulthood. a Feeding paradigm in the present study. b Body weight of the offspring. n = 8 mouse/group. Different letters show statistically significant differences (P < 0.05 by Tukey’s HSD test) between the groups

Full size image

Fatty acid analysis of brain lipid fractions

The offspring that exposed to behavioral analyses [12] and maintained under free-feeding conditions were deeply anesthetized by intraperitoneal injection of sodium pentobarbital (> 75 mg/kg body weight), euthanized by cervical dislocation, and decapitated, and the brains were dissected from the surrounding tissues. To obtain the ventral midbrain, 1-mm-thick coronal sections were prepared using a brain slicer (BS-Z 2000C, Muromachi Kikai, Tokyo, Japan), and the ventral midbrain was manually dissected from the relevant section based on the mouse brain atlas [25]. The fatty acid composition of the ventral midbrains obtained from three offspring per group was evaluated using the gas chromatography as previously described [12, 26,27,28]. The gas chromatography was performed once. Three offspring data were averaged in different groups. Each peak area in the chromatogram was obtained through the data analysis software. The ratio of the peak area of each fatty acid to the peak area of the internal standard (tricosanoic acid) was calculated, and then the amount of each fatty acid in the analyte was calculated by multiplying the above ratio by the amount of the internal standard used. Recovery of the internal standard was 98.9% in average.

Statistical analysis

To compare all the pairs of groups, Tukey’s honestly significant difference (HSD) test was used for each experiment by using SPSS Statistics (IBM, Armonk, NY). Differences with a P value < 0.05 were considered statistically significant. Normality of data was not evaluated. Sample size was determined based on our previous study [12]. The investigators were not blinded to the experiments. All summary data are presented as the mean ± SEM.

Results

Mice in every group grew similarly, and we confirmed that their body weight in adulthood was similar (Fig. 1b).

Next, the levels of n-6 and n-3 PUFAs in the ventral midbrain of these mice were evaluated (Additional file 1: Fig. S1 and Table S2). The levels of total n-6 PUFAs, especially LA (18:2) and n-6 DPA (22:5), were increased in the gestation and life-long groups, respectively, compared to the control group (Fig. 2a). The level of docosatetraenoic acid (22:4) was slightly decreased in the lactation group compared to the control group (Fig. 2a). Regarding n-3 PUFAs, the level of DHA (22:6) was decreased in every group (in the gestation, lactation, postweaning, and life-long groups) compared to the control group (Fig. 2b). We also found that the n-6/n-3 ratio in the ventral midbrain was increased in the gestation and life-long groups compared to the control group (Fig. 2c). These data show that the composition of n-6 or n-3 PUFAs in the adult ventral midbrain was differently or similarly affected, respectively, by exposure to an n-6high/n-3low diet during specific life stages.

Fig. 2
figure 2

Fatty acid profile in the ventral midbrain of the offspring exposed to the n-6high/n-3low diet during specific life stages. Levels of n-6 PUFAs (a), n-3 PUFAs (b), SFAs (d), and MUFAs (e) and the n-6/n-3 ratio (c) in the offspring’s ventral midbrain (n = 3 mouse/group). Fatty acids with more than 1% total fatty acids in either group are shown. Different letters show statistically significant differences (P < 0.05 by Tukey’s HSD test) between the groups

Full size image

We also evaluated the levels of SFAs and MUFAs in the ventral midbrain (Additional file 1: Fig. S1 and Table S2). The level of total SFAs, especially palmitic acid (PA; 16:0), was increased in the gestation and postweaning groups compared to the control group (Fig. 2d). On the other hand, the total MUFA levels, especially oleic acid (OA; 18:1n-9) and to a lesser extent eicosenoic acid (20:1), were decreased in the gestation group compared to the control group (Fig. 2e). These data show that the composition of SFAs and MUFAs in the adult ventral midbrain was affected by gestational exposure to an n-6high/n-3low diet and that of SFAs was also affected by postweaning exposure to an n-6high/n-3low diet.

Discussion

The level of DHA in the ventral midbrain may be differentially controlled compared to that in other brain regions. We have previously reported that exposure to the n-6high/n-3low diet during the gestation period in mice decreased the level of DHA in the embryonic whole brain [11], which was totally recovered in the adult whole brain by postnatal exposure to diets adequate in ALA [23]. It has also been reported that exposure to an n-6high/n-3low diet during the gestation period in rhesus monkeys decreased the DHA level in the frontal cortex at birth, but this reduction was completely recovered by postnatal exposure to a diet adequate in ALA for 2–3 years [29]. These reports suggest that reduced DHA in most brain regions can be recovered by postnatal dietary ALA in mice and monkeys. Thus, it is surprising that the DHA level in the ventral midbrain was decreased in every group in this study compared to the control group. Our data suggest that DHA in the ventral midbrain is vulnerable to reduction induced by dietary deficiency in n-3 PUFAs throughout life, and reduced DHA in the ventral midbrain that occurs in any life stage is not recovered by dietary ALA.

n-6 DPA is synthesized from adrenic acid, an n-6 PUFA, when dietary deficiency in n-3 PUFAs is prolonged and is thought to compensate for reduced DHA in the cellular membrane [5]. In line with this notion, we found that n-6 DPA and DHA in the ventral midbrain were increased and decreased, respectively, in the life-long group. However, in the gestation, lactation, and postweaning groups, n-6 DPA was not increased compared to that in the control group, despite reduced DHA. These results suggest that n-6 DPA does not play a role in compensating for reduced DHA in the ventral midbrain when exposure to an n-6high/n-3low diet is limited to specific life stages.

Are any fatty acids in the ventral midbrain responsible for the increased sucrose intake in the offspring exposed to the n-6high/n-3low diet? We have previously shown that offspring in the gestation and life-long groups, but not in the lactation or postweaning groups, showed increased sucrose intake compared to that of the control group [12]. However, in the present study, we did not find any fatty acids in the ventral midbrain that showed changes common in the gestation and life-long groups but not in the lactation or postweaning groups. As another possible mechanism by which exposure to the n-6high/n-3low diet during the gestation period increased offspring sucrose intake in adulthood, we found that offspring in the gestation and life-long groups, but not in the lactation or postweaning groups, had an increased number of dopaminergic neurons in the ventral midbrain [12]. The production of dopaminergic neurons is only observed in the embryonic brain; thus, it is possible that increased dopaminergic neurogenesis in the embryonic midbrain caused by in utero exposure to an n-6high/n-3low diet increases sucrose intake in adult offspring. The relationships between the levels of n-6 and n-3 PUFAs in the ventral midbrain and increased sucrose intake and between increased dopaminergic neurogenesis and increased sucrose intake warrant further investigations.

Limitations

  • We used the diets containing only ALA as an n-3 PUFA; however, n-3 PUFAs in human diets include not only ALA but also eicosapentaenoic acid and DHA [2, 3].

  • The n-6/n-3 ratio in the n-6high/n-3low diet is approximately 120/1, which is much higher than that in modern human diets, whose n-6/n-3 ratio is generally within the range of 4/1 to 20/1 [18]. Future study to investigate the effects of various dietary n-6/n-3 ratios on the brain fatty acid profile is warranted.

  • We used male offspring in this study because female offspring exposed to the n-6high/n-3low diet did not show increased sucrose intake compared to the female offspring exposed to the control diet [12]; however, we confirmed that there are sexual differences in the fatty acid profile of the whole brain between male and female mice [23]. Investigating the fatty acid profile of the ventral midbrain of female offspring exposed to the n-6high/n-3low diet should be performed in future studies.

Availability of data and materials

The datasets generated during this study are available from the corresponding author on reasonable request.

Abbreviations

ALA:

α-Linolenic acid

ARA:

Arachidonic acid

DHA:

Docosahexaenoic acid

DPA:

Docosapentaenoic acid

HSD:

Honestly significant difference

n-6high/n-3low :

High in n-6 PUFAs and low in n-3 PUFAs

LA:

Linoleic acid

MUFA:

Monounsaturated fatty acid

OA:

Oleic acid

PA:

Palmitic acid

PUFA:

Polyunsaturated fatty acid

SFA:

Saturated fatty acid

References

  1. Sakayori N, Kimura R, Osumi N. Impact of lipid nutrition on neural stem/progenitor cells. Stem Cells Int. 2013;2013: 973508.

    Article  Google Scholar 

  2. Elmadfa I, Kornsteiner M. Dietary fat intake—a global perspective. Ann Nutr Metab. 2009;54(Suppl 1):8–14.

    CAS  Article  Google Scholar 

  3. Otsuka R, Kato Y, Imai T, Ando F, Shimokata H. Higher serum EPA or DHA, and lower ARA compositions with age independent fatty acid intake in japanese aged 40 to 79. Lipids. 2013;48:719–27.

    CAS  Article  Google Scholar 

  4. Soderberg M, Edlund C, Kristensson K, Dallner G. Fatty acid composition of brain phospholipids in aging and in Alzheimer’s disease. Lipids. 1991;26:421–5.

    CAS  Article  Google Scholar 

  5. Okuyama H, Kobayashi T, Watanabe S. Dietary fatty acids–the N-6/N-3 balance and chronic elderly diseases. Excess linoleic acid and relative N-3 deficiency syndrome seen in Japan. Prog Lipid Res. 1996;35:409–57.

    CAS  Article  Google Scholar 

  6. Kawakita E, Hashimoto M, Shido O. Docosahexaenoic acid promotes neurogenesis in vitro and in vivo. Neuroscience. 2006;139:991–7.

    CAS  Article  Google Scholar 

  7. Sakayori N, Maekawa M, Numayama-Tsuruta K, Katura T, Moriya T, Osumi N. Distinctive effects of arachidonic acid and docosahexaenoic acid on neural stem/progenitor cells. Genes Cells. 2011;16:778–90.

    CAS  Article  Google Scholar 

  8. Sakayori N, Osumi N. Polyunsaturated fatty acids and their metabolites in neural development and implications for psychiatric disorders. Curr Psychopharmacol. 2013;2:73–83.

    CAS  Article  Google Scholar 

  9. Dyall SC, Mandhair HK, Fincham RE, Kerr DM, Roche M, Molina-Holgado F. Distinctive effects of eicosapentaenoic and docosahexaenoic acids in regulating neural stem cell fate are mediated via endocannabinoid signalling pathways. Neuropharmacology. 2016;107:387–95.

    CAS  Article  Google Scholar 

  10. Coti Bertrand P, O’Kusky JR, Innis SM. Maternal dietary (n-3) fatty acid deficiency alters neurogenesis in the embryonic rat brain. J Nutr. 2006;136:1570–5.

    Article  Google Scholar 

  11. Sakayori N, Kikkawa T, Tokuda H, Kiryu E, Yoshizaki K, Kawashima H, et al. Maternal dietary imbalance between omega-6 and omega-3 polyunsaturated fatty acids impairs neocortical development via epoxy metabolites. Stem Cells. 2016;34:470–82.

    CAS  Article  Google Scholar 

  12. Sakayori N, Katakura M, Hamazaki K, Higuchi O, Fujii K, Fukabori R, et al. Maternal dietary imbalance between omega-6 and omega-3 fatty acids triggers the offspring’s overeating in mice. Commun Biol. 2020;3:473.

    CAS  Article  Google Scholar 

  13. Harauma A, Yasuda H, Hatanaka E, Nakamura MT, Salem N Jr, Moriguchi T. The essentiality of arachidonic acid in addition to docosahexaenoic acid for brain growth and function. Prostaglandins Leukot Essent Fatty Acids. 2017;116:9–18.

    CAS  Article  Google Scholar 

  14. Harauma A, Hatanaka E, Yasuda H, Nakamura MT, Salem N Jr, Moriguchi T. Effects of arachidonic acid, eicosapentaenoic acid and docosahexaenoic acid on brain development using artificial rearing of delta-6-desaturase knockout mice. Prostaglandins Leukot Essent Fatty Acids. 2017;127:32–9.

    CAS  Article  Google Scholar 

  15. Hashimoto M, Katakura M, Tanabe Y, Al Mamun A, Inoue T, Hossain S, et al. n-3 fatty acids effectively improve the reference memory-related learning ability associated with increased brain docosahexaenoic acid-derived docosanoids in aged rats. Biochem Biophys Acta. 2015;1851:203–9.

    CAS  PubMed  Google Scholar 

  16. Simopoulos AP. Evolutionary aspects of the dietary omega-6:omega-3 fatty acid ratio: medical implications. World Rev Nutr Diet. 2009;100:1–21.

    CAS  Article  Google Scholar 

  17. Blasbalg TL, Hibbeln JR, Ramsden CE, Majchrzak SF, Rawlings RR. Changes in consumption of omega-3 and omega-6 fatty acids in the United States during the 20th century. Am J Clin Nutr. 2011;93:950–62.

    CAS  Article  Google Scholar 

  18. Simopoulos AP. An increase in the Omega-6/Omega-3 fatty acid ratio increases the risk for obesity. Nutrients. 2016;8:128.

    Article  Google Scholar 

  19. Hajnal A, Norgren R. Accumbens dopamine mechanisms in sucrose intake. Brain Res. 2001;904:76–84.

    CAS  Article  Google Scholar 

  20. Zimmer L, Delion-Vancassel S, Durand G, Guilloteau D, Bodard S, Besnard JC, et al. Modification of dopamine neurotransmission in the nucleus accumbens of rats deficient in n-3 polyunsaturated fatty acids. J Lipid Res. 2000;41:32–40.

    CAS  Article  Google Scholar 

  21. Kim H, Kim H, Lee E, Kim Y, Ha EH, Chang N. Association between maternal intake of n-6 to n-3 fatty acid ratio during pregnancy and infant neurodevelopment at 6 months of age: results of the MOCEH cohort study. Nutr J. 2017;16:23.

    Article  Google Scholar 

  22. Hamazaki K, Matsumura K, Tsuchida A, Kasamatsu H, Tanaka T, Ito M, et al. Maternal dietary intake of fish and PUFAs and child neurodevelopment at 6 months and 1 year of age: a nationwide birth cohort-the Japan Environment and Children’s Study (JECS). Am J Clin Nutr. 2020;112:1295–303.

    Article  Google Scholar 

  23. Sakayori N, Tokuda H, Yoshizaki K, Kawashima H, Innis SM, Shibata H, et al. Maternal nutritional imbalance between linoleic acid and alpha-linolenic acid increases offspring’s anxious behavior with a sex-dependent manner in mice. Tohoku J Exp Med. 2016;240:31–7.

    CAS  Article  Google Scholar 

  24. Reeves PG, Nielsen FH, Fahey GC Jr. AIN-93 purified diets for laboratory rodents: final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet. J Nutr. 1993;123:1939–51.

    CAS  Article  Google Scholar 

  25. Paxinos G, Franklin K. The mouse brain in stereotaxic coordinates. 2nd ed. Cambridge: Academic Press; 2001.

    Google Scholar 

  26. Hashimoto M, Shinozuka K, Gamoh S, Tanabe Y, Hossain MS, Kwon YM, et al. The hypotensive effect of docosahexaenoic acid is associated with the enhanced release of ATP from the caudal artery of aged rats. J Nutr. 1999;129:70–6.

    CAS  Article  Google Scholar 

  27. Inoue T, Hashimoto M, Katakura M, Tanabe Y, Al Mamun A, Matsuzaki K, et al. Effects of chronic administration of arachidonic acid on lipid profiles and morphology in the skeletal muscles of aged rats. Prostaglandins Leukot Essent Fatty Acids. 2014;91:119–27.

    CAS  Article  Google Scholar 

  28. Muramatsu H, Akimoto N, Hashimoto M, Sugibayashi K, Katakura M. Influence of Polyunsaturated Fatty Acid Intake on Kidney Functions of Rats with Chronic Renal Failure. Mar Drugs. 2021;19:692.

    CAS  Article  Google Scholar 

  29. Anderson GJ, Neuringer M, Lin DS, Connor WE. Can prenatal N-3 fatty acid deficiency be completely reversed after birth? Effects on retinal and brain biochemistry and visual function in rhesus monkeys. Pediatr Res. 2005;58:865–72.

    CAS  Article  Google Scholar 

Download references

Acknowledgements

We thank Ms. Chiaki Kanno at Fukushima Medical University for animal care and Nisshin OilliO Group, Ltd. (Tokyo, Japan) for providing the high-linoleic safflower oil.

Funding

This work was supported by JSPS KAKENHI Grant Numbers JP17J10395 and JP21H03357 (to N.S.) and the Lotte Research Promotion Grant (to N.S.). These funders do not have any role in the design, analysis, or reporting of the study.

Author information

Authors and Affiliations

  1. Department of Physiology and Oral Physiology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, 734-8553, Japan

    Nobuyuki Sakayori & Makoto Sugita

  2. Department of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University, Fukushima, 960-1295, Japan

    Nobuyuki Sakayori, Susumu Setogawa & Kazuto Kobayashi

  3. Japan Society for the Promotion of Science, Chiyoda-ku, Tokyo, 102-0083, Japan

    Nobuyuki Sakayori & Susumu Setogawa

  4. Laboratory of Nutritional Physiology, Department of Pharmaceutical Sciences, Faculty of Pharmacy and Pharmaceutical Sciences, Josai University, Saitama, 350-0295, Japan

    Masanori Katakura

  5. Department of Physiology, Osaka Metropolitan University Graduate School of Medicine, Osaka, 545-8585, Japan

    Susumu Setogawa

Authors
  1. Nobuyuki Sakayori
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Masanori Katakura
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Susumu Setogawa
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Makoto Sugita
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Kazuto Kobayashi
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

NS conceived the study, performed the experiments, analyzed the data, and wrote the paper; MK performed the experiments and analyzed the data; and SS, MS, and KK analyzed the data. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Nobuyuki Sakayori.

Ethics declarations

Ethics approval and consent to participate

All animal experiments were performed in accordance with the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals and were approved by the committee for animal experimentation of our university.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interest.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Additional file 1

: Fig. S1. Representative chromatograms obtained from the gas chromatography of the brain lipids. Chromatograms of the the control (a), gestation (b), lactation (c), postweaning (d), and life-long (e) groups. Table S1. Fatty acid composition of the dietary oils. Fatty acid composition is shown as % of total fatty acids (n = 3 dietary oils/group). Table S2. Retention time and peak area of each fatty acid in the chromatograms (n = 3 mouse/group).

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and Permissions

About this article

Verify currency and authenticity via CrossMark

Cite this article

Sakayori, N., Katakura, M., Setogawa, S. et al. Characterization of the fatty acid profile in the ventral midbrain of mice exposed to dietary imbalance between omega-6 and omega-3 fatty acids during specific life stages. BMC Res Notes 15, 285 (2022). https://doi.org/10.1186/s13104-022-06175-0

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s13104-022-06175-0

Keywords

  • Omega-6
  • Omega-3
  • Fatty acid profile
  • Midbrain
  • Life stage

BMC Research Notes

ISSN: 1756-0500

Contact us