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Prevalence of obesity among infants and children below 5 years of age is rising dramatically, and early childhood obesity is a forerunner of obesity and obesity-associated diseases in adulthood. Childhood obesity is hence one of the most serious public health challenges today. Here, we have identified a mother-to-child lipid signaling that protects from obesity. We have found that breast milk-specific lipid species, so-called alkylglycerol-type (AKG-type) ether lipids, which are absent from infant formula and adult-type diets, maintain beige adipose tissue (BeAT) in the infant and impede the transformation of BeAT into lipid-storing white adipose tissue (WAT). Breast milk AKGs are metabolized by adipose tissue macrophages (ATMs) to platelet-activating factor (PAF), which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of AKG intake in infancy leads to a premature loss of BeAT and increases fat accumulation. AKG signaling is specific for infants and is inactivated in adulthood. However, in obese adipose tissue, ATMs regain their ability to metabolize AKGs, which reduces obesity. In summary, AKGs are specific lipid signals of breast milk that are essential for healthy adipose tissue development.

Docosahexaenoic acid (DHA), is the major polyunsaturated fatty acid in the brain and is important for both the structure and the function of the nervous system. Mice were fed either an n-3 fatty acid deficient (n-3 Def) or adequate (n-3 Adq) diet for two generations. The mice were housed under two conditions, as a group or in isolation and the major point of the study was to determine whether n-3 fatty acid deficiency would enhance isolation-induced anxiety. Isolation stress was assessed using the novelty suppressed feeding paradigm (NSF) after a 3-week period and the test lasted a maximal duration of 10 min. The number of successful mice consuming food pellets within 5 min in the n-3 Def diet group was low in both housing conditions (group housing, 33% and isolated, 30%), but was 92% in the group housed and 50% in the isolated group when fed the n-3 Adq diet. In the subsequent 5 min period, the isolated housing group consuming the n-3 Adq diet increased up to 79% and the group housed animals fed the n-3 Def diet increased to 67%. However, those that consumed the n-3 deficient diet combined with isolation stress exhibited no increase. These results suggested that the n-3 deficient mice had increased anxiety that was enhanced by the chronic mild stress of social isolation.

Obesity is not only a risk factor for lifestyle-related diseases but also causes skin barrier dysfunction, which leads to a reduced quality of life due to dryness, itching, and scratching, and thus requires appropriate treatment. However, there are no studies on this issue. Therefore, this study aimed to examine whether oral intake of linseed oil is effective for skin barrier function in obesity and to confirm how the effect is demonstrated. TSOD mice received either sterile distilled water (Control group) or linseed oil (Omega group), containing a high level of omega-3 fatty acids, including α-linolenic acid, orally for eight weeks. Mice were then irradiated with ultraviolet B (UVB) and three days later, transepidermal water loss (TEWL), which is the primary outcome of skin barrier function, was measured and gross skin appearance was observed. Hematoxylin and eosin (HE) staining and Ki-67 immunostaining were performed on skin samples. mRNA expression levels of the inflammatory markers , , , and were measured by real-time reverse transcriptase-polymerase chain reaction (RT-PCR). We also performed fatty acid analysis of skin and erythrocytes by gas chromatography. Statistical analysis was performed using unpaired Student's t-test and Pearson's correlation analysis. Compared with the Control group, the Omega group exhibited lower TEWL values and little skin erythema. Histological analysis revealed thinner epidermis and fewer Ki-67 positive cells. Additionally, in the Omega group, mRNA levels of four inflammation-related genes were lower, α-linolenic acid levels in both skin and erythrocytes were higher, and a lower n-6/n-3 ratio was observed. And α-linolenic acid levels in the skin were negatively correlated with the expression levels of inflammation-related genes. Oral intake of linseed oil was found to inhibit skin barrier dysfunction in obesity. This effect was mediated by α-linolenic acid, a major component of linseed oil with anti-inflammatory properties, which was taken up by erythrocytes and supplied to the skin. Therefore, oral intake of linseed oil is expected to be a useful therapeutic method for skin barrier dysfunction in obesity.

In many mammals, early interactions between caregivers and offspring involve rich physical contact during which offspring typically remain calm near the caregiver. Such contact is thought to support emotional regulation during infancy, but how prior experience shapes these mechanisms remains unclear. Here, we show that back stroking induces a calming response in human infants and mouse pups, with reduced movement. In mouse pups, back stroking further reduces heart rate, facilitates sleep onset, and attenuates stress-induced corticosterone elevations. These sleep-promoting and stress-buffering effects are absent in artificially reared pups deprived of postnatal maternal care, suggesting that early experience tunes the calming response to stroking. Transcriptomic analysis reveals reduced hypothalamic expression of the calcium channel subunit gene Cacna1b in artificially reared pups, and knockdown of hypothalamic Cacna1b in maternally reared pups abolishes stroking-induced calming. Thus, early-life maternal care and associated physical contact may shape hypothalamic circuits supporting behavioral and physiological regulation. Back stroking rapidly calms human infants and mouse pups, markedly reducing movement. This shared response requires early-life maternal care and depends on hypothalamic Cav2.2 channel activity, linking caregiving to arousal regulation.

Decreases in brain docosahexaenoic acid (DHA) have been associated with losses in brain function leading to an interest in the conditions which lead to such brain decreases, and such variables as age. Also of relevance would be the rate of repletion of DHA when the n-3 dietary deficiency is reversed. This experiment describes dietary deficiency in n-3 fatty acids induced in weanling (3 week) and young adult (7 week) mice. There was an immediate and continuous loss of brain DHA with similar rates in the two age groups. Serum DHA declined more rapidly in younger animals with respect to similarly treated adults. Brain and serum docosapentaenoic acid (DPAn-6) increased more rapidly and to higher levels in the younger animals. A second experiment determined the rates of normalization of brain fatty acid profiles when alpha-linolenic acid was added to the diets of n-3 deficient mice. Brain DHA recovery occurred at a faster rate (half-time, T 1/2  = 1.4 weeks) when begun at weaning relative to young adult mice ( T 1/2  = 3.5 weeks). Correspondingly, brain DPAn-6 recovered faster in the younger animals; the adult group had a half-time of more than twice that of the 3-week old group. This study therefore demonstrates that the young adult mouse brain DHA is somewhat plastic and can be partially depleted via a low n-3 fatty acid diet and subsequently restored when dietary n-3 fatty acids are repleted. Relevance of these findings for human nutrition is discussed.

Fatty acids and their derivatives play a role in the response to retinal injury. The effects of dietary arachidonic acid (AA) supplementation on N-methyl-N-nitrosourea (MNU)-induced retinal degeneration was investigated in young Lewis rats during the gestational, lactational and post-weaning periods. Dams were fed 0·1, 0·5 or 2·0 % AA diets or a basal ( < 0·01 % AA) diet. On postnatal day 21 (at weaning), male pups received a single intraperitoneal injection of 50 mg MNU/kg or vehicle, and were fed the same diet as their mother for 7 d. Retinal apoptosis was analysed by the terminal deoxynucleotidyl transferase-mediated dUTP digoxigenin nick-end labelling (TUNEL) assay 24 h after the MNU treatment, and retinal morphology was examined 7 d post-MNU. Histologically, all rats that received MNU and were fed the basal and 0·1 % AA diets developed retinal degeneration characterised by the loss of photoreceptor cells (disappearance of the outer nuclear layer and the photoreceptor layer) in the central retina. The 0·5 and 2·0 % AA diets rescued rats from retinal damage. Morphometrically, in parallel with the AA dose (0·5 and 2·0 % AA), the photoreceptor ratio significantly increased and the retinal damage ratio decreased in the central retina, compared with the corresponding ratios in basal diet-fed rats. In parallel with the increase in serum and retinal AA levels and the AA:DHA ratio, the apoptotic index in the central retina was dose-dependently decreased in rats fed the 0·5 and 2·0 % AA diets. In conclusion, an AA-rich diet during the gestation, lactation and post-weaning periods rescued young Lewis rats from MNU-induced retinal degeneration via the inhibition of photoreceptor apoptosis. Therefore, an AA-enriched diet in the prenatal and postnatal periods may be an important strategy to suppress the degree of photoreceptor injury in humans.

We investigated the postpartum mental health of women who had consumed perilla oil or fish oil containing various omega-3 fatty acids for 12 weeks starting in mid-pregnancy. The association between fatty acids in maternal erythrocytes and mental health risk factors was also examined. Healthy Japanese primiparas in mid-pregnancy (gestational weeks 18–25) were randomly divided into two groups and consumed approximately 2.0 g/day of omega-3 fatty acids in either perilla oil (the ALA dose was 2.4 g/day) or fish oil (the EPA + DHA dose was 1.7 g/day) for 12 weeks. Maternal mental health was assessed using the Edinburgh Postnatal Depression Scale (EPDS) as the primary measure and the Mother-to-Infant Bonding Scale (MIBS) as the secondary measure. Data from an observational study were used as a historical control. Maternal blood, cord blood, and colostrum samples were collected for fatty acid composition analysis. In addition, completers of the observational studies were enrolled in a case–control study, wherein logistic regression analysis was performed to examine the association between maternal fatty acids and EPDS score. The proportion of participants with a high EPDS score (≥9) was significantly lower in the perilla oil group (12.0%, p = 0.044) but not in the fish oil group (22.3%, p = 0.882) compared with the historical control (21.6%), while the proportions between the former groups also tended to be lower (p = 0.059). No marked effect of omega-3 fatty acid intake was observed from the MIBS results. In the case–control study of the historical control, high levels of α-linolenic acid in maternal erythrocytes were associated with an EPDS score of <9 (odds ratio of 0.23, 95% confidence interval: 0.06, 0.84, p = 0.018 for trend). The results of this study suggest that consumption of α-linolenic acid during pregnancy may stabilize postpartum mental health.

The aim of this study was to investigate the effects of the administration of oral arachidonic acid (AA) in rats with or without dextran sulphate sodium (DSS)-induced inflammatory bowel disease. Male Wistar rats were administered AA at 0, 5, 35 or 240 mg/kg daily by gavage for 8 weeks. Inflammatory bowel disease was induced by replacing drinking water with 3 % DSS solution during the last 7 d of the AA dosing period. These animals passed loose stools, diarrhoea and red-stained faeces. Cyclo-oxygenase-2 concentration and myeloperoxidase activity in the colonic tissue were significantly increased in the animals given AA at 240 mg/kg compared with the animals given AA at 0 mg/kg. Thromboxane B2 concentration in the medium of cultured colonic mucosae isolated from these groups was found to be dose-dependently increased by AA, and the increase was significant at 35 and 240 mg/kg. Leukotriene B4 concentration was also significantly increased and saturated at 5 mg/kg. In addition, AA at 240 mg/kg promoted DSS-induced colonic mucosal oedema with macrophage infiltration. In contrast, administration of AA for 8 weeks, even at 240 mg/kg, showed no effects on the normal rats. These results suggest that in rats with bowel disease AA metabolism is affected by oral AA, even at 5 mg/kg per d, and that excessive AA may aggravate inflammation, whereas AA shows no effects in rats without inflammatory bowel disease.

Docosahexaenoic acid (DHA) supply to the fetal brain depends upon the dam's dietary intake of n-3 fats. In this study, we measured the incorporation of DHA into the fetal brain and liver in n-3 fatty acid deficient (0.1% alpha-linolenate) mice upon switching to an n-3 fatty acid adequate (2.1% alpha-linolenate) diet. Second generation mice raised and maintained on an n-3 deficient diet during mating were switched to an n-3 adequate diet on embryonic day 1 (ED 1) or ED 13. Fatty acid analysis was performed on fetal brains and livers and on maternal serum on ED 13, 15, 17, and 19. Although fetal brain and liver DHA began at a very low level (both exhibited an 85% decline), recovery was nearly complete by ED 15 in the group switched near conception but thereafter diverged. The maternal serum and fetal liver were very similar in their DHA and docosapentaenoic acid time courses. However, when repletion began on ED 13, brain DHA recovery was only about 44%. These results suggest that a nutritional intervention with alpha-linolenic acid can nearly but incompletely rescue the mouse fetal DHA deficiency if began at the time of conception but that the third trimester is too late, thus leaving a large DHA gap.