Docosahexaenoic acid increases cellular adiponectin mRNA and secreted adiponectin protein, as well as PPARγ mRNA, in 3T3-L1 adipocytes

Oster, Richard T.; Tishinsky, Justine M.; Yuan, Zongfei; Robinson, Lindsay E.

doi:10.1139/h10-076

Cited by 99 publications

(98 citation statements)

References 35 publications

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“…An increased waist circumference has previously been reported in children at 2.5 y of age whose mothers were supplemented with DHA during lactation (5). Although, to our knowledge, our study is the first study to determine the effect of prenatal DHA supplementation on insulin sensitivity, our findings were unexpected because of existing data from in vitro and experimental animal studies that suggested that DHA increases insulin sensitivity (25,26). Although it is possible that the observed differences in insulin sensitivity and the waist:hip ratio may indicate a true underlying adverse effect of DHA supplementation, these differences were secondary outcomes and, as such, require confirmation.…”

Section: Discussionmentioning

confidence: 59%

DHA supplementation during pregnancy does not reduce BMI or body fat mass in children: follow-up of the DHA to Optimize Mother Infant Outcome randomized controlled trial

Mühlhäusler

Yelland

McDermott

et al. 2016

The American Journal of Clinical Nutrition

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Background: The omega-3 (n-3) long-chain polyunsaturated fatty acid (LCPUFA) docosahexaenoic acid (DHA) has proven effective at reducing fat storage in animal studies. However, a systematic review of human trials showed a lack of quality data to support or refute this hypothesis. Objective: We sought to determine whether maternal DHA supplementation during the second half of pregnancy results in a lower body mass index (BMI) and percentage of body fat in children. Design: We conducted a follow-up at 3 and 5 y of age of children who were born to mothers enrolled in the DOMInO (DHA to Optimize Mother Infant Outcome) double-blind, randomized controlled trial, in which women with a singleton pregnancy were provided with DHArich fish-oil capsules (800 mg DHA/d) or vegetable-oil capsules (control group) in the second half of pregnancy. Primary outcomes were the BMI z score and percentage of body fat at 3 and 5 y of age. Potential interactions between prenatal DHA and the peroxisome proliferatoractivated receptor-g (PPARg) genotype as a measure of the genetic predisposition to obesity were investigated. Results: A total of 1614 children were eligible for the follow-up. Parent or caregiver consent was obtained for 1531 children (95%), and these children were included in the analysis. BMI z scores and percentages of body fat of children in the DHA group did not differ from those of children in the control group at either 3 y of age [BMI z score adjusted mean difference: 0.03 (95% CI: 20.07, 0.13; P = 0.61); percentage of body fat adjusted mean difference: 20.26 (95% CI: 20.99, 0.46; P = 0.47)] or 5 y of age [BMI z score adjusted mean difference: 0.02 (95% CI: 20.08, 0.12; P = 0.66); percentage of body fat adjusted mean difference: 0.11 (95% CI: 20.60, 0.82; P = 0.75)]. No treatment effects were modified by the PPARg genotype of the child. Conclusion: Independent of a genetic predisposition to obesity, maternal intake of DHA-rich fish oil during the second half of pregnancy does not affect the growth or body composition of children at 3 or 5 y of age. This trial was registered at www.anzctr.org. au as ACTRN1260500056906 and ACTRN12611001127998. Am J Clin Nutr 2016;103:1489-96.

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Section: Discussionmentioning

confidence: 59%

DHA supplementation during pregnancy does not reduce BMI or body fat mass in children: follow-up of the DHA to Optimize Mother Infant Outcome randomized controlled trial

Mühlhäusler

Yelland

McDermott

et al. 2016

The American Journal of Clinical Nutrition

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“…DHA supplementation in vitro can induce adiponectin expression at both the mRNA and protein levels in 3T3-L1 adipocytes (Oster et al 2010). The stimulating effect of n-3 PUFAs on adiponectin secretion from human adipocytes is believed to be dependent on PPARg (Tishinsky 2013).…”

Section: Induction Of Adipokinesmentioning

confidence: 99%

n-3 polyunsaturated fatty acids and insulin secretion

Wang,

Chan

2014

Journal of Endocrinology

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n-3 polyunsaturated fatty acids (PUFAs) are a subgroup of fatty acids with broad health benefits, such as lowering blood triglycerides and decreasing the risk of some types of cancer. A beneficial effect of n-3 PUFAs in diabetes is indicated by results from some studies. Defective insulin secretion is a fundamental pathophysiological change in both types 1 and 2 diabetes. Emerging studies have provided evidence of a connection between n-3 PUFAs and improved insulin secretion from pancreatic b-cells. This review summarizes the recent findings in this regard and discusses the potential mechanisms by which n-3 PUFAs influence insulin secretion from pancreatic b-cells.

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“…Culture, differentiation, and identification of 3T3-L1 preadipocytes were conducted as described in a previous report (Oster et al, 2010). Cells were maintained in high-glucose DMEM medium supplemented with 10% fetal bovine serum in a humid atmosphere containing 5% CO 2 at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Lentinan depresses 3T3-L1 fat cell formation by inhibiting PPARγ/AKT signaling pathway

Sun

et al. 2015

Genet. Mol. Res.

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ABSTRACT.We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferatoractivated receptor gamma (PPARg)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARg activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARg and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARg mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARg mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARg mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARg/AKT signaling pathway.

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Docosahexaenoic acid increases cellular adiponectin mRNA and secreted adiponectin protein, as well as PPARγ mRNA, in 3T3-L1 adipocytes

Cited by 99 publications

References 35 publications

DHA supplementation during pregnancy does not reduce BMI or body fat mass in children: follow-up of the DHA to Optimize Mother Infant Outcome randomized controlled trial

DHA supplementation during pregnancy does not reduce BMI or body fat mass in children: follow-up of the DHA to Optimize Mother Infant Outcome randomized controlled trial

n-3 polyunsaturated fatty acids and insulin secretion

Lentinan depresses 3T3-L1 fat cell formation by inhibiting PPARγ/AKT signaling pathway

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