|ZHOU, BINGJIE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|ICHIKAWA, REIKO - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|NOEL, SABRINA - University Of Massachusetts|
|ZHANG, XIYUAN - University Of Massachusetts|
|BHUPATHIRAJU, SHILPA - Harvard School Of Public Health|
|SMITH, CAREN - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|TUCKER, KATHERINE - University Of Massachusetts|
|ORDOVAS, JOSE - Jean Mayer Human Nutrition Research Center On Aging At Tufts University|
|Lai, Chao Qiang|
Submitted to: Journal of Obesity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/13/2020
Publication Date: 5/1/2020
Citation: Zhou, B., Ichikawa, R., Parnell, L.D., Noel, S.E., Zhang, X., Bhupathiraju, S., Smith, C., Tucker, K.L., Ordovas, J.M., Lai, C. 2020. Metabolomic links between sugar-sweetened beverage intake and obesity. Journal of Obesity. https://doi.org/10.1155/2020/7154738.
Interpretive Summary: Sugar-sweetened beverage (SSB) consumption is an important dietary factor that contributes to obesity and obesity-related diseases, but the biological mechanism that connects SSB intake to obesity is not understood. For preventing obesity and reducing the risk of obesity-related diseases that are associated with SSB intake, there is a need to understand the molecular mechanisms of such association. We examined the relationship of biochemicals found in the blood of participants in the Boston Puerto Rican Health Study with their SSB intake and body mass index, and identified 28 compounds, many of them related to metabolism of the lipid components of cell membranes that link SSB intake to obesity. Our findings suggest that SSB intake is associated with an abnormal increase of a group of membrane lipids, which would disrupt membrane-lipid metabolism, and then contribute to an increased risk of obesity. In addition, we found that persons with different versions of genes that function in cell membrane-lipid processes experience different degree of weight gains associated with SSB consumption. Our results imply that high SSB intake increased the risk of obesity in part by disturbing cell membrane-lipid metabolism. Moreover, certain genetic differences in membrane lipid-related genes amplify the effects of SSB consumption in elevating the risk of obesity.
Technical Abstract: Background: Sugar sweetened beverage (SSB) consumption is highly associated with obesity, but the metabolic mechanism underlying this correlation is not understood. Objective: Our objective was to examine metabolomic links between SSB intake and obesity to understand metabolic mechanisms. Methods: We examined the association of plasma metabolomic profiles with SSB intake and obesity risk in 781 participants, aged 45-75y, in the Boston Puerto Rican Health Study (BPRHS) using generalized linear models, controlling for potential confounding factors. Based on identified metabolites, we conducted pathway enrichment analysis to identify potential metabolic pathways that link SSB intake and obesity risk. Genetic variants in genes encoding enzymes known to function in identified metabolic pathways were examined for their interactions with SSB intake on obesity. Results: SSB intake was correlated with BMI (ß = 0.607, P =0.045). Among 526 measured metabolites, 86 metabolites showed significant correlation with SSB intake and 148 metabolites with BMI (P = 0.05); and 28 were correlated with both SSB intake and BMI. Pathway enrichment analysis identified the phosphatidylcholine and lysophospholipid pathways as linking SSB intake to obesity, after correction for multiple testing. Furthermore, eight of 10 genes functioning in these two pathways showed strong interactions with SSB intake on BMI. Conclusions: We identified two key metabolic pathways that link SSB intake to obesity, revealing the potential of phosphatidylcholine and lysophospholipid to modulate how SSB intake increases obesity risk. The interaction between genetic variants in these pathway and SSB intake on obesity further supports the mechanism.