The overconsumption of n-6 polyunsaturated fatty acids (PUFA), resulting in a high ratio of n-6 to n-3 PUFA, may contribute to the increased pathogenesis of obesity and osteoporosis by promoting low-grade chronic inflammation (LGCI). As evidence suggests, both obesity and osteoporosis are linked on a cellular and systemic basis. This review will analyze if a relationship exists between LGCI, fat, bone, and n-3 PUFA. During the life cycle, inflammation increases, fat mass accumulates, and bone mass declines, thus suggesting that a connection exists. This review will begin by examining how the current American diet and dietary guidelines may fall short of providing an anti-inflammatory dose of the n-3 PUFA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). It will then define LGCI and outline the evidence for a relationship between fat and bone. Inflammation as it pertains to obesity and osteoporosis and how EPA and DHA can alleviate the associated inflammation will be discussed, followed by some preliminary evidence to show how mesenchymal stem cell (MSC) lineage commitment may be altered by inflammation to favor adipogenesis. Our hypothesis is that n-3 PUFA positively influence obesity and osteoporosis by reducing LGCI, ultimately leading to a beneficial shift in MSC lineage commitment. This hypothesis essentially relates the need for more focused research in several areas such as determining age and lifestyle factors that promote the shift in MSC commitment and if current intakes of EPA and DHA are optimal for fat and bone.
Keywords: 2010 DG; 2010 Dietary Guidelines for Americans; 5-Lox; 5-lipoxygenase; AA; AHA; ALA; AMDR; American Heart Association; BMD; C-reactive protein; CB2; CRP; Cox-2; DHA; DPA; EPA; IFNγ; IL-6; Inflammation; LA; LGCI; LTB(4); LTB(5); MCP-1; MSC; Mesenchymal stem cells; NHANES; NO; National Health and Nutrition Examination Survey; Obesity; Omega-3 fatty acids; Osteoporosis; PGE(2); PUFA; SDA; TNF-α; acceptable macronutrient distribution ranges; arachidonic acid; bone mineral density; cannabinoid receptor type 2; cyclooxygenase-2; docosahexaenoic acid; docosapentaenoic acid; eicosapentaenoic acid; interferon-γ; interleukin-6; leukotriene B(4); leukotriene B(5); linoleic acid; low-grade chronic inflammation; mesenchymal stem cell; monocyte chemoattractant protein–1; nitric oxide; polyunsaturated fatty acids; prostaglandin E2; stearidonic acid; tumor necrosis factor–α; α-linolenic acid.
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