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Review
. 2018 Dec 31;20(1):128.
doi: 10.3390/ijms20010128.

Etiology of Metabolic Syndrome and Dietary Intervention

Hang Xu  1 , Xiaopeng Li  2   3 , Hannah Adams  4 , Karen Kubena  5 , Shaodong Guo  6
Affiliations
Review

Etiology of Metabolic Syndrome and Dietary Intervention

Hang Xu et al. Int J Mol Sci. .

Abstract

The growing prevalence of metabolic syndrome (MetS) in the U.S. and even worldwide is becoming a serious health problem and economic burden. MetS has become a crucial risk factor for the development of type 2 diabetes mellitus (T2D) and cardiovascular diseases (CVD). The rising rates of CVD and diabetes, which are the two leading causes of death, simultaneously exist. To prevent the progression of MetS to diabetes and CVD, we have to understand how MetS occurs and how it progresses. Too many causative factors interact with each other, making the investigation and treatment of metabolic syndrome a very complex issue. Recently, a number of studies were conducted to investigate mechanisms and interventions of MetS, from different aspects. In this review, the proposed and demonstrated mechanisms of MetS pathogenesis are discussed and summarized. More importantly, different interventions are discussed, so that health practitioners can have a better understanding of the most recent research progress and have available references for their daily practice.

Keywords: dietary intervention; insulin resistance; metabolic syndrome; obesity; personal nutrition.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The role of kinases in the insulin signaling cascades and its interaction with nutrients in control of FOXO1-mediated physiological function. AA—amino acids; FFA—free fatty acids; HGP—hepatic glucose production; Agt—angiotensinogen; Hmox-1—heme oxygenase-1; G6pc—glucose-6-phosphatase catalytic subunit; Agrp—agouti-related peptide; pY—tyrosine phosphorylation; pS/T—serine/threonine phosphorylation; OGT—O-GlcNAc transferase; HBP—hexosamine biosynthetic pathway; PIP2—phosphatidylinositol-4,5-biphosphate; PIP3—phosphatidylinositol-3,4,5-triphosphate; PTP1B—protein tyrosine phosphatase; PTEN—phosphatase and tensin homolog; PDK—phosphoinositide-dependent protein kinase; PI3K—phosphatidylinositide 3-kinase; PIKKs—PI3K-related kinase family; IR—insulin receptor.
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