The Role of Chemerin in Metabolic and Cardiovascular Disease: A Literature Review of Its Physiology and Pathology from a Nutritional Perspective

Abstract

Chemerin is a novel adipokine that plays a major role in adipogenesis and lipid metabolism. It also induces inflammation and affects insulin signaling, steroidogenesis and thermogenesis. Consequently, it likely contributes to a variety of metabolic and cardiovascular diseases, including atherosclerosis, diabetes, hypertension and pre-eclampsia. This review describes its origin and receptors, as well as its role in various diseases, and subsequently summarizes how nutrition affects its levels. It concludes that vitamin A, fat, glucose and alcohol generally upregulate chemerin, while omega-3, salt and vitamin D suppress it. Dietary measures rather than drugs acting as chemerin receptor antagonists might become a novel tool to suppress chemerin effects, thereby potentially improving the aforementioned diseases. However, more detailed studies are required to fully understand chemerin regulation.

Statins Prevent the Deleterious Consequences of Placental Chemerin Upregulation in Preeclampsia

“…Circulating chemerin is, at least partly, adipose tissue-derived, and this may explain its correlation with BMI. 6 , 7 However, the placenta is another well-known source of chemerin, and thus, its upregulated levels in preeclampsia are likely of placental origin. 10 , 13 Indeed, the elevated chemerin release from preeclamptic placentas supports this concept.…”

“…As such, it might serve as a biomarker for preeclampsia and its fetal complications on top of the sFlt-1/PlGF ratio. Chemerin not only acts as a proinflammatory adipokine 6 , 7 but also exerts constrictor effects. Interestingly, statins suppressed the placental release of chemerin, as well as its constrictor effects, and these effects were the largest for a statin that passed the placental barrier best.…”

“…4,5 Chemerin is an adipokine that, under nonpregnant conditions, is primarily secreted by the liver and adipose tissue, contributing to multiple metabolic and inflammatory processes. [6][7][8] Chemerin synthesis and secretion have been linked to the low-density lipoprotein receptor (LDLR), and the expression of both chemerin and the LDLR is regulated by the transcription factor SREBP2 (sterol regulatory element-binding protein 2). 9 In pregnant women, circulating chemerin exhibits an increase in concentration during pregnancy and subsequently undergoes a rapid decline after delivery.…”

“… 6 A second receptor, CCRL2 (CC motif chemokine receptor-like 2), functions as a chaperone receptor, concentrating chemerin locally and thereby allowing optimal chemerin-CMKLR1 interaction. 6 CMKLR1 activation is responsible for the deleterious effects observed in pregnant mice with placental chemerin overexpression. 10 This receptor also upregulates constrictor responses.…”

Genetic and Lifestyle-Related Factors Influencing Serum Hyper-Propionylcarnitine Concentrations and Their Association with Metabolic Syndrome and Cardiovascular Disease Risk

“…Other genes among the selected genetic variants are related to similar metabolic processes. CMKLR1 is linked to nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and insulin signaling [29], and kinesin family member 5B (KIF5B) is associated with insulin resistance and obesity [30]. KIF5B plays a role in growth factors and transforming the growth factor-beta (TGF-β) pathways [31].…”