Cardiometabolic health benefits of dairy-milk polar lipids

Abstract

Low-quality dietary patterns impair cardiometabolic health by increasing the risk of obesity-related disorders. Cardiometabolic risk relative to dairy-food consumption continues to be a controversial topic, due to recommendations that endorse low-fat and nonfat dairy foods over full-fat varieties despite accumulated evidence that does not strongly support these recommendations. Controlled human studies and mechanistic preclinical investigations support that full-fat dairy foods decrease cardiometabolic risk by promoting gut health, reducing inflammation, and managing dyslipidemia. These gut- and systemic-level cardiometabolic benefits are attributed, at least in part, to milk polar lipids (MPLs) derived from the phospholipid- and sphingolipid-rich milk fat globule membrane that is of higher abundance in full-fat dairy milk. The controversy surrounding full-fat dairy food consumption is discussed in this review relative to cardiometabolic health and MPL bioactivities that alleviate dyslipidemia, shift gut microbiota composition, and reduce inflammation. This summary, therefore, is expected to advance the understanding of full-fat dairy foods through their MPLs and the need for translational research to establish evidence-based dietary recommendations.

Keywords: dairy milk; milk fat globule membrane; milk phospholipids; milk polar lipids; milk sphingomyelin.

Figure 1

Distribution of polar lipids in raw milk from cows. The polar lipid content of bovine milk is 12.8–40.0 mg/100 g, with total phospholipid concentrations approximately doubling those of total sphingolipid concentrations.^, Phospholipids contain a phosphoglycerol backbone, with a saturated fatty acid at R₁, an unsaturated fatty acid at R₂, and 1 of several alcohols (ie, ethanolamine, serine, inositol, or choline) at the polar head of X₁. Sphingolipids consist of an amide-containing sphingoid backbone (primarily sphingosine in milk). Similar to phospholipids, R₁ is a saturated fatty acid, whereas X₂ is substituted with phosphocholine, phosphoethanolamine, or a sugar. Abbreviations: GluCer, glucosyl ceramide; LacCer, lactosyl ceramide; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin

Figure 2

Milk polar lipid content in fluid cow’s milk. Although the relative proportions of specific milk polar lipids are unaffected, the total quantity of milk polar lipid is reduced by ≤40% in SSM (1.5% fat, weight per weight) and skim milk (0.1%) compared with FFM (3.5%). Data from Rombaut et al.Abbreviations: FFM, full-fat milk; GluCer, glucosyl ceramide; LacCer, lactosyl ceramide; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin; SSM, semi-skim milk

Figure 3

Summary of cardiometabolic activities of milk polar lipids (MPLs) in humans and rodent models. MPLs consisting of LacCer, GluCer, SM, and glycerophospholipids (PE, PC, PI, and PS) and several membrane-associated proteins are present in the MFGM trilayer. PC, SM, and PS are generally localized to the outer membrane; PE, PC, SM, and PS are more enriched in the inner membrane; and PI and PS compose the majority of the inner monolayer. MPLs, especially SM, were noted in this review to have significant cardioprotective activities; the appearance of a rodent and/or human image in the figure denotes model system-specific benefits of MPL on cardiometabolic health outcomes. The most compelling evidence in humans, and supported by rodent studies, indicates that MPLs reduce circulating cholesterol levels by intraluminal emulsification activities that limit intestinal cholesterol absorption. Although studies in humans are lacking, evidence from rodent models support MPLs as improving liver health and gastrointestinal health, potentially involving prebiotic and/or antimicrobial activities on gut microbiota. Although relatively more limited in study regardless of model system, MPL in rodents reduces adiposity, possibly through a mechanism involving the browning of adipose tissue. Note: Schematic representation of MFGM is not drawn to scale. Abbreviations: ADPH, adipophilin; BTN, butyrophilin; CD36, cluster of differentiation 36; CHOL, cholesterol; FABP, fatty acid–binding protein; GPL, glycerophospholipid; GluCer, glucosyl ceramide; LacCer, lactosyl ceramide; LDL-C, low-density lipoprotein cholesterol; MFG-EGF8, milk fat globule–epidermal growth factor 8 protein; MFGM, milk fat globule membrane; MPL, PC, phosphatidylcholine; PE, phosphatidylethanolamine; PI, phosphatidylinositol; PS, phosphatidylserine; SM, sphingomyelin; TJP, tight junction protein; VLDL-C, very-low-density lipoprotein cholesterol; XO, xanthine oxidase