Genetic variability of milk fatty acids.

The milk fatty acid (FA) profile is far from the optimal fat composition in regards to human health. The natural sources of variation, such as feeding or genetics, could be used to increase the concentrations of unsaturated fatty acids. The impact of feeding is well described. However, genetic effects on the milk FA composition begin to be extensively studied. This paper summarizes the available information about the genetic variability of FAs. The greatest breed differences in FA composition are observed between Holstein and Jersey milk. Milk fat of the latter breed contains higher concentrations of saturated FAs, especially short-chain FAs. The variation of the delta-9 desaturase activity estimated from specific FA ratios could explain partly these breed differences. The choice of a specific breed seems to be a possibility to improve the nutritional quality of milk fat. Generally, the proportions of FAs in milk are more heritable than the proportions of these same FAs in fat. Heritability estimates range from 0.00 to 0.54. The presence of some single nucleotide polymorphisms could explain partly the observed individual genetic variability. The polymorphisms detected on SCD1 and DGAT1 genes influence the milk FA composition. The SCD1 V allele increases the unsaturation of C16 and C18. The DGAT1 A allele is related to the unsaturation of C18. So, a combination of the molecular and quantitative approaches should be used to develop tools helping farmers in the selection of their animals to improve the nutritional quality of the produced milk fat

Heteromeric Solute Carriers: Function, Structure, Pathology and Pharmacology

Solute carriers form one of three major superfamilies of membrane transporters in humans, and include uniporters, exchangers and symporters. Following several decades of molecular characterisation, multiple solute carriers that form obligatory heteromers with unrelated subunits are emerging as a distinctive principle of membrane transporter assembly. Here we comprehensively review experimentally established heteromeric solute carriers: SLC3-SLC7 amino acid exchangers, SLC16 monocarboxylate/H+ symporters and basigin/embigin, SLC4A1 (AE1) and glycophorin A exchanger, SLC51 heteromer Ost α-Ost β uniporter, and SLC6 heteromeric symporters. The review covers the history of the heteromer discovery, transporter physiology, structure, disease associations and pharmacology - all with a focus on the heteromeric assembly. The cellular locations, requirements for complex formation, and the functional role of dimerization are extensively detailed, including analysis of the first complete heteromer structures, the SLC7-SLC3 family transporters LAT1-4F2hc, b0,+AT-rBAT and the SLC6 family heteromer B0AT1-ACE2. We present a systematic analysis of the structural and functional aspects of heteromeric solute carriers and conclude with common principles of their functional roles and structural architecture