Genetic ancestry modifies fatty acid concentrations in different adipose tissue depots and milk fat

Abstract

The objective of this study was to determine the effect of cow genetic strain on fatty acid (FA) profiles in adipose tissue and milk. Adipose samples from two subcutaneous (shoulder and tail-head) and three visceral (kidney channel, mesenteric and omental) depots were obtained post mortem from New Zealand (NZ; n = 8) and North American (NA; n = 8) Holstein-Friesian cows. At the time of slaughter cows were in similar body condition (NZ: 4.0 ± 0.03, NA: 4.0 ± 0.02; ± SD) and stage of lactation (NZ: 90 ± 11.2 d; NA: 83 ± 4.3 d; ± SD). Milk was collected during the a.m. milking prior to slaughter and milk fat was extracted. Adipose and milk fat FA were quantified using gas chromatography. NZ cows had a lower proportion of saturated FA in shoulder, tail-head and omental adipose tissue and a greater proportion of mono-unsaturated FA and an elevated Δ9-desaturase index in shoulder and tail-head adipose tissue. The proportions of individual FA differed between adipose depots, with proportions of de-novo FA greater in subcutaneous compared with visceral adipose depots. Milk from NZ cows contained greater concentrations of short chain FA (C8 : 0-12 : 0) and CLA, and less cis-9 18 : 1 than milk from NA cows. Regression analysis identified moderate associations between milk FA and shoulder adipose tissue FA for 18 : 2 (R(2) = 0.24), 18 : 3 n - 3 (R(2) = 0.39), and polyunsaturated fatty acids (R(2) = 0.38). Results from this study support the hypothesis that genetic strain dictates FA profiles in adipose tissue and milk and may alter the metabolic status of the various adipose depots differently. The data further support the premise that genetic strain affects the metabolic status of the various adipose depots differently. Elucidating the mechanisms that regulate the different adipose depots in the NZ and NA strains will increase our understanding of tissue mobilization and replenishment.

Estimation of genetic and crossbreeding parameters of fatty acid concentrations in milk fat predicted by mid-infrared spectroscopy in New Zealand dairy cattle

“…There are studies reporting genetic strain (Meier et al 2013) and breed (MacGibbon & McLennan, 1987; MacGibbon, 1996) differences for fatty acids in New Zealand dairy cattle, but as far as is known by the authors, there is a lack of estimates of other genetic parameters such as heterosis effects and genetic variances and heritabilities for FA. Heterosis is defined as the superiority expressed from the first crossbred cows compared with the average of the parental breeds.…”

Hepatic pyruvate carboxylase expression differed prior to hyperketonemia onset in transition dairy cows

“…The major FA in adipose tissue are C16:0, C18:0, and C18:1 [8][9][10] and are expected to be increased in plasma postpartum as cows mobilize FA from adipose tissue, as was observed with increased postpartum plasma C16:0 and C18:1 relative to prepartum plasma in both HYK and nonHYK cows in the current study. Although both groups mobilized adipose tissue, the greater BCS loss and elevated NEFA of HYK cows would suggest that FA derived from adipose Expression of PC, PC: PCK1, and PC:PCK2 were log transformed for analysis to achieve normal residuals and thus are reported using the 67% confidence interval.…”

“…Prior work has demonstrated that subcutaneous adipose tissue FA profile does not change across the transition period [8], making it unlikely that preferential mobilization plays a major role in differential FA metabolism, at least within the subcutaneous depots. Relative to C16:0 and C18:1, C18:0 is present in lower proportions in subcutaneous fat, but at a greater proportion in internal fat stores [9,10] which are also mobilized during the peripartum period [32]. It is unknown if the difference in FA profiles and metabolic activity between adipose tissue depots [33] may impact the circulating FA profile or preferential mobilization and metabolism.…”

“…Although the general etiology of HYK has been described, the effects of HYK status on nutrient metabolism, specifically the potential for preferential FA use for hepatic fates, are not fully understood. The primary non-esterified fatty acid (NEFA) circulating in plasma during negative EB are C16:0, C18:0, and C18:1, which are derived from adipose tissue depots where they are stored [8][9][10]. Compared to cows restricted to maintenance energy intake prepartum, cows fed above maintenance requirements prepartum to induce fatty liver had increased blood NEFA and increased C16:0 and C18:1 in plasma and liver postpartum [8].…”

ADSA Foundation Scholar Award: Influencing hepatic metabolism: Can nutrient partitioning be modulated to optimize metabolic health in the transition dairy cow?

“…Despite the potential gaps in understanding of mechanism or regulation of lipolysis, our understanding of the metabolism and regulatory effect of mobilized NEFA continues to increase. In ruminants, primary adipose tissue fatty acids are C16:0, C18:0, and C18:1 (Rukkwamsuk et al, 2000;Sato and Inoue, 2006;Meier et al, 2013), which are thus expected to be increased in plasma postpartum, as cows mobilize fatty acids from adipose tissue. Although the majority of in vivo research on adipose tissue focuses on subcutaneous depots due to accessibility, we cannot ignore other adipose depots and must acknowledge that the regulation and metabolic activity of these visceral depots may be different (Ji et al, 2014).…”