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  • In both families GPR A mRNA in kidney

    2021-09-17

    In both families, GPR109A mRNA in kidney fat was positively correlated with NEFA as a tendency. A positive correlation between this fat depot and insulin was observed in lean-type cows. In fat-type cows, mesenteric GPR109A mRNA correlated positively with insulin and negatively with urea on a moderate level (Figure 3A and 3B). In mesenteric fat of the lean-type family, GPR109A mRNA showed a strong negative correlation to BHBA. Within the fat-type group, AdipoQ mRNA in SCback was strongly related to BHBA, and AdipoR2 in the same AT depot to NEFA. In the lean-type group, AdipoQ mRNA in kidney fat correlated positively with BHBA at a moderate level but correlated strongly and negatively with glucose. In liver, the amount of AdipoR2 mRNA was 3-fold higher than that of AdipoR1 mRNA (P≤0.001). In liver, GPR109A mRNA correlated positively with fat concentration (P≤0.05; r=0.76) in fat-type animals, whereas AdipoR1 mRNA tended to correlate negatively with hepatic glycogen content within the lean-type group.
    Discussion In this study, we present data about differential mRNA expression of AdipoQ, its receptors, and GPR109A mRNA in liver, s.c. fat, and 3 v.c. fat depots of 2 cattle families that differ in fat accretion but have a common genetic background. Correlation of mRNA abundance data with different fat masses and blood metabolites revealed clear differences between the families. Prior work has shown that abundance of AdipoQ mRNA is correlated negatively with subcutaneous AT back fat in cattle (Taniguchi et al., 2008). The AdipoQ mRNA correlated less in fatter Hereford × Aberdeen Angus steers than in Charolais × Red Angus steers. However, that study was based on 2 breeds with different genetic backgrounds, and no information was provided about AdipoQ receptors and kainic acid australia GPR109A, which are related to insulin sensitivity and kainic acid australia metabolism. Likewise, v.c. adipose depots were not analyzed but, from studies in humans, it is known that v.c. adipocytes secrete more AdipoQ than do those from s.c. AT (Motoshima et al., 2002) and more AdipoQ mRNA is found in v.c. AT compared with s.c. AT in mice (Altomonte et al., 2003). In general, AdipoQ expression is positively related to insulin sensitivity and negatively associated with obesity and gluconeogenesis (Combs et al., 2001; Kadowaki et al., 2006).
    Conclusions We found clear differences in mRNA abundance of the AdipoQ system and GPR109A between 2 dairy cow families that differed in body fat accretion and milk secretion but had a common genetic background. Visceral AT in both families was of central importance in interacting with the AdipoQ system and GPR109A mRNA. The effect of AdipoQ secretion, especially by visceral AT depots, on liver metabolism should be clarified. Autocrine as well as paracrine effects in AT might be significant.
    Acknowledgments The study was supported by the core budget of the FBN Dummerstorf (Dummerstorf, Germany). The authors acknowledge Ralf Pfuhl and the staff of the experimental slaughterhouse at FBN Dummerstorf for performing extensive slaughtering and dissection. The authors give thanks to Isabella Israel and Inga Hofs (Institute of Animal Science, Physiology and Hygiene Unit, University of Bonn, Germany) for excellent technical assistance.
    Niacin, a vitamin of the B complex, has been used for almost 50 years as an anti-dyslipidemic drug with a favorable profile for all lipoprotein classes. In particular, niacin is the most potent agent to raise high density lipoprotein cholesterol (HDL-c)., , Numerous clinical studies have shown the beneficial effects of niacin, namely a reduction of coronary artery disease and overall mortality., However, extensive use of niacin is limited due to transient skin vasodilatation (flushing) affecting most of the patients. Extended release formulations of niacin (e.g., Niaspan®) show a reduction in flushing events, but are not able to overcome this side effect completely., In addition, doses of extended release niacin formulations are limited due to hepatotoxicity caused by niacin metabolites., It has been proposed that niacin’s main mode of action is inhibiting lipolysis in the adipose tissue. As a consequence, free fatty acid (FFA) levels in plasma and liver are lowered leading to a decreased production of very low density lipoprotein cholesterol (VLDL-c). This results in a reduction of total plasma cholesterol (TC), triglyceride (TG), and LDL-c levels. Due to the lower number of TG rich lipoprotein particles in plasma, fewer modifications of the HDL-c particles via the cholesteryl ester transfer protein (CETP) occur, which leads to a decrease in HDL-c catabolism., A niacin-mediated direct inhibition of lipoprotein A-I HDL-c (LpAI-HDL-c) particle uptake by the liver, which would contribute to the overall HDL-c raising properties of niacin, has also been proposed. In addition, the anti-dyslipidemic effects of niacin are discussed in the context of its diacylglycerol acyltransferase 2 (DGAT2) inhibitory effects.