scholarly journals The interplay between non-esterified fatty acids and bovine peroxisome proliferator-activated receptors: results of an in vitro hybrid approach

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Sebastiano Busato ◽  
Massimo Bionaz
Keyword(s):  
Fatty Acids ◽  
Hybrid Approach ◽  
Peroxisome Proliferator ◽  
Esterified Fatty Acids ◽  
Peroxisome Proliferator Activated Receptors

scholarly journals The Interplay Between Non-Esterified Fatty Acids and Bovine Peroxisome Proliferator-Activated Receptors: Results of an In Vivo-In Vitro Hybrid Approach

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1245-1245
Author(s):  
Sebastiano Busato ◽  
Massimo Bionaz
Keyword(s):  
Fatty Acids ◽  
Solid Phase ◽  
Hybrid Approach ◽  
Dietary Lipids ◽  
Dietary Fatty Acids ◽  
Peroxisome Proliferator ◽  
Dependent Manner ◽  
Esterified Fatty Acids ◽  
Peroxisome Proliferator Activated Receptors

Abstract Objectives Metabolic stressors and energy deficiency related to parturition induce lipolysis in dairy cows with a subsequent increase in circulating non-esterified fatty acids (NEFA). We hypothesized that circulating NEFA directly activate the Peroxisome Proliferator-Activated Receptors (PPAR), a transcription factor with known nutrigenomics response to fatty acids, in a dose-dependent manner. Methods Whole-blood samples were collected from five cows at different times between −40 and +10 days relative to parturition to isolate serum. NEFA were extracted from said samples through solid-phase extraction. A bioluminescent reported, bound to a PPAR response element, was used to assess PPAR activation in response to the treatments. To estimate individual PPAR isotype activation, PPAR isotype-specific antagonists were used, along with the treatments. Results Isolated NEFA activate PPAR linearly up to 400 μM, with a decrease in their effect when albumin is introduced. A hybrid approach, treating cells with bovine serum from different stages of parturition, revealed that much of the PPAR activation can be explained by the amount of NEFA in the serum, and that its activation follows a quadratic tendency (calculated maximum activation at 1.47 mM NEFA of 4.8-fold vs. DMEM control, R2 = 0.91). Further analysis of the effect of serum NEFA on PPAR revealed that they mostly activate PPARδ and PPARγ, but not PPARα. However, addition of palmitic acid to the media activate PPARδ and PPARα, but not PPARγ, and only when circulating NEFA are low (0.16 mM, prepartum), while additional palmitate did not increase PPAR activation in serum with high NEFA (0.71 mM, postpartum). Finally, the addition of lipoprotein lipase to the serum, in order to mimic release of NEFA from VLDL, increased PPAR activation, recapitulating the role of dietary lipids in the regulation of PPAR. Conclusions Taken together, our results support the activation of PPAR by NEFA, helping to explain prior observations on PPAR activation in peripartum cows. Additionally, we outlined the role of dietary fatty acids in activating PPAR and their interaction with serum NEFA. Our results aid in setting the foundation for nutrigenomics approaches in ruminant nutrition. Funding Sources This study was funded by the Oregon Beef Council.

Oxidized fatty acids from Clematis species activate peroxisome proliferator activated receptors (PPARs) in vitro

Planta Medica ◽  
2014 ◽  
Vol 80 (16) ◽  
Author(s):  
EM Pferschy-Wenzig ◽  
B Lugger ◽  
AG Atanasov ◽  
C Malainer ◽  
EH Heiss ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors ◽  
Oxidized Fatty Acids

scholarly journals Two antibacterial and PPARα/γ-agonistic unsaturated keto fatty acids from a coral-associated actinomycete of the genus Micrococcus

2020 ◽  
Vol 16 ◽  
pp. 297-304 ◽  
Author(s):  
Amit Raj Sharma ◽  
Enjuro Harunari ◽  
Naoya Oku ◽  
Nobuyasu Matsuura ◽  
Agus Trianto ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Spectroscopic Analysis ◽  
Culture Broth ◽  
Peroxisome Proliferator ◽  
Simulation Studies ◽  
Fish Pathogen ◽  
Chemical Structures ◽  
Agonistic Activity ◽  
Isoform Specificity ◽  
Peroxisome Proliferator Activated Receptors

A pair of geometrically isomeric unsaturated keto fatty acids, (6E,8Z)- and (6E,8E)-5-oxo-6,8-tetradecadienoic acids (1 and 2), were isolated from the culture broth of an actinomycete of the genus Micrococcus, which was associated with a stony coral, Catalaphyllia sp. Their chemical structures were elucidated by spectroscopic analysis including NMR and MS, with special assistance of spin system simulation studies for the assignment of an E geometry at C8 in 2. As metabolites of microbes, compounds 1 and 2 are unprecedented in terms of bearing a 2,4-dienone system. Both 1 and 2 showed antibacterial activity against the plant pathogen Rhizobium radiobacter and the fish pathogen Tenacibaculum maritimum, with a contrasting preference that 1 is more effective to the former strain while 2 is so to the latter. In addition, compounds 1 and 2 displayed agonistic activity against peroxisome proliferator-activated receptors (PPARs) with an isoform specificity towards PPARα and PPARγ.

scholarly journals Molecular Recognition of Fatty Acids by Peroxisome Proliferator–Activated Receptors

1999 ◽  
Vol 3 (3) ◽  
pp. 397-403 ◽  
Author(s):  
H.Eric Xu ◽  
Millard H Lambert ◽  
Valerie G Montana ◽  
Derek J Parks ◽  
Steven G Blanchard ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Molecular Recognition ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptors

Inhibition of binding of gonadal steroids to serum binding proteins by non-esterified fatty acids: the influence of chain length and degree of unsaturation

1989 ◽  
Vol 120 (2) ◽  
pp. 175-179 ◽  
Author(s):  
C. Street ◽  
R. J. S. Howell ◽  
L. Perry ◽  
S. Al-Othman ◽  
T. Chard
Keyword(s):  
Fatty Acids ◽  
Protein Binding ◽  
Unsaturated Fatty Acids ◽  
Late Pregnancy ◽  
Sex Hormone Binding Globulin ◽  
Partial Purification ◽  
Normal Female ◽  
Esterified Fatty Acids ◽  
Vitro Binding

Abstract. The effect of non-esterified fatty acids (NEFA) on the in vitro binding of testosterone, 5-alpha dihydrotestosterone and estradiol E2 to sex hormone binding globulin (SHBG) was examined using pooled normal female serum, and SHBG and albumin fractions obtained from the partial purification of late pregnancy serum. A range of saturated and unsaturated fatty acids were examined for their effect on steroid-protein binding. In normal female serum, NEFA added at physiological concentrations disrupted steroid-protein binding. The shorter chain (C8–C12) saturated acids and the poly-unsaturated acids proved to be more effective inhibitors than the longer chain saturated or mono-unsaturated acids. The greatest inhibition was obtained with E2 whereas the binding of dihydrotestosterone was least affected. With partially purified SHBG, the same concentrations of NEFA were less effective at inhibiting the binding of dihydrotestosterone and testosterone but elicited the same effect with E2. The binding of steroids to albumin appeared to be unaffected by these concentrations of NEFA.

scholarly journals Peroxisome Proliferator-Activated Receptor Delta: A Conserved Director of Lipid Homeostasis through Regulation of the Oxidative Capacity of Muscle

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-7 ◽  
Author(s):  
Pieter de Lange ◽  
Assunta Lombardi ◽  
Elena Silvestri ◽  
Fernando Goglia ◽  
Antonia Lanni ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acids ◽  
Oxidative Capacity ◽  
Whole Body ◽  
Lipid Homeostasis ◽  
Peroxisome Proliferator ◽  
Transcriptional Program ◽  
Peroxisome Proliferator Activated Receptor ◽  
Peroxisome Proliferator Activated Receptors ◽  
Metabolic Action

The peroxisome proliferator-activated receptors (PPARs), which are ligand-inducible transcription factors expressed in a variety of tissues, have been shown to perform key roles in lipid homeostasis. In physiological situations such as fasting and physical exercise, one PPAR subtype, PPARδ, triggers a transcriptional program in skeletal muscle leading to a switch in fuel usage from glucose/fatty acids to solely fatty acids, thereby drastically increasing its oxidative capacity. The metabolic action of PPARδ has also been verified in humans. In addition, it has become clear that the action of PPARδ is not restricted to skeletal muscle. Indeed, PPARδ has been shown to play a crucial role in whole-body lipid homeostasis as well as in insulin sensitivity, and it is active not only in skeletal muscle (as an activator of fat burning) but also in the liver (where it can activate glycolysis/lipogenesis, with the produced fat being oxidized in muscle) and in the adipose tissue (by incrementing lipolysis). The main aim of this review is to highlight the central role for activated PPARδ in the reversal of any tendency toward the development of insulin resistance.

scholarly journals Omega-3 Fatty Acids and PPARγin Cancer

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-14 ◽  
Author(s):  
Iris J. Edwards ◽  
Joseph T. O'Flaherty
Keyword(s):  
Fatty Acids ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Anticancer Agents ◽  
Dietary Fatty Acids ◽  
Human Populations ◽  
Peroxisome Proliferator ◽  
Omega 3 ◽  
New Paradigm

Omega-3 (or n-3) polyunsaturated fatty acids (PUFAs) and their metabolites are natural ligands for peroxisome proliferator receptor activator (PPAR)γand, due to the effects of PPARγon cell proliferation, survival, and differentiation, are potential anticancer agents. Dietary intake of omega-3 PUFAs has been associated with a reduced risk of certain cancers in human populations and in animal models. In vitro studies have shown that omega-3 PUFAs inhibit cell proliferation and induce apoptosis in cancer cells through various pathways but one of which involves PPARγactivation. The differential activation of PPARγand PPARγ-regulated genes by specific dietary fatty acids may be central to their distinct roles in cancer. This review summarizes studies relating PUFAs to PPARγand cancer and offers a new paradigm relating an n-3 PUFA through PPARγto the expression of the cell surface proteoglycan, syndecan-1, and to the death of cancer cells.

Sign in / Sign up

Export Citation Format

Share Document