Differential expression of Pparγ target genes in testis of rats under theinfluence of paternal trans fatty acid and vitamin-E.

Fat intake in children: Is there a need for revised recommendations?

Peroxisome Proliferator-activated Receptor (PPAR)-2 Controls Adipocyte Differentiation and Adipose Tissue Function through the Regulation of the Activity of the Retinoid X Receptor/PPARγ Heterodimer

Trans–fatty acid levels in sperm are associated with sperm concentration among men from an infertility clinic

Magnolol enhances adipocyte differentiation and glucose uptake in 3T3-L1 cells

To assess the intake of trans fatty acids (TFA) and other fatty acids in 14 Western European countries. A maximum of 100 foods per country were sampled and centrally analysed. Each country calculated the intake of individual trans and other fatty acids, clusters of fatty acids and total fat in adults and/or the total population using the best available national food consumption data set. A wide variation was observed in the intake of total fat and (clusters) of fatty acids in absolute amounts. The variation in proportion of energy derived from total fat and from clusters of fatty acids was less. Only in Finland, Italy, Norway and Portugal total fat did provide on average less than 35% of energy intake. Saturated fatty acids (SFA) provided on average between 10% and 19% of total energy intake, with the lowest contribution in most Mediterranean countries. TFA intake ranged from 0.5% (Greece, Italy) to 2.1% (Iceland) of energy intake among men and from 0.8% (Greece) to 1.9% among women (Iceland) (1.2-6.7 g/d and 1.7-4.1 g/d, respectively). The TFA intake was lowest in Mediterranean countries (0.5-0.8 en%) but was also below 1% of energy in Finland and Germany. Moderate intakes were seen in Belgium, The Netherlands, Norway and UK and highest intake in Iceland. Trans isomers of C18:1 were the most TFA in the diet. Monounsaturated fatty acids contributed 9-12% of mean daily energy intake (except for Greece, nearly 18%) and polyunsaturated fatty acids 3-7%. The current intake of TFA in most Western European countries does not appear to be a reason for major concern. In several countries a considerable proportion of energy was derived from SFA. It would therefore be prudent to reduce intake of all cholesterol-raising fatty acids, TFA included.

The involvement of peroxisome proliferator-activated receptor gamma (PPARγ) in anti-inflammatory activity of N-stearoylethanolamine

Dietary mono- or di-trans fatty acids with chain lengths of 18-22 increase the risk of cardiovascular diseases because they increase LDL cholesterol and decrease HDL cholesterol in the plasma. However, the effects of trans isomers of PUFAs on lipid metabolism remain unknown. Dietary PUFAs, especially eicosapentaenoic acid (EPA) in marine oils, improve serum lipid profiles by suppressing liver X receptor alpha (LXRalpha) activity in the liver. In this study, we compared the effects of trans geometric isomers of eicosapentaenoic acid (TEPA) on triacylglycerol synthesis induced by a synthetic LXRalpha agonist (T0901317) with the effects of EPA in HepG2 cells. TEPA significantly decreased the amount of cellular triacylglycerol and the expression of mRNAs encoding fatty acid synthase, stearoyl-CoA desaturase-1, and glycerol-3-phosphate acyltransferase induced by T0901317 compared with EPA. However, there was no significant difference between the suppressive effect of TEPA or EPA on the expression of sterol-regulatory element binding protein-1c (SREBP-1c) induced by T0901317. We found that TEPA, but not EPA, decreased the mRNA expression of peroxisome proliferator-activated receptor gamma coactivator 1beta (PGC-1beta), which is a coactivator of both LXRalpha and SREBP-1. These results suggest that the hypolipidemic effect of TEPA can be attributed to a decrease not only in SREBP-1 but also in PGC-1beta expression.

Falcarindiol, a typical polyacetylene compound found in Apiaceae vegetables, activates peroxisome proliferator-activated receptor γ (PPARγ). However, whether it induces the browning of adipocytes through PPARγ activation is unclear. In this study, we aimed to clarify the effects of falcarindiol on adipocyte browning and mitochondrial respiration in human preadipocyte-derived adipocytes. Human primary cultured cells were differentiated for 8 days in the presence of falcarindiol. The expression of PPARγ target and beige adipocyte-related genes was measured using quantitative real-time PCR, and the accumulation of lipid droplets and uncoupling protein 1 (UCP1) protein expression were evaluated using immunohistochemistry. The oxygen consumption rate was measured using a Seahorse flux analyzer. Falcarindiol increased the expression of PPARγ target genes, including PPARγ, FABP4, SLC2A4, and ADIPOQ. It also increased the expression of beige adipocyte-related genes, such as PPARGC1A, PPARA, CITED1, and TBX1, and increased the expression of UCP1 protein. Falcarindiol also significantly increased basal respiration, ATP-linked respiration, maximal respiration, spare capacity, and proton-leak respiration, and significantly decreased the coupling efficiency in a concentration-dependent manner. These results indicate that falcarindiol promotes a beige adipocyte-like phenotype and oxygen consumption of adipocytes in vitro, suggesting that dietary intake of falcarindiol and falcarindiol-containing Apiaceae vegetables may be effective in obesity prevention.

It has been demonstrated that peroxisome proliferator-activated receptor γ (PPARγ) can regulate the transcription of its target gene, insulin-degrading enzyme (IDE), and thus enhance the expression of the IDE protein. The protein can degrade β amyloid (Aβ), a core pathological product of Alzheimer’s disease (AD). PPARγ can also regulate the transcription of other target gene, β-amyloid cleavage enzyme 1 (BACE1), and thus inhibit the expression of the BACE1 protein. BACE1 can hydrolyze amyloid precursor protein (APP), the precursor of Aβ. In adipose tissue, PPARγ agonists can inhibit the phosphorylation of PPARγ by inhibiting cyclin-dependent kinase 5 (CDK5), which in turn affects the expression of target genes regulated by PPARγ. PPARγ agonists may also exert inhibitory effects on the phosphorylation of PPARγ in the brain, thereby affecting the expression of the aforementioned PPARγ target genes and reducing Aβ levels. The present study confirmed this hypothesis by showing that PPARγ agonist pioglitazone attenuated the neuronal apoptosis of primary rat hippocampal neurons induced by Aβ1–42, downregulated CDK5 expression, weakened the binding of CDK5 to PPARγ, reduced PPARγ phosphorylation, increased the expression of PPARγ and IDE, decreased the expression of BACE1, reduced APP production, and downregulated intraneuronal Aβ1–42 levels. These effects were inhibited by the PPARγ antagonist GW9662. After CDK5 silencing with CDK5 shRNA, the above effect of pioglitazone was not observed, except when upregulating the expression of PPARγ in Aβ1–42 treated neurons. In conclusion, this study demonstrated that pioglitazone could inhibit the phosphorylation of PPARγ in vitro by inhibiting CDK5 expression, which in turn affected the expression of PPARγ target genes Ide and Bace1, thereby promoting Aβ degradation and reducing Aβ production. This reduced Aβ levels in the brain, thereby exerting neuroprotective effects in an AD model.

A large body of data from epidemiologic, clinical trial, animal, and in vitro studies demonstrate adverse consequences of industrially synthesized trans fatty acids (TFAs) on the risk of coronary heart disease (CHD). A growing database of more recent research from virtually all experimental models demonstrates evidence of detrimental consequences of TFAs on the risk of diabetes. Evidence is accumulating about the physiological and cellular mechanisms of action that account for the many adverse effects TFAs have on CHD and diabetes. In a relatively short period of time (i.e., from around the early 1990s to the present time, or almost 20 years), we have gained a good understanding of the health effects of TFAs from epidemiologic studies, clinical trials/studies, animal research, and in vitro experiments that collectively justify current dietary recommendations made by numerous government agencies and health organizations to consume a diet with as little TFAs as possible. Public policy actions have been impl...

V. Adopting Healthful Lifestyle Habits to Lower LDL Cholesterol andReduce CHD Risk

ObjectiveTo investigate the influences of high trans fatty acids (TFA) intake on fatty-acid constitution ratios of erythrocyte membrane in rabbits.Method32 New Zealand white rabbits were randomly divided into four groups:...

Trans fatty acids are unsaturated fatty acids produced by the partial hydrogenation of polyunsaturated oils. Over the last few years, an increasing interest on these fatty acids has been shown because of their role in the pathogenesis of cardiovascular diseases. To date, major scientific associations strongly recommend consuming a low intake of trans fatty acids for the prevention of cardiovascular diseases, but data on the consumption of these fatty acids in the general population are still lacking. We conducted this observational study on a population of Italian teenagers in order to evaluate the consumption of trans fatty acids in the diet. We studied 81 Italian teenagers, 45 males and 36 females, with a median age of 16 years. To assess their consumption of trans fatty acids, we used the "High School Survey", a questionnaire prepared by the Harvard Medical School. Total calories of the studied population were 2359.2 +/- 591.5 kcal/day with a mean intake of trans fatty acids of 3.24 +/- 1.48 g/day, corresponding to 1.23% of the total energy. A relevant proportion of subjects, namely 51 (62.9%), exceeded the limit contribution of 1% of energy from trans fatty acids. Their intake of total calories and trans fatty acids significantly increased according to their increasing age (p = 0.0003 for trend). Our data, therefore, obtained in a limited population of Italian adolescents, showed that a consistent proportion of adolescents does not follow the nutritional recommendations for intake of trans fatty acids, likely increasing their risk of cardiovascular diseases.

Previously, we found that the basic helix-loop-helix transcriptional repressor DEC1 interacts with the PPARγ:RXRα heterodimer, a master transcription factor for adipogenesis and lipogenesis, to suppress transcription from PPARγ target genes (Noshiro et al., Genes to Cells, 2018, 23:658-669). Because the expression of PPARγ and several of its target genes exhibits circadian rhythmicity in white adipose tissue (WAT), we examined the expression profiles of PPARγ target genes in wild-type and Dec1-/- mice. We found that the expression of PPARγ target genes responsible for lipid metabolism, including the synthesis of triacylglycerol from free fatty acids (FFAs), lipid storage and the lipolysis of triacylglycerol to FFAs, oscillates in a circadian manner in WAT. Moreover, DEC1 deficiency led to a marked increase in the expression of these genes at night (Zeitgeber times 16 and 22), resulting in disruption of circadian rhythms. Serum FFA levels in wild-type mice also showed circadian oscillations, but these were disrupted by DEC1 deficiency, leading to reduced FFA levels. These results suggest that PPARγ:RXRα and DEC1 cooperatively generate the circadian expression of PPARγ target genes through PPAR-responsive elements in WAT.

Multi-omics analysis of the active components and mechanisms of Baojin Chenfei formula in silica-induced murine silicosis.