PPARs in Rhythmic Metabolic Regulation and Implications in Health and Disease

Charoensuksai, Purin; Xu, Wei

doi:10.1155/2010/243643

Cited by 38 publications

(38 citation statements)

References 55 publications

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“…This study therefore presents an underestimation of the in-terpretation of the total transcriptional effects of SFA and MUFA challenges. However, those gene expression changes might also reflect changes over time, as circadian effects on gene expression have been described [32]. The amount of fat used (95g, 88 energy-%) is relatively high and does not reflect a common meal.…”

Section: Discussionmentioning

confidence: 99%

High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects

Esser

Dijk

Oosterink

et al. 2015

Molecular Nutrition Food Res

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Section: Discussionmentioning

confidence: 99%

High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects

Esser

Dijk

Oosterink

et al. 2015

Molecular Nutrition Food Res

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“…PPARs are closely related to energy status and metabolism. An aberration of PPARs leads to abnormal expression of genes in metabolic pathways, thereby contributing to etiology of metabolic syndrome 39 . In addition, PPARs are the major regulators of lipid and fatty acid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Ochratoxin A induced early hepatotoxicity: new mechanistic insights from microRNA, mRNA and proteomic profiling studies

Yang

Chen

et al. 2014

Sci Rep

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The mycotoxin ochratoxin A (OTA) is found widely in agricultural commodities. OTA can induce various toxicities. In this study, rats were gavaged with OTA for different weeks. Then, the expression of microRNAs, mRNAs and proteins were measured in the rat livers treated with OTA for 13 weeks. Our sequencing data suggests that the medial and the high doses of OTA exert different effects on livers. Five distinctive pathways were induced after OTA treatment as collectively demonstrated at miRNA, mRNA and protein levels. Two (primary bile acid biosynthesis, and metabolism of xenobiotics by cytochrome P450) are directly associated with liver damage, whereas the remaining pathways (arginine and proline metabolism, cysteine and methionine metabolism, and PPAR signaling pathway) cause metabolic disease. This study reveals OTA-induced early hepatotoxicity for the first time by combining multi-omics methods. The novel metabolic pathways may contribute to the pathogenesis of metabolic diseases later in life.O chratoxin A (OTA) is a low molecular weight mycotoxin produced by certain strains of filamentous fungi of the Aspergillus and Penicillium genera and has been detected in a large variety of agricultural commodities. OTA carries potential health-associated risks and has been classified as a possible human carcinogen (group 2B) by the International Agency for Research on Cancer 1 . OTA has previously been found to induce various toxic effects including nephrotoxicity, hepatotoxicity, immunotoxicity, genotoxicity, carcinogenicity, teratogenicity, neurotoxicity and mutagenicity.The liver is one of the major target organs of OTA biotransformation. Although, some early hepatotoxicity studies employed relative high concentrations of OTA and found remarkable liver lesion 2,3 , lower doses of OTA did not provoke significant pathological changes 4-6 . Most of the previous studies have been extensively focused on OTA-induced kidney damage, less on liver. However, it is still unknown how OTA affects the liver which is the largest detoxification organ of body. Therefore, the identification of early hepatotoxicity can be helpful to understand the mechanism of some diseases that may be developed and progressed by OTA in later stage, and to prevent these diseases in early stage to improve human health.Omics approaches, such as transcriptome and proteome, are promising to detect the pathological changes of liver at a molecular level. Till date, omics technology has been employed only in a few studies to understand the mechanism of OTA hepatotoxicity. Moreover, a high-throughput microarray profiling study on HepG2 liver cell transcriptome demonstrated that multiple hepatic metabolism genes are modulated by OTA exposure 7 . In addition, proteomic approaches have helped identify key proteins in the livers of pigs treated with OTA 8 . These omics approaches have widened our view about OTA hepatotoxicity, however the mechanism of OTA actions remains largely unknown.Recently, microRNAs (miRNAs) in animals and plants are shown to play an impor...

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“…PPARγ is a regulator of adipogenesis and fat storage; it induces the differentiation of pre-adipocytes in mature fat cells, modulates the activation of genes involved in lipogenesis and storage of triglycerides, and also regulates insulin sensitivity in adipose tissue (Charoensuksai & Xu, 2010). Pparg is rhythmically expressed, and its circadian oscillation is driven by binding of DBP and E4BP4 to first exon D-sites with functional promoter activity .…”

Section: Vdr (Nr1i1) Vitamin D3 Receptormentioning

confidence: 99%

Clock Genes and Clock-Controlled Genes in the Regulation of Metabolic Rhythms

Mazzoccoli

Pazienza

Vinciguerra

2012

Chronobiology International

149

109

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Daily rotation of the Earth on its axis and yearly revolution around the Sun impose to living organisms adaptation to nyctohemeral and seasonal periodicity. Terrestrial life forms have developed endogenous molecular circadian clocks to synchronize their behavioral, biological, and metabolic rhythms to environmental cues, with the aim to perform at their best over a 24-h span. The coordinated circadian regulation of sleep/wake, rest/activity, fasting/feeding, and catabolic/anabolic cycles is crucial for optimal health. Circadian rhythms in gene expression synchronize biochemical processes and metabolic fluxes with the external environment, allowing the organism to function effectively in response to predictable physiological challenges. In mammals, this daily timekeeping is driven by the biological clocks of the circadian timing system, composed of master molecular oscillators within the suprachiasmatic nuclei of the hypothalamus, pacing self-sustained and cell-autonomous molecular oscillators in peripheral tissues through neural and humoral signals. Nutritional status is sensed by nuclear receptors and coreceptors, transcriptional regulatory proteins, and protein kinases, which synchronize metabolic gene expression and epigenetic modification, as well as energy production and expenditure, with behavioral and light-dark alternance. Physiological rhythmicity characterizes these biological processes and body functions, and multiple rhythms coexist presenting different phases, which may determine different ways of coordination among the circadian patterns, at both the cellular and whole-body levels. A complete loss of rhythmicity or a change of phase may alter the physiological array of rhythms, with the onset of chronodisruption or internal desynchronization, leading to metabolic derangement and disease, i.e., chronopathology.

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PPARs in Rhythmic Metabolic Regulation and Implications in Health and Disease

Cited by 38 publications

References 55 publications

High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects

High fat challenges with different fatty acids affect distinct atherogenic gene expression pathways in immune cells from lean and obese subjects

Ochratoxin A induced early hepatotoxicity: new mechanistic insights from microRNA, mRNA and proteomic profiling studies

Clock Genes and Clock-Controlled Genes in the Regulation of Metabolic Rhythms

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