scholarly journals Roles of Vitamin A Metabolism in the Development of Hepatic Insulin Resistance

2013 ◽  
Vol 2013 ◽  
pp. 1-21 ◽  
Author(s):  
Guoxun Chen
Keyword(s):  
Insulin Resistance ◽  
Transcription Factors ◽  
Retinoic Acid ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Hepatic Insulin Resistance ◽  
Glucose And Lipid Metabolism ◽  
Hepatic Genes

The increase in the number of people with obesity- and noninsulin-dependent diabetes mellitus has become a major public health concern. Insulin resistance is a common feature closely associated with human obesity and diabetes. Insulin regulates metabolism, at least in part, via the control of the expression of the hepatic genes involved in glucose and fatty acid metabolism. Insulin resistance is always associated with profound changes of the expression of hepatic genes for glucose and lipid metabolism. As an essential micronutrient, vitamin A (VA) is needed in a variety of physiological functions. The active metablite of VA, retinoic acid (RA), regulates the expression of genes through the activation of transcription factors bound to the RA-responsive elements in the promoters of RA-targeted genes. Recently, retinoids have been proposed to play roles in glucose and lipid metabolism and energy homeostasis. This paper summarizes the recent progresses in our understanding of VA metabolism in the liver and of the potential transcription factors mediating RA responses. These transcription factors are the retinoic acid receptor, the retinoid X receptor, the hepatocyte nuclear factor 4α, the chicken ovalbumin upstream promoter-transcription factor II, and the peroxisome proliferator-activated receptor β/δ. This paper also summarizes the effects of VA status and RA treatments on the glucose and lipid metabolism in vivo and the effects of retinoid treatments on the expression of insulin-regulated genes involved in the glucose and fatty acid metabolism in the primary hepatocytes. I discuss the roles of RA production in the development of insulin resistance in hepatocytes and proposes a mechanism by which RA production may contribute to hepatic insulin resistance. Given the large amount of information and progresses regarding the physiological functions of VA, this paper mainly focuses on the findings in the liver and hepatocytes and only mentions the relative findings in other tissues and cells.

scholarly journals Glucocorticoids and fatty acid metabolism in humans: fuelling fat redistribution in the metabolic syndrome

2008 ◽  
Vol 197 (2) ◽  
pp. 189-204 ◽  
Author(s):  
David P Macfarlane ◽  
Shareen Forbes ◽  
Brian R Walker
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Fatty Acid ◽  
Glucose Metabolism ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Hepatic Insulin Resistance ◽  
Induce Insulin Resistance ◽  
The Metabolic Syndrome

Glucocorticoid hormones constitute an integral component of the response to stress, and many of the manifestations of glucocorticoid excess (Cushing's syndrome) are predictable on the basis of their acute effects to raise blood pressure, induce insulin resistance, increase protein catabolism and elevate plasma glucose. However, it appears to be a paradox that the acute lipolytic effect of glucocorticoids is not manifest in long-term weight loss in humans. The effects of glucocorticoids on glucose metabolism are well characterised, involving impaired peripheral glucose uptake and hepatic insulin resistance, and there is mounting evidence that subtle abnormalities in glucocorticoid concentrations in the plasma and/or in tissue sensitivity to glucocorticoids are important in metabolic syndrome. The effects of glucocorticoids on fatty acid metabolism are less well understood than their influence on glucose metabolism. In this article, we review the literature describing the effects of glucocorticoids on fatty acid metabolism, with particular reference to in vivo human studies. We consider the implications for contrasting acute versus chronic effects of glucocorticoids on fat accumulation, effects in different adipose depots and the potential role of glucocorticoid signalling in the pathogenesis and therapy of metabolic syndrome.

scholarly journals Identification of differentially expressed genes and pathways between intramuscular and abdominal fat-derived preadipocyte differentiation of chickens in vitro

BMC Genomics ◽  
2019 ◽  
Vol 20 (1) ◽  
Author(s):  
Meng Zhang ◽  
Fang Li ◽  
Xiang-fei Ma ◽  
Wen-ting Li ◽  
Rui-rui Jiang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Differentially Expressed Genes ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Adipogenic Differentiation ◽  
Abdominal Fat ◽  
Receptor Interaction ◽  
Preadipocyte Differentiation ◽  
Factors Affecting

Abstract Background The distribution and deposition of fat tissue in different parts of the body are the key factors affecting the carcass quality and meat flavour of chickens. Intramuscular fat (IMF) content is an important factor associated with meat quality, while abdominal fat (AbF) is regarded as one of the main factors affecting poultry slaughter efficiency. To investigate the differentially expressed genes (DEGs) and molecular regulatory mechanisms related to adipogenic differentiation between IMF- and AbF-derived preadipocytes, we analysed the mRNA expression profiles in preadipocytes (0d, Pre-) and adipocytes (10d, Ad-) from IMF and AbF of Gushi chickens. Results AbF-derived preadipocytes exhibited a higher adipogenic differentiation ability (96.4% + 0.6) than IMF-derived preadipocytes (86.0% + 0.4) (p < 0.01). By Ribo-Zero RNA sequencing, we obtained 4403 (2055 upregulated and 2348 downregulated) and 4693 (2797 upregulated and 1896 downregulated) DEGs between preadipocytes and adipocytes in the IMF and Ad groups, respectively. For IMF-derived preadipocyte differentiation, pathways related to the PPAR signalling pathway, ECM-receptor interaction and focal adhesion pathway were significantly enriched. For AbF-derived preadipocyte differentiation, the steroid biosynthesis pathways, calcium signaling pathway and ECM-receptor interaction pathway were significantly enriched. A large number of DEGs related to lipid metabolism, fatty acid metabolism and preadipocyte differentiation, such as PPARG, ACSBG2, FABP4, FASN, APOA1 and INSIG1, were identified in our study. Conclusion This study revealed large transcriptomic differences between IMF- and AbF-derived preadipocyte differentiation. A large number of DEGs and transcription factors that were closely related to fatty acid metabolism, lipid metabolism and preadipocyte differentiation were identified in the present study. Additionally, the microenvironment of IMF- and AbF-derived preadipocyte may play a significant role in adipogenic differentiation. This study provides valuable evidence to understand the molecular mechanisms underlying adipogenesis and fat deposition in chickens.

Intracellular Fatty Acid Metabolism in Skeletal Muscle and Insulin Resistance

2005 ◽  
Vol 1 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Eun Koh ◽  
Woo Lee ◽  
Min-Seon Kim ◽  
Joong-Yeol Park ◽  
In Lee ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism

scholarly journals Aberrant fatty acid metabolism in skeletal muscle contributes to insulin resistance in zinc transporter 7 (znt7)-knockout mice

2018 ◽  
Vol 293 (20) ◽  
pp. 7549-7563 ◽  
Author(s):  
Liping Huang ◽  
Surapun Tepaamorndech ◽  
Catherine P. Kirschke ◽  
John W. Newman ◽  
William R. Keyes ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Knockout Mice ◽  
Acid Metabolism ◽  
Zinc Transporter

scholarly journals Lipid Metabolism Profiles in Rheumatic Diseases

2021 ◽  
Vol 12 ◽  
Author(s):  
Weilin Chen ◽  
Qi Wang ◽  
Bin Zhou ◽  
Lihua Zhang ◽  
Honglin Zhu
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Rheumatic Diseases ◽  
Fatty Acid Metabolism ◽  
High Mortality ◽  
Acid Metabolism ◽  
Cell Metabolism ◽  
Therapeutic Strategies ◽  
Clinical Applications ◽  
Multiple Organs

Rheumatic diseases are a group of chronic autoimmune disorders that involve multiple organs or systems and have high mortality. The mechanisms of these diseases are still ill-defined, and targeted therapeutic strategies are still challenging for physicians. Recent research indicates that cell metabolism plays important roles in the pathogenesis of rheumatic diseases. In this review, we mainly focus on lipid metabolism profiles (dyslipidaemia, fatty acid metabolism) and mechanisms in rheumatic diseases and discuss potential clinical applications based on lipid metabolism profiles.

scholarly journals Multi-Omics Analysis of Fatty Acid Metabolism in Thyroid Carcinoma

2021 ◽  
Vol 11 ◽  
Author(s):  
Jinghui Lu ◽  
Yankun Zhang ◽  
Min Sun ◽  
Changyuan Ding ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Thyroid Carcinoma ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Metabolic Reprogramming ◽  
Clinical Samples ◽  
Integrated Analysis ◽  
Additional Energy

ObjectivePapillary thyroid carcinoma (PTC) accounts for the majority of thyroid cancer and affects a large number of individuals. The pathogenesis of PTC has not been completely elucidated thus far. Metabolic reprogramming is a common feature in tumours. Our previous research revealed the reprogramming of lipid metabolism in PTC. Further studies on lipid metabolism reprogramming may help elucidate the pathogenesis of PTC.MethodsClinical samples of PTC and para-tumour tissue were analysed using lipidomic, proteomic, and metabolomic approaches. A multi-omics integrative strategy was adopted to identify the important pathways in PTC. The findings were further confirmed using western blotting, tissue microarray, bioinformatics, and cell migration assays.ResultsMulti-omics data and the results of integrated analysis revealed that the three steps of fatty acid metabolism (hydrolysis, transportation, and oxidation) were significantly enhanced in PTC. Especially, the expression levels of LPL, FATP2, and CPT1A, three key enzymes in the respective steps, were elevated in PTC. Moreover, LPL, FATP2 and CPT1A expression was associated with the TNM stage, lymph node metastasis of PTC. Moreover, high levels of FATP2 and CPT1A contributed to poor prognosis of PTC. In addition, ectopic overexpression of LPL, FATP2 and CPT1A can each promote the migration of thyroid cancer cells.ConclusionsOur data suggested that enhanced fatty acid metabolism supplied additional energy and substrates for PTC progression. This may help elucidating the underlying mechanism of PTC pathogenesis and identifying the potential therapeutic targets for PTC.

scholarly journals Interplay and cooperation between SREBF1 and master transcription factors regulate lipid metabolism and tumor-promoting pathways in squamous cancer

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Li-Yan Li ◽  
Qian Yang ◽  
Yan-Yi Jiang ◽  
Wei Yang ◽  
Yuan Jiang ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Fatty Acid ◽  
Lipid Metabolism ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Human Cancer ◽  
Regulatory Element ◽  
Regulatory Elements ◽  
Gene Set Enrichment Analysis ◽  
Transcriptional Dysregulation

AbstractSquamous cell carcinomas (SCCs) comprise one of the most common histologic types of human cancer. Transcriptional dysregulation of SCC cells is orchestrated by tumor protein p63 (TP63), a master transcription factor (TF) and a well-researched SCC-specific oncogene. In the present study, both Gene Set Enrichment Analysis (GSEA) of SCC patient samples and in vitro loss-of-function assays establish fatty-acid metabolism as a key pathway downstream of TP63. Further studies identify sterol regulatory element binding transcription factor 1 (SREBF1) as a central mediator linking TP63 with fatty-acid metabolism, which regulates the biosynthesis of fatty-acids, sphingolipids (SL), and glycerophospholipids (GPL), as revealed by liquid chromatography tandem mass spectrometry (LC-MS/MS)-based lipidomics. Moreover, a feedback co-regulatory loop consisting of SREBF1/TP63/Kruppel like factor 5 (KLF5) is identified, which promotes overexpression of all three TFs in SCCs. Downstream of SREBF1, a non-canonical, SCC-specific function is elucidated: SREBF1 cooperates with TP63/KLF5 to regulate hundreds of cis-regulatory elements across the SCC epigenome, which converge on activating cancer-promoting pathways. Indeed, SREBF1 is essential for SCC viability and migration, and its overexpression is associated with poor survival in SCC patients. Taken together, these data shed light on mechanisms of transcriptional dysregulation in cancer, identify specific epigenetic regulators of lipid metabolism, and uncover SREBF1 as a potential therapeutic target and prognostic marker in SCC.

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