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Article ; Online: Diet-induced differential effects on plasma lipids secretion by the inositol-requiring transmembrane kinase/endoribonuclease 1α

Jahangir Iqbal / Ali Al Qarni / Ahmed Bakillah

Frontiers in Bioscience-Landmark, Vol 26, Iss 5, Pp 11-

2021 Volume 21

Abstract: Intestinal and hepatic lipid metabolism plays an essential role in regulating plasma lipid levels. These lipids are mobilized on apolipoprotein B (apoB)-containing lipoproteins and their plasma homeostasis is maintained by balancing production and ... ...

Abstract	Intestinal and hepatic lipid metabolism plays an essential role in regulating plasma lipid levels. These lipids are mobilized on apolipoprotein B (apoB)-containing lipoproteins and their plasma homeostasis is maintained by balancing production and catabolism. Microsomal triglyceride transfer protein (MTP) which is expressed mainly in the intestine and liver plays an essential role in regulating the assembly and secretion of apoB-lipoproteins. Any imbalance in the production or clearance of lipoproteins leads to hyperlipidemia which is a major risk factor for atherosclerosis, obesity, diabetes, and metabolic syndrome. Here, we identify a new role of inositol-requiring transmembrane kinase/endoribonuclease 1α (IRE1α) in the regulation of plasma lipids. We generated intestine specific IRE1α knockout mice to study whether intestinal IRE1α regulates plasma lipids by modulating intestinal lipid absorption. Intestine specific deletion of Ire1a gene in mice fed chow diet, significantly reduced plasma cholesterol and triglycerides by 29% and 43% in Ire1a-⁣/- mice (P < 0.01 & P < 0.001, respectively). These changes were not associated with any alteration of MTP activity nor its mRNA expression. On the other hand, Western diet increased plasma triglyceride by 37% (P < 0.01) without affecting total plasma cholesterol in Ire1a-⁣/- mice. Interestingly, this effect was associated with a significant increase in the intestinal MTP activity and its mRNA expression (25%, P < 0.01 and 70%, P < 0.05, respectively). Collectively, our findings reveal key role of intestinal IRE1α in the regulation of plasma lipids that may provide a therapeutic target for disorders of lipid metabolism.
Keywords	lipoproteins ; lipids ; atherosclerosis ; obesity ; diabetes ; endoplasmic reticulum ; unfolded protein response ; microsomal triglyceride transfer protein ; Biochemistry ; QD415-436 ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2021-04-01T00:00:00Z
Publisher	IMR Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Regulation of Sphingolipid Metabolism by MicroRNAs

Zainab Jahangir / Ahmed Bakillah / Jahangir Iqbal

Diseases, Vol 6, Iss 3, p

A Potential Approach to Alleviate Atherosclerosis

2018 Volume 82

Abstract: The rapidly expanding field of bioactive lipids is exemplified by the many sphingolipids, which are structurally and functionally diverse molecules with significant physiologic functions. These sphingolipids are main constituents of cellular membranes ... ...

Abstract	The rapidly expanding field of bioactive lipids is exemplified by the many sphingolipids, which are structurally and functionally diverse molecules with significant physiologic functions. These sphingolipids are main constituents of cellular membranes and have been found associated with plasma lipoproteins, and their concentrations are altered in several metabolic disorders such as atherosclerosis, obesity, and diabetes. Understanding the mechanisms that regulate their biosynthesis and secretion may provide novel information that might be amenable to therapeutic targeting in the treatment of these diseases. Several sphingolipid synthesis genes have been targeted as potential therapeutics for atherosclerosis. In recent years, significant progress has been made in studying the role of microRNAs (miRNAs) in lipid metabolism. However, little effort has been made to investigate their role in sphingolipid metabolism. Sphingolipid biosynthetic pathways involve various enzymes that lead to the formation of several key molecules implicated in atherosclerosis, and the identification of miRNAs that regulate these enzymes could help us to understand these complex pathways better and may prove beneficial in alleviating atherosclerosis.
Keywords	atherosclerosis ; ceramides ; lipids ; lipoproteins ; miRNA ; sphingolipids ; sphingomyelin ; Medicine ; R
Language	English
Publishing date	2018-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Profiling of G-Protein Coupled Receptors in Adipose Tissue and Differentiating Adipocytes Offers a Translational Resource for Obesity/Metabolic Research

Saeed Al Mahri / Meshail Okla / Mamoon Rashid / Shuja Shafi Malik / Jahangir Iqbal / Maria Al Ibrahim / Ghida Dairi / Amer Mahmood / Manikandan Muthurangan / Ahmed Yaqinuddin / Sameer Mohammad

Cells, Vol 12, Iss 377, p

2023 Volume 377

Abstract: G protein-coupled receptors (GPCRs) are expressed essentially on all cells, facilitating cellular responses to external stimuli, and are involved in nearly every biological process. Several members of this family play significant roles in the regulation ... ...

Abstract	G protein-coupled receptors (GPCRs) are expressed essentially on all cells, facilitating cellular responses to external stimuli, and are involved in nearly every biological process. Several members of this family play significant roles in the regulation of adipogenesis and adipose metabolism. However, the expression and functional significance of a vast number of GPCRs in adipose tissue are unknown. We used a high-throughput RT-PCR panel to determine the expression of the entire repertoire of non-sensory GPCRs in mouse white, and brown adipose tissue and assess changes in their expression during adipogenic differentiation of murine adipocyte cell line, 3T3-L1. In addition, the expression of GPCRs in subcutaneous adipose tissues from lean, obese, and diabetic human subjects and in adipocytes isolated from regular chow and high-fat fed mice were evaluated by re-analyzing RNA-sequencing data. We detected a total of 292 and 271 GPCRs in mouse white and brown adipose tissue, respectively. There is a significant overlap in the expression of GPCRs between the two adipose tissue depots, but several GPCRs are specifically expressed in one of the two tissue types. Adipogenic differentiation of 3T3-L1 cells had a profound impact on the expression of several GPCRs. RNA sequencing of subcutaneous adipose from healthy human subjects detected 255 GPCRs and obesity significantly changed the expression of several GPCRs in adipose tissue. High-fat diet had a significant impact on adipocyte GPCR expression that was similar to human obesity. Finally, we report several highly expressed GPCRs with no known role in adipose biology whose expression was significantly altered during adipogenic differentiation, and/or in the diseased human subjects. These GPCRs could play an important role in adipose metabolism and serve as a valuable translational resource for obesity and metabolic research.
Keywords	adipose tissue ; adipogenesis ; G-protein-coupled receptors ; thermogenesis ; obesity ; metabolic syndrome ; Biology (General) ; QH301-705.5
Subject code	616 ; 571
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: A comparative study of functional outcome of treatment of intra articular fractures of distal radius fixed with percutaneous Kirschner's wires vs T-plate.

Khan, Jahangir Iqbal / Hussain, Faisal Nazeer / Mehmood, Tahir / Adil, Omer

Pakistan journal of medical sciences

2017 Volume 33, Issue 3, Page(s) 709–713

Abstract: Background & objective: Fractures of the distal radius are common with a variable prognosis in case of intra articular extension. The available options include Plaster, External fixation, Prefabricated Splintage using Ligamentotaxis, K-wire fixation, ... ...

Abstract	Background & objective: Fractures of the distal radius are common with a variable prognosis in case of intra articular extension. The available options include Plaster, External fixation, Prefabricated Splintage using Ligamentotaxis, K-wire fixation, and open reduction internal fixation with T-plate without an as yet clear advantage of one over the others. If these fractures are allowed to collapse, radial shortening, angulation and articular incongruity may cause permanent deformity and loss of function. This limited small scale study was intended to compare the functional results of treatment of these fractures with a T plate and K-wires. Methods: This was a prospective experimental study conducted at department of Orthopedics of PGMI/Lahore General Hospital, Lahore. Total 30 patients were included and randomized into two groups of 15 patients each. Group-A patients were treated with Krischner's wires and Group-B patients were treated with a T-Plate with open reduction. Informed consent was taken. Post operative follow up was done for 12 weeks for the outcome parameters (Green and O'Brien score). Results: Mean age of patients in Group-A and B was 36.13±9.81 and 44.73±7.86 years respectively. In Group-A there were 10 male and 5 female patients and in Group-B there were 8 male and seven female patients respectively. In Group-A nine patients presented with Fernandez type-II and six patients presented with Fernandez type-III fracture. While in Group-B 10 patients presented with Fernandez type-II and five patients presented with Fernandez type-III fracture. Among Group-A patient's final outcome was excellent in 86.67% patients while in Group-B only 53.33% patients had excellent outcome at three months follow up. Conclusion: Percutaneous Kirschner's wires appeared to be more effective as compared to T-Plate fixation in terms of functional outcome for treating intra-articular distal radius fractures.
Language	English
Publishing date	2017-08-01
Publishing country	Pakistan
Document type	Journal Article
ZDB-ID	2032827-8
ISSN	1681-715X ; 1682-024X ; 1017-4699
ISSN (online)	1681-715X
ISSN	1682-024X ; 1017-4699
DOI	10.12669/pjms.333.11421
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Hexim1 heterozygosity stabilizes atherosclerotic plaque and decreased steatosis in ApoE null mice fed atherogenic diet

Dhar-Mascareno, Manya / Daniel Beckles / Eduardo Mascareno / Inna Rozenberg / Jahangir Iqbal / M. Mahmood Hussain

international journal of biochemistry & cell biology. 2017 Feb., v. 83

2017

Abstract: Hexim-1 is an inhibitor of RNA polymerase II transcription elongation. Decreased Hexim-1 expression in animal models of chronic diseases such as left ventricular hypertrophy, obesity and cancer triggered significant changes in adaptation and remodeling. ... ...

Abstract	Hexim-1 is an inhibitor of RNA polymerase II transcription elongation. Decreased Hexim-1 expression in animal models of chronic diseases such as left ventricular hypertrophy, obesity and cancer triggered significant changes in adaptation and remodeling. The main aim of this study was to evaluate the role of Hexim1 in lipid metabolism focused in the progression of atherosclerosis and steatosis. We used the C57BL6 apolipoprotein E (ApoE null) crossed bred to C57BL6Hexim1 heterozygous mice to obtain ApoE null − Hexim1 heterozygous mice (ApoE-HT). Both ApoE null backgrounds were fed high fat diet for twelve weeks. Then, we evaluated lipid metabolism, atherosclerotic plaque formation and liver steatosis. In order to understand changes in the transcriptome of both backgrounds during the progression of steatosis, we performed Affymetrix mouse 430 2.0 microarray. After 12 weeks of HFD, ApoE null and ApoE-HT showed similar increase of cholesterol and triglycerides in plasma. Plaque composition was altered in ApoE-HT. Additionally, liver triglycerides and steatosis were decreased in ApoE-HT mice. Affymetrix analysis revealed that decreased steatosis might be due to impaired inducible SOCS3 expression in ApoE-HT mice. In conclusion, decreased Hexim-1 expression does not alter cholesterol metabolism in ApoE null background after HFD. However, it promotes stable atherosclerotic plaque and decreased steatosis by promoting the anti-inflammatory TGFβ pathway and blocking the expression of the inducible and pro-inflammatory expression of SOCS3 respectively.
Keywords	animal models ; apolipoprotein E ; atherosclerosis ; cholesterol ; cholesterol metabolism ; chronic diseases ; DNA-directed RNA polymerase ; fatty liver ; heterozygosity ; high fat diet ; hypertrophy ; liver ; mice ; microarray technology ; neoplasms ; obesity ; transcriptome ; transforming growth factor beta ; triacylglycerols
Language	English
Dates of publication	2017-02
Size	p. 56-64.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	1228429-4
ISSN	1878-5875 ; 1357-2725
ISSN (online)	1878-5875
ISSN	1357-2725
DOI	10.1016/j.biocel.2016.12.010
Database	NAL-Catalogue (AGRICOLA)

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Article: Novel role of a triglyceride-synthesizing enzyme: DGAT1 at the crossroad between triglyceride and cholesterol metabolism

Sachdev, Vinay / Albert K. Groen / Andreas Zimmer / Andrew V. Turnbull / Bernhard Scheicher / Christina Leopold / Dagmar Kolb / Dagmar Kratky / Gerald Hoefler / Jahangir Iqbal / Jay V. Patankar / M. Mahmood Hussain / Madeleine Goeritzer / Marcela Doktorova / Raimund Bauer / Renze Boverhof / Sascha Obrowsky

Biochimica et biophysica acta. 2016 Sept., v. 1861, no. 9

2016

Abstract: Acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1) is a key enzyme in triacylglycerol (TG) biosynthesis. Here we show that genetic deficiency and pharmacological inhibition of DGAT1 in mice alters cholesterol metabolism. Cholesterol absorption, as ... ...

Abstract	Acyl-CoA:diacylglycerol acyltransferase 1 (DGAT1) is a key enzyme in triacylglycerol (TG) biosynthesis. Here we show that genetic deficiency and pharmacological inhibition of DGAT1 in mice alters cholesterol metabolism. Cholesterol absorption, as assessed by acute cholesterol uptake, was significantly decreased in the small intestine and liver upon DGAT1 deficiency/inhibition. Ablation of DGAT1 in the intestine (I-DGAT1−/−) alone is sufficient to cause these effects. Consequences of I-DGAT1 deficiency phenocopy findings in whole-body DGAT1−/− and DGAT1 inhibitor-treated mice. We show that deficiency/inhibition of DGAT1 affects cholesterol metabolism via reduced chylomicron size and increased trans-intestinal cholesterol excretion. These effects are independent of cholesterol uptake at the apical surface of enterocytes but mediated through altered dietary fatty acid metabolism. Our findings provide insight into a novel role of DGAT1 and identify a pathway by which intestinal DGAT1 deficiency affects whole-body cholesterol homeostasis in mice. Targeting intestinal DGAT1 may represent a novel approach for treating hypercholesterolemia.
Keywords	absorption ; biosynthesis ; cholesterol ; cholesterol metabolism ; dietary fat ; enterocytes ; excretion ; fatty acid metabolism ; homeostasis ; hypercholesterolemia ; liver ; mice ; small intestine ; triacylglycerols
Language	English
Dates of publication	2016-09
Size	p. 1132-1141.
Publishing place	Elsevier B.V.
Document type	Article
ISSN	1388-1981
DOI	10.1016/j.bbalip.2016.06.014
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Mycobacterial Metabolic Syndrome

Amanda J Martinot / Mary Farrow / Lu Bai / Emilie Layre / Tan-Yun Cheng / Jennifer H Tsai / Jahangir Iqbal / John W Annand / Zuri A Sullivan / M Mahmood Hussain / James Sacchettini / D Branch Moody / Jessica C Seeliger / Eric J Rubin

PLoS Pathogens, Vol 12, Iss 1, p e

LprG and Rv1410 Regulate Triacylglyceride Levels, Growth Rate and Virulence in Mycobacterium tuberculosis.

2016 Volume 1005351

Abstract: Mycobacterium tuberculosis (Mtb) mutants lacking rv1411c, which encodes the lipoprotein LprG, and rv1410c, which encodes a putative efflux pump, are dramatically attenuated for growth in mice. Here we show that loss of LprG-Rv1410 in Mtb leads to ... ...

Abstract	Mycobacterium tuberculosis (Mtb) mutants lacking rv1411c, which encodes the lipoprotein LprG, and rv1410c, which encodes a putative efflux pump, are dramatically attenuated for growth in mice. Here we show that loss of LprG-Rv1410 in Mtb leads to intracellular triacylglyceride (TAG) accumulation, and overexpression of the locus increases the levels of TAG in the culture medium, demonstrating a role of this locus in TAG transport. LprG binds TAG within a large hydrophobic cleft and is sufficient to transfer TAG from donor to acceptor membranes. Further, LprG-Rv1410 is critical for broadly regulating bacterial growth and metabolism in vitro during carbon restriction and in vivo during infection of mice. The growth defect in mice is due to disrupted bacterial metabolism and occurs independently of key immune regulators. The in vivo essentiality of this locus suggests that this export system and other regulators of metabolism should be considered as targets for novel therapeutics.
Keywords	Immunologic diseases. Allergy ; RC581-607 ; Biology (General) ; QH301-705.5
Subject code	572
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Lack of MTTP Activity in Pluripotent Stem Cell-Derived Hepatocytes and Cardiomyocytes Abolishes apoB Secretion and Increases Cell Stress

Ying Liu / Donna M. Conlon / Xin Bi / Katherine J. Slovik / Jianting Shi / Hailey I. Edelstein / John S. Millar / Ali Javaheri / Marina Cuchel / Evanthia E. Pashos / Jahangir Iqbal / M. Mahmood Hussain / Robert A. Hegele / Wenli Yang / Stephen A. Duncan / Daniel J. Rader / Edward E. Morrisey

Cell Reports, Vol 19, Iss 7, Pp 1456-

2017 Volume 1466

Abstract: Abetalipoproteinemia (ABL) is an inherited disorder of lipoprotein metabolism resulting from mutations in microsomal triglyceride transfer protein (MTTP). In addition to expression in the liver and intestine, MTTP is expressed in cardiomyocytes, and ... ...

Abstract	Abetalipoproteinemia (ABL) is an inherited disorder of lipoprotein metabolism resulting from mutations in microsomal triglyceride transfer protein (MTTP). In addition to expression in the liver and intestine, MTTP is expressed in cardiomyocytes, and cardiomyopathy has been reported in several ABL cases. Using induced pluripotent stem cells (iPSCs) generated from an ABL patient homozygous for a missense mutation (MTTPR46G), we show that human hepatocytes and cardiomyocytes exhibit defects associated with ABL disease, including loss of apolipoprotein B (apoB) secretion and intracellular accumulation of lipids. MTTPR46G iPSC-derived cardiomyocytes failed to secrete apoB, accumulated intracellular lipids, and displayed increased cell death, suggesting intrinsic defects in lipid metabolism due to loss of MTTP function. Importantly, these phenotypes were reversed after the correction of the MTTPR46G mutation by CRISPR/Cas9 gene editing. Together, these data reveal clear cellular defects in iPSC-derived hepatocytes and cardiomyocytes lacking MTTP activity, including a cardiomyocyte-specific regulated stress response to elevated lipids.
Keywords	abetaliproteinemia ; induced pluripotent stem cells ; iPSC-derived hepatocytes and cardiomyocytes ; lipid accumulation ; apoB ; cardiac stress ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2017-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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