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Article ; Online: Oxidative stress in obesity-associated hepatocellular carcinoma: sources, signaling and therapeutic challenges.

Brahma, Manoja K / Gilglioni, Eduardo H / Zhou, Lang / Trépo, Eric / Chen, Pengyu / Gurzov, Esteban N

2021 Volume 40, Issue 33, Page(s) 5155–5167

Abstract: Obesity affects more than 650 million individuals worldwide and is a well-established risk factor for the development of hepatocellular carcinoma (HCC). Oxidative stress can be considered as a bona fide tumor promoter, contributing to the initiation and ... ...

Abstract	Obesity affects more than 650 million individuals worldwide and is a well-established risk factor for the development of hepatocellular carcinoma (HCC). Oxidative stress can be considered as a bona fide tumor promoter, contributing to the initiation and progression of liver cancer. Indeed, one of the key events involved in HCC progression is excessive levels of reactive oxygen species (ROS) resulting from the fatty acid influx and chronic inflammation. This review provides insights into the different intracellular sources of obesity-induced ROS and molecular mechanisms responsible for hepatic tumorigenesis. In addition, we highlight recent findings pointing to the role of the dysregulated activity of BCL-2 proteins and protein tyrosine phosphatases (PTPs) in the generation of hepatic oxidative stress and ROS-mediated dysfunctional signaling, respectively. Finally, we discuss the potential and challenges of novel nanotechnology strategies to prevent ROS formation in obesity-associated HCC.
MeSH term(s)	Carcinoma, Hepatocellular ; Humans ; Liver Neoplasms ; Oxidative Stress ; Signal Transduction
Language	English
Publishing date	2021-07-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-01950-y
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Zs.A 2218: Show issues

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Article ; Online: HAMSAB diet ameliorates dysfunctional signaling in pancreatic islets in autoimmune diabetes.

Vandenbempt, Valerie / Eski, Sema Elif / Brahma, Manoja K / Li, Ao / Negueruela, Javier / Bruggeman, Ylke / Demine, Stéphane / Xiao, Peng / Cardozo, Alessandra K / Baeyens, Nicolas / Martelotto, Luciano G / Singh, Sumeet Pal / Mariño, Eliana / Gysemans, Conny / Gurzov, Esteban N

iScience

2023 Volume 27, Issue 1, Page(s) 108694

Abstract: An altered gut microbiota is associated with type 1 diabetes (T1D), affecting the production of short-chain fatty acids (SCFA) and glucose homeostasis. We previously demonstrated that enhancing serum acetate and butyrate using a dietary supplement ( ... ...

Abstract	An altered gut microbiota is associated with type 1 diabetes (T1D), affecting the production of short-chain fatty acids (SCFA) and glucose homeostasis. We previously demonstrated that enhancing serum acetate and butyrate using a dietary supplement (HAMSAB) improved glycemia in non-obese diabetic (NOD) mice and patients with established T1D. The effects of SCFA on immune-infiltrated islet cells remain to be clarified. Here, we performed single-cell RNA sequencing on islet cells from NOD mice fed an HAMSAB or control diet. HAMSAB induced a regulatory gene expression profile in pancreas-infiltrated immune cells. Moreover, HAMSAB maintained the expression of β-cell functional genes and decreased cellular stress. HAMSAB-fed mice showed preserved pancreatic endocrine cell identity, evaluated by decreased numbers of poly-hormonal cells. Finally, SCFA increased insulin levels in human β-like cells and improved transplantation outcome in NOD/SCID mice. Our findings support the use of metabolite-based diet as attractive approach to improve glucose control in T1D.
Language	English
Publishing date	2023-12-10
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108694
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Article ; Online: Differential regulation of pro-inflammatory cytokine signalling by protein tyrosine phosphatases in pancreatic β-cells.

Stanley, William J / Trivedi, Prerak M / Sutherland, Andrew P / Thomas, Helen E / Gurzov, Esteban N

Journal of molecular endocrinology

2017 Volume 59, Issue 4, Page(s) 325–337

Abstract: Type 1 diabetes (T1D) is characterized by the destruction of insulin-producing β-cells by immune cells in the pancreas. Pro-inflammatory including TNF-α, IFN-γ and IL-1β are released in the islet during the autoimmune assault and signal in β-cells ... ...

Abstract	Type 1 diabetes (T1D) is characterized by the destruction of insulin-producing β-cells by immune cells in the pancreas. Pro-inflammatory including TNF-α, IFN-γ and IL-1β are released in the islet during the autoimmune assault and signal in β-cells through phosphorylation cascades, resulting in pro-apoptotic gene expression and eventually β-cell death. Protein tyrosine phosphatases (PTPs) are a family of enzymes that regulate phosphorylative signalling and are associated with the development of T1D. Here, we observed expression of PTPN6 and PTPN1 in human islets and islets from non-obese diabetic (NOD) mice. To clarify the role of these PTPs in β-cells/islets, we took advantage of CRISPR/Cas9 technology and pharmacological approaches to inactivate both proteins. We identify PTPN6 as a negative regulator of TNF-α-induced β-cell death, through JNK-dependent BCL-2 protein degradation. In contrast, PTPN1 acts as a positive regulator of IFN-γ-induced STAT1-dependent gene expression, which enhanced autoimmune destruction of β-cells. Importantly, PTPN1 inactivation by pharmacological modulation protects β-cells and primary mouse islets from cytokine-mediated cell death. Thus, our data point to a non-redundant effect of PTP regulation of cytokine signalling in β-cells in autoimmune diabetes.
MeSH term(s)	Animals ; Cell Death/genetics ; Cell Death/immunology ; Cytokines/metabolism ; Gene Expression ; Gene Knockout Techniques ; Gene Targeting ; Humans ; Inflammation Mediators/metabolism ; Insulin-Secreting Cells/metabolism ; JNK Mitogen-Activated Protein Kinases/metabolism ; Mice ; Mice, Inbred NOD ; Phosphorylation ; Protein Tyrosine Phosphatase, Non-Receptor Type 1/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 1/metabolism ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/genetics ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/metabolism ; Protein Tyrosine Phosphatases/genetics ; Protein Tyrosine Phosphatases/metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Cytokines ; Inflammation Mediators ; Tumor Necrosis Factor-alpha ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Protein Tyrosine Phosphatase, Non-Receptor Type 1 (EC 3.1.3.48) ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 (EC 3.1.3.48) ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2017-08-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645012-x
ISSN	1479-6813 ; 0952-5041
ISSN (online)	1479-6813
ISSN	0952-5041
DOI	10.1530/JME-17-0089
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Zs.A 2406: Show issues

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Article ; Online: Protein tyrosine phosphatases: molecular switches in metabolism and diabetes.

Gurzov, Esteban N / Stanley, William J / Brodnicki, Thomas C / Thomas, Helen E

Trends in endocrinology and metabolism: TEM

2015 Volume 26, Issue 1, Page(s) 30–39

Abstract: Protein tyrosine phosphatases (PTPs) are a large family of enzymes that generally oppose the actions of protein tyrosine kinases (PTKs). Genetic polymorphisms for particular PTPs are associated with altered risk of both type 1 diabetes (T1D) and type 2 ... ...

Abstract	Protein tyrosine phosphatases (PTPs) are a large family of enzymes that generally oppose the actions of protein tyrosine kinases (PTKs). Genetic polymorphisms for particular PTPs are associated with altered risk of both type 1 diabetes (T1D) and type 2 diabetes (T2D). Moreover, recent evidence suggests that PTPs play crucial roles in metabolism. They can act as regulators of liver homeostasis, food intake, or immune-mediated pancreatic b cell death. In this review we describe the mechanisms by which different members of the non-receptor PTP (PTPN) family influence metabolic physiology. This 'metabolic job' of PTPs is discussed in depth and the role of these proteins in different cell types compared. Understanding the pathways regulated by PTPs will provide novel therapeutic strategies for the treatment of diabetes.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Energy Metabolism/genetics ; Genes, Switch/physiology ; Humans ; Immunity, Cellular/genetics ; Insulin-Secreting Cells/metabolism ; Metabolism/genetics ; Models, Molecular ; Polymorphism, Genetic ; Protein Tyrosine Phosphatases/genetics ; Protein Tyrosine Phosphatases/physiology
Chemical Substances	Protein Tyrosine Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2015-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2014.10.004
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Zs.A 2999: Show issues

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Article ; Online: The JAK/STAT pathway in obesity and diabetes.

Gurzov, Esteban N / Stanley, William J / Pappas, Evan G / Thomas, Helen E / Gough, Daniel J

The FEBS journal

2016 Volume 283, Issue 16, Page(s) 3002–3015

Abstract: Diabetes mellitus are complex, multi-organ metabolic pathologies characterized by hyperglycemia. Emerging evidence shows that the highly conserved and potent JAK/STAT signaling pathway is required for normal homeostasis, and, when dysregulated, ... ...

Abstract	Diabetes mellitus are complex, multi-organ metabolic pathologies characterized by hyperglycemia. Emerging evidence shows that the highly conserved and potent JAK/STAT signaling pathway is required for normal homeostasis, and, when dysregulated, contributes to the development of obesity and diabetes. In this review, we analyze the role of JAK/STAT activation in the brain, liver, muscle, fat and pancreas, and how this affects the course of the disease. We also consider the therapeutic implications of targeting the JAK/STAT pathway in treatment of obesity and diabetes.
MeSH term(s)	Adipose Tissue/enzymology ; Adipose Tissue/metabolism ; Animals ; Brain/enzymology ; Brain/metabolism ; Diabetes Mellitus/enzymology ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/therapy ; Fatty Liver/metabolism ; Humans ; Insulin-Secreting Cells/enzymology ; Insulin-Secreting Cells/metabolism ; Janus Kinases/antagonists & inhibitors ; Janus Kinases/metabolism ; Mice ; Muscle, Skeletal/enzymology ; Muscle, Skeletal/metabolism ; Obesity/enzymology ; Obesity/metabolism ; Obesity/therapy ; STAT Transcription Factors/antagonists & inhibitors ; STAT Transcription Factors/metabolism ; Signal Transduction
Chemical Substances	STAT Transcription Factors ; Janus Kinases (EC 2.7.10.2)
Language	English
Publishing date	2016-08
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.13709
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Zs.A 260: Show issues

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Article ; Online: STAT3 Regulates Mitochondrial Gene Expression in Pancreatic β-Cells and Its Deficiency Induces Glucose Intolerance in Obesity.

Schaschkow, Anaïs / Pang, Lokman / Vandenbempt, Valerie / Elvira, Bernat / Litwak, Sara A / Vekeriotaite, Beata / Maillard, Elisa / Vermeersch, Marjorie / Paula, Flavia M M / Pinget, Michel / Perez-Morga, David / Gough, Daniel J / Gurzov, Esteban N

Diabetes

2021 Volume 70, Issue 9, Page(s) 2026–2041

Abstract: Most obese and insulin-resistant individuals do not develop diabetes. This is the result of the capacity of β-cells to adapt and produce enough insulin to cover the needs of the organism. The underlying mechanism of β-cell adaptation in obesity, however, ...

Abstract	Most obese and insulin-resistant individuals do not develop diabetes. This is the result of the capacity of β-cells to adapt and produce enough insulin to cover the needs of the organism. The underlying mechanism of β-cell adaptation in obesity, however, remains unclear. Previous studies have suggested a role for STAT3 in mediating β-cell development and human glucose homeostasis, but little is known about STAT3 in β-cells in obesity. We observed enhanced cytoplasmic expression of STAT3 in severely obese subjects with diabetes. To address the functional role of STAT3 in adult β-cells, we generated mice with tamoxifen-inducible partial or full deletion of STAT3 in β-cells and fed them a high-fat diet before analysis. Interestingly, β-cell heterozygous and homozygous STAT3-deficient mice showed glucose intolerance when fed a high-fat diet. Gene expression analysis with RNA sequencing showed that reduced expression of mitochondrial genes in STAT3 knocked down human EndoC-β
MeSH term(s)	Animals ; Blood Glucose/metabolism ; Diet, High-Fat ; Genes, Mitochondrial ; Glucose Intolerance/genetics ; Glucose Intolerance/metabolism ; Humans ; Insulin/metabolism ; Insulin-Secreting Cells/metabolism ; Mice ; Mice, Knockout ; Mitochondria/genetics ; Mitochondria/metabolism ; Obesity/genetics ; Obesity/metabolism ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism
Chemical Substances	Blood Glucose ; Insulin ; STAT3 Transcription Factor
Language	English
Publishing date	2021-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db20-1222
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Uh III Zs.175: Show issues

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Article ; Online: Metabolite-based dietary supplementation in human type 1 diabetes is associated with microbiota and immune modulation.

Bell, Kirstine J / Saad, Sonia / Tillett, Bree J / McGuire, Helen M / Bordbar, Sara / Yap, Yu Anne / Nguyen, Long T / Wilkins, Marc R / Corley, Susan / Brodie, Shannon / Duong, Sussan / Wright, Courtney J / Twigg, Stephen / de St Groth, Barbara Fazekas / Harrison, Leonard C / Mackay, Charles R / Gurzov, Esteban N / Hamilton-Williams, Emma E / Mariño, Eliana

Microbiome

2022 Volume 10, Issue 1, Page(s) 9

Abstract: Background: Short-chain fatty acids (SCFAs) produced by the gut microbiota have beneficial anti-inflammatory and gut homeostasis effects and prevent type 1 diabetes (T1D) in mice. Reduced SCFA production indicates a loss of beneficial bacteria, commonly ...

Abstract	Background: Short-chain fatty acids (SCFAs) produced by the gut microbiota have beneficial anti-inflammatory and gut homeostasis effects and prevent type 1 diabetes (T1D) in mice. Reduced SCFA production indicates a loss of beneficial bacteria, commonly associated with chronic autoimmune and inflammatory diseases, including T1D and type 2 diabetes. Here, we addressed whether a metabolite-based dietary supplement has an impact on humans with T1D. We conducted a single-arm pilot-and-feasibility trial with high-amylose maize-resistant starch modified with acetate and butyrate (HAMSAB) to assess safety, while monitoring changes in the gut microbiota in alignment with modulation of the immune system status. Results: HAMSAB supplement was administered for 6 weeks with follow-up at 12 weeks in adults with long-standing T1D. Increased concentrations of SCFA acetate, propionate, and butyrate in stools and plasma were in concert with a shift in the composition and function of the gut microbiota. While glucose control and insulin requirements did not change, subjects with the highest SCFA concentrations exhibited the best glycemic control. Bifidobacterium longum, Bifidobacterium adolescentis, and vitamin B7 production correlated with lower HbA1c and basal insulin requirements. Circulating B and T cells developed a more regulatory phenotype post-intervention. Conclusion: Changes in gut microbiota composition, function, and immune profile following 6 weeks of HAMSAB supplementation were associated with increased SCFAs in stools and plasma. The persistence of these effects suggests that targeting dietary SCFAs may be a mechanism to alter immune profiles, promote immune tolerance, and improve glycemic control for the treatment of T1D. Trial registration: ACTRN12618001391268. Registered 20 August 2018, https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=375792 Video Abstract.
MeSH term(s)	Animals ; Diabetes Mellitus, Type 1 ; Diabetes Mellitus, Type 2/microbiology ; Dietary Supplements ; Fatty Acids, Volatile ; Gastrointestinal Microbiome ; Humans ; Mice ; Microbiota
Chemical Substances	Fatty Acids, Volatile
Language	English
Publishing date	2022-01-19
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
ZDB-ID	2697425-3
ISSN	2049-2618 ; 2049-2618
ISSN (online)	2049-2618
ISSN	2049-2618
DOI	10.1186/s40168-021-01193-9
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Article: RNA interference against Hec1 inhibits tumor growth in vivo.

Gurzov, E N / Izquierdo, M

Gene therapy

2006 Volume 13, Issue 1, Page(s) 1–7

Abstract: Hec1 (highly expressed in cancer) plays an important role in chromosome segregation by interacting with a subset of checkpoint proteins that survey proper chromosome alignment and bipolar spindle attachment. In order to disrupt mitotic progression of ... ...

Abstract	Hec1 (highly expressed in cancer) plays an important role in chromosome segregation by interacting with a subset of checkpoint proteins that survey proper chromosome alignment and bipolar spindle attachment. In order to disrupt mitotic progression of tumor cell lines, we have used retrovirus and adenovirus vectors that inhibit Hec1 synthesis. Vector-expressed short hairpin RNAs (shRNAs) caused very efficient depletion of the target protein, cellular arrest and considerable mitotic catastrophe induction 96 h post infection in human cervix-adenocarcinoma (HeLa) and glioblastoma (U-373-MG) cell lines. Furthermore, adenocarcinomas induced in the flanks of nude mice show significant reduction in size compared with control when treated with either Hec1-shRNA retroviruses or adenoviruses. These results indicate that depletion of Hec1 could be used as a new strategy to block the dividing cell, and therefore against cancer.
MeSH term(s)	Adenocarcinoma/pathology ; Adenocarcinoma/therapy ; Adenoviridae/genetics ; Animals ; Brain Neoplasms/pathology ; Brain Neoplasms/therapy ; Chromosome Segregation/drug effects ; Female ; Flow Cytometry ; Genetic Therapy/methods ; Genetic Vectors/genetics ; Genetic Vectors/therapeutic use ; Glioblastoma/pathology ; Glioblastoma/therapy ; HeLa Cells ; Humans ; Mice ; Mice, Nude ; Microscopy, Fluorescence ; Mitosis/drug effects ; Neoplasm Transplantation ; Neoplasms/pathology ; Neoplasms/therapy ; Nuclear Proteins/genetics ; RNA Interference ; RNA, Small Interfering/genetics ; Retroviridae/genetics ; Uterine Cervical Neoplasms/pathology ; Uterine Cervical Neoplasms/therapy
Chemical Substances	NDC80 protein, human ; Nuclear Proteins ; RNA, Small Interfering
Language	English
Publishing date	2006-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1191036-7
ISSN	1476-5462 ; 0969-7128
ISSN (online)	1476-5462
ISSN	0969-7128
DOI	10.1038/sj.gt.3302595
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Zs.A 3991: Show issues

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Article: The JAK/STAT pathway in obesity and diabetes

Gurzov, Esteban N / Daniel J. Gough / Evan G. Pappas / Helen E. Thomas / William J. Stanley

FEBS journal. 2016 Aug., v. 283, no. 16

2016

Abstract: Diabetes mellitus are complex, multiâorgan metabolic pathologies characterized by hyperglycemia. Emerging evidence shows that the highly conserved and potent JAK/STAT signaling pathway is required for normal homeostasis, and, when dysregulated, ... ...

Abstract	Diabetes mellitus are complex, multiâorgan metabolic pathologies characterized by hyperglycemia. Emerging evidence shows that the highly conserved and potent JAK/STAT signaling pathway is required for normal homeostasis, and, when dysregulated, contributes to the development of obesity and diabetes. In this review, we analyze the role of JAK/STAT activation in the brain, liver, muscle, fat and pancreas, and how this affects the course of the disease. We also consider the therapeutic implications of targeting the JAK/STAT pathway in treatment of obesity and diabetes.
Keywords	brain ; diabetes mellitus ; disease course ; homeostasis ; hyperglycemia ; liver ; muscles ; obesity ; pancreas ; signal transduction
Language	English
Dates of publication	2016-08
Size	p. 3002-3015.
Publishing place	John Wiley & Sons, Ltd
Document type	Article
Note	REVIEW
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.13709
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Article: Cyclin E1 knockdown induces apoptosis in cancer cells.

Gurzov, Esteban N / Izquierdo, Marta

Neurological research

2006 Volume 28, Issue 5, Page(s) 493–499

Abstract: Objectives: Cyclin E1 is expressed during the late G1 phase of the cell cycle and mediates the initiation of DNA synthesis by activating cyclin-dependent kinases 2 (CDK2). Abnormally high levels of cyclin E1 expression have frequently been found in ... ...

Abstract	Objectives: Cyclin E1 is expressed during the late G1 phase of the cell cycle and mediates the initiation of DNA synthesis by activating cyclin-dependent kinases 2 (CDK2). Abnormally high levels of cyclin E1 expression have frequently been found in cancer cells. Here, we investigate the effect of cyclin E1 knockdown on cancer cells. Methods: RNA interference, expressed from a DNA-based retroviral vector, was used to knockdown cyclin E1 in adenocarcinoma (HeLa), breast (MDA-MB-31) and glioblastoma (U-373-MG) cell lines and an explant from one glioma patient (GB-LP-2). Results: We have obtained very efficient depletion of cyclin E1 protein (over 80%) and considerable apoptotic induction (50-70%) after 96 hours post-infection. The ability of U-373-MG cells to induce tumor growth in nude mice was also abolished after cyclin E1 knockdown. Discussion: Our results indicate that retrovirus carrying the DNA to be transcribed into a short hairpin RNA (shRNA) against cyclin E1 could be used as a therapeutic agent for cancer therapy.
MeSH term(s)	Animals ; Apoptosis/genetics ; Blotting, Western ; Cell Cycle/physiology ; Cell Proliferation ; Cyclin E/antagonists & inhibitors ; Cyclin E/genetics ; Cyclin E/metabolism ; Female ; Fluorescent Antibody Technique ; Genetic Therapy/methods ; Genetic Vectors ; HeLa Cells ; Humans ; Mice ; Mice, Nude ; Neoplasms, Experimental/genetics ; Neoplasms, Experimental/therapy ; Oncogene Proteins/antagonists & inhibitors ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; RNA Interference ; Retroviridae ; Transfection
Chemical Substances	CCNE1 protein, human ; Cyclin E ; Oncogene Proteins
Language	English
Publishing date	2006-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	424428-x
ISSN	1743-1328 ; 0161-6412
ISSN (online)	1743-1328
ISSN	0161-6412
DOI	10.1179/016164106X115143
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Zs.A 1491: Show issues

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