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Article ; Online: Functional Recovery Caused by Human Adipose Tissue Mesenchymal Stem Cell-Derived Extracellular Vesicles Administered 24 h after Stroke in Rats.

Rohden, Francieli / Teixeira, Luciele Varaschini / Bernardi, Luis Pedro / Ferreira, Pamela Cristina Lukasewicz / Colombo, Mariana / Teixeira, Geciele Rodrigues / de Oliveira, Fernanda Dos Santos / Cirne Lima, Elizabeth Obino / Guma, Fátima Costa Rodrigues / Souza, Diogo Onofre

International journal of molecular sciences

2021 Volume 22, Issue 23

Abstract: Ischemic stroke is a major cause of death and disability, intensely demanding innovative and accessible therapeutic strategies. Approaches presenting a prolonged period for therapeutic intervention and new treatment administration routes are promising ... ...

Abstract	Ischemic stroke is a major cause of death and disability, intensely demanding innovative and accessible therapeutic strategies. Approaches presenting a prolonged period for therapeutic intervention and new treatment administration routes are promising tools for stroke treatment. Here, we evaluated the potential neuroprotective properties of nasally administered human adipose tissue mesenchymal stem cell (hAT-MSC)-derived extracellular vesicles (EVs) obtained from healthy individuals who underwent liposuction. After a single intranasal EV (200 µg/kg) administered 24 h after a focal permanent ischemic stroke in rats, a higher number of EVs, improvement of the blood-brain barrier, and re-stabilization of vascularization were observed in the recoverable peri-infarct zone, as well as a significant decrease in infarct volume. In addition, EV treatment recovered long-term motor (front paws symmetry) and behavioral impairment (short- and long-term memory and anxiety-like behavior) induced by ischemic stroke. In line with these findings, our work highlights hAT-MSC-derived EVs as a promising therapeutic strategy for stroke.
MeSH term(s)	Administration, Intranasal ; Adult ; Animals ; Blood-Brain Barrier ; Brain/blood supply ; Brain/pathology ; Elevated Plus Maze Test ; Extracellular Vesicles/transplantation ; Female ; Humans ; Male ; Mesenchymal Stem Cells ; Middle Aged ; Neovascularization, Physiologic ; Rats, Wistar ; Recovery of Function ; Stem Cell Transplantation/methods ; Stroke/pathology ; Stroke/therapy ; Rats
Language	English
Publishing date	2021-11-28
Publishing country	Switzerland
Document type	Evaluation Study ; Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms222312860
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Article ; Online: Exogenous expression of caveolin-1 is sufficient for hepatic stellate cell activation.

Ilha, Mariana / Moraes, Ketlen da Silveira / Rohden, Francieli / Martins, Leo Anderson Meira / Borojevic, Radovan / Lenz, Guido / Barbé-Tuana, Florencia / Guma, Fátima Costa Rodrigues

Journal of cellular biochemistry

2019 Volume 120, Issue 11, Page(s) 19031–19043

Abstract: Caveolin-1 (Cav-1) expression is increased in hepatic stellate cells (HSC) upon liver cirrhosis and it functions as an integral membrane protein of lipid rafts and caveolae that regulates and integrates multiple signals as a platform. This study aimed to ...

Abstract	Caveolin-1 (Cav-1) expression is increased in hepatic stellate cells (HSC) upon liver cirrhosis and it functions as an integral membrane protein of lipid rafts and caveolae that regulates and integrates multiple signals as a platform. This study aimed to evaluate the role of Cav-1 in HSC. Thus, the effects of exogenous expression of Cav-1 in GRX cells, a model of activated HSC, were determined. Here, we demonstrated through evaluating well-known HSC activation markers - such as α-smooth muscle actin, collagen I, and glial fibrillary acidic protein - that up regulation of Cav-1 induced GRX to a more activated phenotype. GRX
MeSH term(s)	Caveolin 1/biosynthesis ; Caveolin 1/genetics ; Cell Cycle Checkpoints ; Cell Line ; Gene Expression ; Hepatic Stellate Cells/cytology ; Hepatic Stellate Cells/metabolism ; Humans
Chemical Substances	CAV1 protein, human ; Caveolin 1
Language	English
Publishing date	2019-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.29226
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Zs.A 1114: Show issues

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Article ; Online: Ethylmalonic acid impairs bioenergetics by disturbing succinate and glutamate oxidation and induces mitochondrial permeability transition pore opening in rat cerebellum.

de Moura Alvorcem, Leonardo / Britto, Renata / Cecatto, Cristiane / Cristina Roginski, Ana / Rohden, Francieli / Nathali Scholl, Juliete / Guma, Fátima C R / Figueiró, Fabrício / Umpierrez Amaral, Alexandre / Zanatta, Geancarlo / Seminotti, Bianca / Wajner, Moacir / Leipnitz, Guilhian

Journal of neurochemistry

2021 Volume 158, Issue 2, Page(s) 262–281

Abstract: Tissue accumulation and high urinary excretion of ethylmalonic acid (EMA) are found in ethylmalonic encephalopathy (EE), an inherited disorder associated with cerebral and cerebellar atrophy whose pathogenesis is poorly established. The in vitro and in ... ...

Abstract	Tissue accumulation and high urinary excretion of ethylmalonic acid (EMA) are found in ethylmalonic encephalopathy (EE), an inherited disorder associated with cerebral and cerebellar atrophy whose pathogenesis is poorly established. The in vitro and in vivo effects of EMA on bioenergetics and redox homeostasis were investigated in rat cerebellum. For the in vitro studies, cerebellum preparations were exposed to EMA, whereas intracerebellar injection of EMA was used for the in vivo evaluation. EMA reduced state 3 and uncoupled respiration in vitro in succinate-, glutamate-, and malate-supported mitochondria, whereas decreased state 4 respiration was observed using glutamate and malate. Furthermore, mitochondria permeabilization and succinate supplementation diminished the decrease in state 3 with succinate. EMA also inhibited the activity of KGDH, an enzyme necessary for glutamate oxidation, in a mixed manner and augmented mitochondrial efflux of α-ketoglutarate. ATP levels were markedly reduced by EMA, reflecting a severe bioenergetic disruption. Docking simulations also indicated interactions between EMA and KGDH and a competition with glutamate and succinate for their mitochondrial transporters. In vitro findings also showed that EMA decreased mitochondrial membrane potential and Ca
MeSH term(s)	Animals ; Cerebellum/drug effects ; Cerebellum/metabolism ; Energy Metabolism/drug effects ; Glutamates/metabolism ; Ketoglutaric Acids/metabolism ; Malates/metabolism ; Male ; Malonates/toxicity ; Membrane Potential, Mitochondrial/drug effects ; Mitochondrial Permeability Transition Pore ; Mitochondrial Proteins/drug effects ; Mitochondrial Proteins/metabolism ; Molecular Docking Simulation ; Oxidation-Reduction ; Oxygen Consumption/drug effects ; Rats ; Rats, Wistar ; Succinates/metabolism ; Succinates/pharmacology
Chemical Substances	Glutamates ; Ketoglutaric Acids ; Malates ; Malonates ; Mitochondrial Permeability Transition Pore ; Mitochondrial Proteins ; Succinates ; ethylmalonic acid (432NF49DFG) ; malic acid (817L1N4CKP)
Language	English
Publishing date	2021-04-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.15363
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Ui II Zs.170: Show issues

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Article ; Online: Caveolin-1 influences mitochondrial plasticity and function in hepatic stellate cell activation.

Ilha, Mariana / Meira Martins, Leo A / da Silveira Moraes, Ketlen / Dias, Camila K / Thomé, Marcos P / Petry, Fernanda / Rohden, Francieli / Borojevic, Radovan / Trindade, Vera M T / Klamt, Fábio / Barbé-Tuana, Florência / Lenz, Guido / Guma, Fátima C R

Cell biology international

2022 Volume 46, Issue 11, Page(s) 1787–1800

Abstract: Caveolin-1 (Cav-1) is an integral membrane protein present in all organelles, responsible for regulating and integrating multiple signals as a platform. Mitochondria are extremely adaptable to external cues in chronic liver diseases, and expression of ... ...

Abstract	Caveolin-1 (Cav-1) is an integral membrane protein present in all organelles, responsible for regulating and integrating multiple signals as a platform. Mitochondria are extremely adaptable to external cues in chronic liver diseases, and expression of Cav-1 may affect mitochondrial flexibility in hepatic stellate cells (HSCs) activation. We previously demonstrated that exogenous expression of Cav-1 was sufficient to increase some classical markers of activation in HSCs. Here, we aimed to evaluate the influence of exogenous expression and knockdown of Cav-1 on regulating the mitochondrial plasticity, metabolism, endoplasmic reticulum (ER)-mitochondria distance, and lysosomal activity in HSCs. To characterize the mitochondrial, lysosomal morphology, and ER-mitochondria distance, we perform transmission electron microscope analysis. We accessed mitochondria and lysosomal networks and functions through a confocal microscope and flow cytometry. The expression of mitochondrial machinery fusion/fission genes was examined by real-time polymerase chain reaction. Total and mitochondrial cholesterol content was measured using Amplex Red. To define energy metabolism, we used the Oroboros system in the cells. We report that GRX cells with exogenous expression or knockdown of Cav-1 changed mitochondrial morphometric parameters, OXPHOS metabolism, ER-mitochondria distance, lysosomal activity, and may change the activation state of HSC. This study highlights that Cav-1 may modulate mitochondrial function and structural reorganization in HSC activation, being a potential candidate marker for chronic liver diseases and a molecular target for therapeutic intervention.
MeSH term(s)	Caveolin 1/genetics ; Caveolin 1/metabolism ; Cholesterol/metabolism ; Hepatic Stellate Cells/metabolism ; Humans ; Liver Cirrhosis/pathology ; Membrane Proteins/metabolism ; Mitochondria/metabolism
Chemical Substances	Caveolin 1 ; Membrane Proteins ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2022-08-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1143453-3
ISSN	1095-8355 ; 1065-6995
ISSN (online)	1095-8355
ISSN	1065-6995
DOI	10.1002/cbin.11876
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Zs.A 1451: Show issues

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Article ; Online: Dipyridamole impairs autophagic flux and exerts antiproliferative activity on prostate cancer cells.

Thomé, Marcos P / Pereira, Luiza C / Onzi, Giovana R / Rohden, Francieli / Ilha, Mariana / Guma, Fátima T / Wink, Márcia R / Lenz, Guido

Experimental cell research

2019 Volume 382, Issue 1, Page(s) 111456

Abstract: Autophagy is a cellular bulk degradation process used as an alternative source of energy and metabolites and implicated in various diseases. Inefficient autophagy in nutrient-deprived cancer cells would be beneficial for cancer therapy making its ... ...

Abstract	Autophagy is a cellular bulk degradation process used as an alternative source of energy and metabolites and implicated in various diseases. Inefficient autophagy in nutrient-deprived cancer cells would be beneficial for cancer therapy making its modulation valuable as a therapeutic strategy for cancer treatment, especially in combination with chemotherapy. Dipyridamole (DIP) is a vasodilator and antithrombotic drug. Its major effects involve the block of nucleoside uptake and phosphodiestesase inhibition, leading to increased levels of intracellular cAMP. Here we report that DIP increases autophagic markers due to autophagic flux blockage, resembling autophagosome maturation and/or closure impairment. Treatment with DIP results in an increased number of autophagosomes and autolysosomes and impairs degradation of SQSTM1/p62. As blockage of autophagic flux decreases the recycling of cellular components, DIP reduced the intracellular ATP levels in cancer cells. Autophagic flux blockage was neither through inhibition of lysosome function nor blockage of nucleoside uptake, but could be prevented by treatment with a PKA inhibitor, suggesting that autophagic flux failure mediated by DIP results from increased intracellular levels of cAMP. Treatment with DIP presented antiproliferative effects in vitro alone and in combination with chemotherapy drugs. Collectively, these data demonstrate that DIP can impair autophagic degradation, by preventing the normal autophagosome maturation, and might be useful in combination anticancer therapy.
MeSH term(s)	Adenocarcinoma/pathology ; Adenosine Triphosphate/metabolism ; Antineoplastic Agents/pharmacology ; Autophagosomes/drug effects ; Autophagosomes/ultrastructure ; Autophagy/drug effects ; Cell Division/drug effects ; Cell Line, Tumor ; Cyclic AMP-Dependent Protein Kinases/physiology ; Dipyridamole/pharmacology ; Drug Resistance, Neoplasm/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Hydrogen-Ion Concentration ; Lysosomes/drug effects ; Lysosomes/enzymology ; Male ; Microtubule-Associated Proteins/biosynthesis ; Microtubule-Associated Proteins/genetics ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; Prostatic Neoplasms/pathology ; Sequestosome-1 Protein/biosynthesis ; Sequestosome-1 Protein/genetics ; Tumor Stem Cell Assay
Chemical Substances	Antineoplastic Agents ; MAP1LC3B protein, human ; Microtubule-Associated Proteins ; Neoplasm Proteins ; SQSTM1 protein, human ; Sequestosome-1 Protein ; Dipyridamole (64ALC7F90C) ; Adenosine Triphosphate (8L70Q75FXE) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
Language	English
Publishing date	2019-06-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1493-x
ISSN	1090-2422 ; 0014-4827
ISSN (online)	1090-2422
ISSN	0014-4827
DOI	10.1016/j.yexcr.2019.06.001
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Zs.A 563: Show issues

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Article ; Online: Neuroprotective Effects of Guanosine Administration on In Vivo Cortical Focal Ischemia in Female and Male Wistar Rats.

Teixeira, Luciele Varaschini / Almeida, Roberto Farina / Rohden, Francieli / Martins, Leo Anderson Meira / Spritzer, Poli Mara / de Souza, Diogo Onofre Gomes

Neurochemical research

2018 Volume 43, Issue 7, Page(s) 1476–1489

Abstract: Guanosine (GUO) has neuroprotective effects in experimental models of brain diseases involving glutamatergic excitotoxicity in male animals; however, its effects in female animals are poorly understood. Thus, we investigated the influence of gender and ... ...

Abstract	Guanosine (GUO) has neuroprotective effects in experimental models of brain diseases involving glutamatergic excitotoxicity in male animals; however, its effects in female animals are poorly understood. Thus, we investigated the influence of gender and GUO treatment in adult male and female Wistar rats submitted to focal permanent cerebral ischemia in the motor cortex brain. Female rats were subdivided into non-estrogenic and estrogenic phase groups by estrous cycle verification. Immediately after surgeries, the ischemic animals were treated with GUO or a saline solution. Open field and elevated plus maze tasks were conducted with ischemic and naïve animals. Cylinder task, immunohistochemistry and infarct volume analyses were conducted only with ischemic animals. Female GUO groups achieved a full recovery of the forelimb symmetry at 28-35 days after the insult, while male GUO groups only partially recovered at 42 days, in the final evaluation. The ischemic insult affected long-term memory habituation to novelty only in female groups. Anxiety-like behavior, astrocyte morphology and infarct volume were not affected. Regardless the estrous cycle, the ischemic injury affected differently female and male animals. Thus, this study points that GUO is a potential neuroprotective compound in experimental stroke and that more studies, considering the estrous cycle, with both genders are recommended in future investigation concerning brain diseases.
MeSH term(s)	Animals ; Brain Ischemia/pathology ; Brain Ischemia/prevention & control ; Cerebral Cortex/drug effects ; Cerebral Cortex/pathology ; Female ; Guanosine/administration & dosage ; Male ; Maze Learning/drug effects ; Maze Learning/physiology ; Neuroprotective Agents/administration & dosage ; Rats ; Rats, Wistar ; Recovery of Function/drug effects ; Recovery of Function/physiology ; Sex Characteristics
Chemical Substances	Neuroprotective Agents ; Guanosine (12133JR80S)
Language	English
Publishing date	2018-05-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	199335-5
ISSN	1573-6903 ; 0364-3190
ISSN (online)	1573-6903
ISSN	0364-3190
DOI	10.1007/s11064-018-2562-3
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Zs.A 1368: Show issues

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Article ; Online: The neuroprotective role of melatonin in a gestational hypermethioninemia model.

Figueiró, Paula W / Moreira, Daniella de S / Dos Santos, Tiago M / Prezzi, Caroline A / Rohden, Francieli / Faccioni-Heuser, Maria Cristina / Manfredini, Vanusa / Netto, Carlos A / Wyse, Angela T S

International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience

2019 Volume 78, Page(s) 198–209

Abstract: Elevated levels of methionine in blood characterize the hypermethioninemia, which may have genetic or non-genetic origin, as for example from high protein diet. Born rats from hypermethioninemic mothers presented cerebral oxidative stress, inhibition of ... ...

Abstract	Elevated levels of methionine in blood characterize the hypermethioninemia, which may have genetic or non-genetic origin, as for example from high protein diet. Born rats from hypermethioninemic mothers presented cerebral oxidative stress, inhibition of Na
MeSH term(s)	Amino Acid Metabolism, Inborn Errors/drug therapy ; Animals ; Brain/drug effects ; Brain/metabolism ; Disease Models, Animal ; Female ; Glycine N-Methyltransferase/deficiency ; Male ; Maze Learning/drug effects ; Melatonin/pharmacology ; Melatonin/therapeutic use ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Oxidative Stress/drug effects ; Pregnancy ; Pregnancy Complications/drug therapy ; Rats ; Rats, Wistar ; Recognition, Psychology/drug effects
Chemical Substances	Neuroprotective Agents ; Glycine N-Methyltransferase (EC 2.1.1.20) ; Melatonin (JL5DK93RCL)
Language	English
Publishing date	2019-08-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	605533-3
ISSN	1873-474X ; 0736-5748
ISSN (online)	1873-474X
ISSN	0736-5748
DOI	10.1016/j.ijdevneu.2019.08.004
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Zs.A 1883: Show issues

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Article ; Online: Guanosine Neuroprotection of Presynaptic Mitochondrial Calcium Homeostasis in a Mouse Study with Amyloid-β Oligomers.

da Silva, Jussemara Souza / Nonose, Yasmine / Rohden, Francieli / Lukasewicz Ferreira, Pâmela C / Fontella, Fernanda Urruth / Rocha, Andréia / Brochier, Andressa Wigner / Apel, Rodrigo Vieira / de Lima, Thais Martins / Seminotti, Bianca / Amaral, Alexandre Umpierrez / Galina, Antonio / Souza, Diogo O

Molecular neurobiology

2020 Volume 57, Issue 11, Page(s) 4790–4809

Abstract: Amyloid-β oligomers (AβOs) toxicity causes mitochondrial dysfunction, leading to synaptic failure in Alzheimer's disease (AD). Considering presynaptic high energy demand and tight ... ...

Abstract	Amyloid-β oligomers (AβOs) toxicity causes mitochondrial dysfunction, leading to synaptic failure in Alzheimer's disease (AD). Considering presynaptic high energy demand and tight Ca
MeSH term(s)	Amyloid beta-Peptides/administration & dosage ; Amyloid beta-Peptides/toxicity ; Animals ; Calcium/metabolism ; Gene Expression Regulation/drug effects ; Glutamic Acid/metabolism ; Guanosine/administration & dosage ; Guanosine/pharmacology ; Hippocampus/drug effects ; Hippocampus/metabolism ; Homeostasis/drug effects ; Male ; Memory/drug effects ; Mice ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Neuroprotection/drug effects ; Oxidative Stress/drug effects ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Synaptosomes/metabolism ; Synaptosomes/ultrastructure
Chemical Substances	Amyloid beta-Peptides ; Guanosine (12133JR80S) ; Glutamic Acid (3KX376GY7L) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2020-08-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-020-02064-4
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Article ; Online: Characterization and antiproliferative activity of glioma-derived extracellular vesicles.

Scholl, Juliete Nathali / de Fraga Dias, Amanda / Pizzato, Pauline Rafaela / Lopes, Daniela Vasconcelos / Moritz, Cesar Eduardo Jacintho / Jandrey, Elisa Helena Farias / Souto, Gabriele Dadalt / Colombo, Mariana / Rohden, Francieli / Sévigny, Jean / Pohlmann, Adriana Raffin / Guterres, Sílvia Stanisçuaski / Battastini, Ana Maria Oliveira / Figueiró, Fabrício

Nanomedicine (London, England)

2020 Volume 15, Issue 10, Page(s) 1001–1018

Abstract: Aim: ...

Abstract	Aim:
MeSH term(s)	Animals ; Brain Neoplasms/drug therapy ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Extracellular Vesicles ; Glioma/drug therapy ; Rats ; Rats, Wistar ; Tumor Microenvironment
Language	English
Publishing date	2020-04-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2277839-1
ISSN	1748-6963 ; 1743-5889
ISSN (online)	1748-6963
ISSN	1743-5889
DOI	10.2217/nnm-2019-0431
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Zs.A 6617: Show issues

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Article ; Online: Obesity associated with type 2 diabetes mellitus is linked to decreased PC1/3 mRNA expression in the Jejunum.

Rohden, Francieli / Costa, Cintia S / Hammes, Thais O / Margis, Rogério / Padoin, Alexandre V / Mottin, Cláudio C / Guaragna, Regina Maria

Obesity surgery

2014 Volume 24, Issue 12, Page(s) 2075–2081

Abstract: Background: Bariatric surgery is the most effective therapeutic option for obesity and its complications, especially in type 2 diabetes. The aim of this study was to investigate the messenger RNA (mRNA) gene expression of proglucagon, glucose-dependent ... ...

Abstract	Background: Bariatric surgery is the most effective therapeutic option for obesity and its complications, especially in type 2 diabetes. The aim of this study was to investigate the messenger RNA (mRNA) gene expression of proglucagon, glucose-dependent insulinotropic peptide (GIP), prohormone convertase 1/3 (PC1/3), and dipeptidyl peptidase-IV (DPP-IV) in jejunum cells of the morbidly obese (OB) non type 2 diabetes mellitus (NDM2) and type 2 diabetes mellitus (T2DM), to determine the molecular basis of incretin secretion after bariatric surgery. Methods: Samples of jejunal mucosa were obtained from 20 NDM2 patients: removal of a section of the jejunum about 60 cm distal to the ligament of Treitz and 18 T2DM patients: removal of a section of the jejunum about 100 cm distal to the ligament of Treitz. Total RNA was extracted using TRIzol. Reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) was carried out. Samples were sequenced to PC1/3 by ACTGene Análises Moleculares Ltd. Immuno content was quantified with a fluorescence microscope. Results: T2DM showed decreased PC1/3 mRNA expression in the primers tested (primer a, p=0.014; primer b, p=0.048). Many patients (36.5 %) did not express PC1/3 mRNA. NDM2 and T2DM subjects showed nonsignificantly different proglucagon, GIP, and DPP-IV mRNA expression. The immuno contents of glucagon-like peptide-1 and GIP decreased in T2DM jejunum, but incubation with high glucose stimulated the immuno contents. Conclusions: The results suggest that bioactivation of pro-GIP and proglucagon could be impaired by the lower expression of PC1/3 mRNA in jejunum cells of obese patients with T2DM. However, after surgery, food could activate this system and improve glucose levels in these patients.
MeSH term(s)	Adult ; Case-Control Studies ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Dipeptidyl Peptidase 4/genetics ; Dipeptidyl Peptidase 4/metabolism ; Female ; Gastric Inhibitory Polypeptide/genetics ; Gastric Inhibitory Polypeptide/metabolism ; Gene Expression Regulation ; Glucagon-Like Peptide 1/genetics ; Glucagon-Like Peptide 1/metabolism ; Humans ; Jejunum/metabolism ; Male ; Middle Aged ; Obesity, Morbid/complications ; Obesity, Morbid/metabolism ; Proprotein Convertase 1/genetics ; Proprotein Convertase 1/metabolism ; RNA, Messenger/metabolism ; Real-Time Polymerase Chain Reaction
Chemical Substances	RNA, Messenger ; pro-glucose-dependent insulinotropic polypeptide ; Gastric Inhibitory Polypeptide (59392-49-3) ; Glucagon-Like Peptide 1 (89750-14-1) ; Dipeptidyl Peptidase 4 (EC 3.4.14.5) ; Proprotein Convertase 1 (EC 3.4.21.93)
Language	English
Publishing date	2014-05-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1070827-3
ISSN	1708-0428 ; 0960-8923
ISSN (online)	1708-0428
ISSN	0960-8923
DOI	10.1007/s11695-014-1279-x
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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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In stock of ZB MED Cologne/Königswinter

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