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  1. Article: GAD65 autoantibodies and its role as biomarker of Type 1 diabetes and Latent Autoimmune Diabetes in Adults (LADA).

    Towns, Roberto / Pietropaolo, Massimo

    Drugs of the future

    2012  Volume 36, Issue 11, Page(s) 847

    Abstract: One of the hallmarks of autoimmune diabetes is the presence of adaptive responses directed to neuroendocrine proteins. One of these proteins is glutamic acid decarboxylase (GAD). While GAD is widely distributed in neuroendocrine tissues, its specific ... ...

    Abstract One of the hallmarks of autoimmune diabetes is the presence of adaptive responses directed to neuroendocrine proteins. One of these proteins is glutamic acid decarboxylase (GAD). While GAD is widely distributed in neuroendocrine tissues, its specific significance in diabetes has paralleled the advances in understanding humoral and cellular immunity in Type 1 diabetes (T1D) and in a subset of Type 2 diabetes (T2D), going from the seminal discoveries of islet autoantibodies to the development and standardization of bioassays as diagnostic tools, to studies on the structure of GAD and its antigenic determinants. GAD65 autoantibodies can accurately predict T1D development in combination with other surrogate humoral biomarkers and they are considered the most sensitive and specific biomarker which identifies a subset of clinically diagnosed T2D termed Latent Autoimmune Diabetes in Adults (LADA). We and others provided evidence indicating that GAD65 autoantibody detection should be part of the diagnostic assessment for clinically diagnosed T2DM mainly because it predicts the rate of progression to insulin requirement in patients affected by LADA. More recently GAD has been used as a "tolerogenic vaccine" to preserve beta cell function in autoimmune diabetes. While the results of Phase III clinical trials did not substantiate the earlier promise of Phase I and II trials, there are still many unanswered questions and approaches that need to be investigated in the applications of GAD in the therapy of T1D and LADA.
    Language English
    Publishing date 2012-08-06
    Publishing country United States
    Document type Journal Article
    ZDB-ID 752959-4
    ISSN 2013-0368 ; 0377-8282
    ISSN (online) 2013-0368
    ISSN 0377-8282
    DOI 10.1358/dof.2011.036.11.1710754
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  2. Article ; Online: AIRE's partnerships: an answer for many questions and new questions in search of answers.

    Towns, Roberto / Pietropaolo, Massimo

    Pediatric diabetes

    2010  Volume 11, Issue 2, Page(s) 85–87

    MeSH term(s) Autoantigens/physiology ; DNA-Binding Proteins/physiology ; Diabetes Mellitus, Type 1/immunology ; Humans ; Immune Tolerance/immunology ; Immune Tolerance/physiology ; RNA Processing, Post-Transcriptional/immunology ; Thymus Gland/immunology ; Transcription Factors/physiology ; AIRE Protein
    Chemical Substances Autoantigens ; DNA-Binding Proteins ; Transcription Factors
    Language English
    Publishing date 2010-04-23
    Publishing country Denmark
    Document type Journal Article
    ZDB-ID 1502504-4
    ISSN 1399-5448 ; 1745-1426 ; 1399-543X
    ISSN (online) 1399-5448
    ISSN 1745-1426 ; 1399-543X
    DOI 10.1111/j.1399-5448.2010.00652.x
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  3. Article ; Online: Humoral autoimmunity in type 1 diabetes: prediction, significance, and detection of distinct disease subtypes.

    Pietropaolo, Massimo / Towns, Roberto / Eisenbarth, George S

    Cold Spring Harbor perspectives in medicine

    2012  Volume 2, Issue 10

    Abstract: Type 1 diabetes mellitus (T1D) is an autoimmune disease encompassing the T-cell-mediated destruction of pancreatic β cells and the production of autoantibodies against islet proteins. In humoral autoimmunity in T1D, the detection of islet autoantibodies ... ...

    Abstract Type 1 diabetes mellitus (T1D) is an autoimmune disease encompassing the T-cell-mediated destruction of pancreatic β cells and the production of autoantibodies against islet proteins. In humoral autoimmunity in T1D, the detection of islet autoantibodies and the examination of their associations with genetic factors and cellular autoimmunity constitute major areas in both basic research and clinical practice. Although insulin is a key autoantigen and may be primus inter pares in importance among T1D autoantigens, an abundant body of research has also revealed other autoantigens associated with the disease process. Solid evidence indicates that autoantibodies against islet targets serve as key markers to enroll newly diagnosed T1D patients and their family members in intervention trials aimed at preventing or halting the disease process. The next challenge is perfecting mechanistic bioassays to be used as end points for disease amelioration following immunomodulatory therapies aimed at blocking immune-mediated β-cell injury and, in turn, preserving β-cell function in type 1 diabetes mellitus.
    MeSH term(s) Autoantibodies/immunology ; Autoimmunity/immunology ; Diabetes Mellitus, Type 1/classification ; Diabetes Mellitus, Type 1/immunology ; Humans ; Immunity, Humoral ; Insulin/immunology ; Insulin-Secreting Cells/immunology ; Risk Factors ; T-Lymphocytes/immunology
    Chemical Substances Autoantibodies ; Insulin
    Language English
    Publishing date 2012-10-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a012831
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: The role of cyclic AMP response element binding protein in transactivation of scavenger receptor class B type I promoter in transfected cells and in primary cultures of rat theca-interstitial cells.

    Towns, Roberto / Menon, K M J

    Molecular and cellular endocrinology

    2005  Volume 245, Issue 1-2, Page(s) 23–30

    Abstract: In the ovary, lutropin (LH) stimulates the selective uptake and transport of cholesterol for steroid biosynthesis from HDL particles via the scavenger receptor class B type I (SR-BI). Furthermore the expression of SR-BI mRNA in the ovary is stimulated by ...

    Abstract In the ovary, lutropin (LH) stimulates the selective uptake and transport of cholesterol for steroid biosynthesis from HDL particles via the scavenger receptor class B type I (SR-BI). Furthermore the expression of SR-BI mRNA in the ovary is stimulated by LH and cyclic AMP (cAMP). Since the promoter of the rat SR-BI gene is devoid of consensus cyclic AMP response element (CRE) sequences, this study examined if cAMP response element binding protein (CREB) plays a role in the transactivation of SR-BI promoter (SR-BIpr). The transactivation of SR-BIpr was examined in transfected 293T cells and human granulosa SVOG-4o cells, and in primary cultures of rat theca-interstitial cells infected with adenoviral constructs containing the SR-BIpr and a luciferase reporter gene. Dose-related increases in SR-BRpr activity ranging from 2- to 4-fold was induces by 293T cells co-transfected with the catalytic subunit of protein kinase A (cPKA). Co-transfections with CREB and cPKA produced a concentration-dependent increase ranging from 6- to 32-fold. The cAMP-mediated transactivation was significantly attenuated by co-transfection with CREB M1, a non-phosphorylatable, dominant-negative form of CREB. An increase in transactivation of SR-BIpr activity was also seen in SVOG-4o cells co-transfected with CREB. In primary cultures of rat theca-interstitial (T-I) cells infected with an adenoviral construct of SR-BIpr, forskolin produced a marked increase in promoter activity. These data indicate that stimulation of the cAMP-PKA-CREB pathway enhances rat SR-BIpr activity and substantiate the role of CREB as an intermediary in this process. The absence of canonical CRE sequences in the rat SR-BIpr suggests that the activation of SR-BI by CREB may occur either through non-canonical CRE sequences or through additional transcription factors that cooperate with CREB in the activation of SR-BI promoter activity.
    MeSH term(s) Animals ; Cell Line ; Cells, Cultured ; Cholesterol, HDL/physiology ; Colforsin/pharmacology ; Cyclic AMP/physiology ; Cyclic AMP Response Element-Binding Protein/genetics ; Cyclic AMP Response Element-Binding Protein/physiology ; Cyclic AMP-Dependent Protein Kinases/genetics ; Cyclic AMP-Dependent Protein Kinases/physiology ; Female ; Gene Expression Regulation/drug effects ; Humans ; Luteinizing Hormone/physiology ; Promoter Regions, Genetic/drug effects ; Promoter Regions, Genetic/genetics ; Promoter Regions, Genetic/physiology ; RNA, Messenger/genetics ; RNA, Messenger/physiology ; Rats ; Rats, Sprague-Dawley ; Scavenger Receptors, Class B/genetics ; Scavenger Receptors, Class B/physiology ; Theca Cells/physiology ; Transcriptional Activation ; Transfection
    Chemical Substances Cholesterol, HDL ; Cyclic AMP Response Element-Binding Protein ; RNA, Messenger ; SCARB1 protein, human ; Scavenger Receptors, Class B ; Colforsin (1F7A44V6OU) ; Luteinizing Hormone (9002-67-9) ; Cyclic AMP (E0399OZS9N) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2005-12-21
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 187438-x
    ISSN 1872-8057 ; 0303-7207
    ISSN (online) 1872-8057
    ISSN 0303-7207
    DOI 10.1016/j.mce.2005.09.013
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Stimulation of autophagy by autoantibody-mediated activation of death receptor cascades.

    Towns, Roberto / Pietropaolo, Massimo / Wiley, John W

    Autophagy

    2008  Volume 4, Issue 5, Page(s) 715–716

    Abstract: Activation of membrane death receptors has been connected to apoptosis and, recently, other non-apoptotic events. For example, we reported recently that sera from either a subset of patients with type 2 diabetes with neuropathy or a subpopulation of ... ...

    Abstract Activation of membrane death receptors has been connected to apoptosis and, recently, other non-apoptotic events. For example, we reported recently that sera from either a subset of patients with type 2 diabetes with neuropathy or a subpopulation of patients with neurogenic chronic intestinal pseudo-obstruction (CIP) stimulate autophagy in SH-SY5Y human neuroblastoma cells via complement-independent, autoantibody-mediated activation of Fas (CD95). Activation of the Fas pathway causes minimal activation of apoptosis in these cells since procaspase-8 shows low constitutive levels of expression in neuroblastoma cells. The observation that anti-Fas autoantibodies induce autophagy is novel and provocative. This finding has implications regarding the pathophysiology of diabetic neuropathy, CIP and, perhaps, other autoimmune disorders. For example, recent reports suggest that expression or activity of proapoptotic caspases can be enhanced by activation of more than one membrane death receptor, as could happen by combinations of cytokines and autoantibodies. The observation that autophagy, a putative cytoprotective pathway that has also been implicated in non-apoptotic cell death, is activated by autoantibodies against Fas, may represent an early cellular protective response. An increase in cytotoxic cytokine levels or the ratio of agonist:antagonist autoantibodies may "tip" the balance of the cellular response to activation of programmed cell death pathways.
    MeSH term(s) Animals ; Autoantibodies/physiology ; Autophagy/immunology ; Cell Line, Tumor ; Diabetic Nephropathies/immunology ; Humans ; Receptors, Death Domain/immunology ; Receptors, Death Domain/physiology ; Signal Transduction/immunology
    Chemical Substances Autoantibodies ; Receptors, Death Domain
    Language English
    Publishing date 2008-05-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.6336
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  6. Article: Inhibitory effect of valproic acid on ovarian androgen biosynthesis in rat theca-interstitial cells

    Fisseha, Senait / Towns, Roberto / Harada, Miyuki / Peegel, Helle / Menon, K. M. J

    Endocrine. 2010 Feb., v. 37, no. 1

    2010  

    Abstract: The objective of the study was to evaluate the effect of valproic acid (VPA) on ovarian androgen biosynthesis in primary cultures of theca-interstitial (T-I) cells isolated from rat ovaries. Ovarian T-I cells were cultured with VPA in the presence or ... ...

    Abstract The objective of the study was to evaluate the effect of valproic acid (VPA) on ovarian androgen biosynthesis in primary cultures of theca-interstitial (T-I) cells isolated from rat ovaries. Ovarian T-I cells were cultured with VPA in the presence or absence of hCG. VPA did not increase basal or hCG-stimulated androgen synthesis when added to primary cultures of T-I cells. However, the addition of VPA caused a marked concentration-dependent inhibitory effect on hCG-stimulated androstendione synthesis. Treatment of T-I cells with 8-Bromo-cAMP resulted in a marked increase in the production of androstenedione, and VPA inhibited this stimulatory effect, suggesting that the mechanism of VPA's inhibitory effect on androstenedione production occurs at a step after second messenger activation. Treatment of T-I cells with hCG resulted in a significant increase in the mRNA expression of steroidogenic enzymes CYP17A1 and 17β-hydroxysteroid dehydrogenase. Addition of VPA sharply blunted the stimulatory effect of hCG, reducing the mRNA expression of the steroidogenic enzymes to basal levels. In conclusion, VPA exerts an inhibitory effect on hCG-stimulated androgen synthesis in rat T-I cells.
    Language English
    Dates of publication 2010-02
    Size p. 187-193.
    Publisher Humana Press Inc
    Publishing place New York
    Document type Article
    ZDB-ID 1194484-5
    ISSN 1355-008X ; 0969-711X
    ISSN 1355-008X ; 0969-711X
    DOI 10.1007/s12020-009-9287-7
    Database NAL-Catalogue (AGRICOLA)

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  7. Article ; Online: Inhibitory effect of valproic acid on ovarian androgen biosynthesis in rat theca-interstitial cells.

    Fisseha, Senait / Towns, Roberto / Harada, Miyuki / Peegel, Helle / Menon, K M J

    Endocrine

    2009  Volume 37, Issue 1, Page(s) 187–193

    Abstract: The objective of the study was to evaluate the effect of valproic acid (VPA) on ovarian androgen biosynthesis in primary cultures of theca-interstitial (T-I) cells isolated from rat ovaries. Ovarian T-I cells were cultured with VPA in the presence or ... ...

    Abstract The objective of the study was to evaluate the effect of valproic acid (VPA) on ovarian androgen biosynthesis in primary cultures of theca-interstitial (T-I) cells isolated from rat ovaries. Ovarian T-I cells were cultured with VPA in the presence or absence of hCG. VPA did not increase basal or hCG-stimulated androgen synthesis when added to primary cultures of T-I cells. However, the addition of VPA caused a marked concentration-dependent inhibitory effect on hCG-stimulated androstendione synthesis. Treatment of T-I cells with 8-Bromo-cAMP resulted in a marked increase in the production of androstenedione, and VPA inhibited this stimulatory effect, suggesting that the mechanism of VPA's inhibitory effect on androstenedione production occurs at a step after second messenger activation. Treatment of T-I cells with hCG resulted in a significant increase in the mRNA expression of steroidogenic enzymes CYP17A1 and 17β-hydroxysteroid dehydrogenase. Addition of VPA sharply blunted the stimulatory effect of hCG, reducing the mRNA expression of the steroidogenic enzymes to basal levels. In conclusion, VPA exerts an inhibitory effect on hCG-stimulated androgen synthesis in rat T-I cells.
    MeSH term(s) 17-Hydroxysteroid Dehydrogenases/genetics ; 17-Hydroxysteroid Dehydrogenases/metabolism ; 8-Bromo Cyclic Adenosine Monophosphate/antagonists & inhibitors ; 8-Bromo Cyclic Adenosine Monophosphate/pharmacology ; Androgens/metabolism ; Androstenedione/metabolism ; Animals ; Antimanic Agents/adverse effects ; Antimanic Agents/pharmacology ; Cells, Cultured ; Chorionic Gonadotropin/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Down-Regulation/drug effects ; Female ; Gene Expression Regulation/drug effects ; Gonadal Steroid Hormones/metabolism ; Osmolar Concentration ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Steroid 17-alpha-Hydroxylase/genetics ; Steroid 17-alpha-Hydroxylase/metabolism ; Theca Cells/drug effects ; Theca Cells/metabolism ; Valproic Acid/adverse effects ; Valproic Acid/pharmacology
    Chemical Substances Androgens ; Antimanic Agents ; Chorionic Gonadotropin ; Gonadal Steroid Hormones ; RNA, Messenger ; 8-Bromo Cyclic Adenosine Monophosphate (23583-48-4) ; Androstenedione (409J2J96VR) ; Valproic Acid (614OI1Z5WI) ; 17-Hydroxysteroid Dehydrogenases (EC 1.1.-) ; Steroid 17-alpha-Hydroxylase (EC 1.14.14.19) ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2009-12-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1194484-5
    ISSN 1559-0100 ; 1355-008X ; 0969-711X
    ISSN (online) 1559-0100
    ISSN 1355-008X ; 0969-711X
    DOI 10.1007/s12020-009-9287-7
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  8. Article: LH/hCG-stimulated androgen production and selective HDL-cholesterol transport are inhibited by a dominant-negative CREB construct in primary cultures of rat theca-interstitial cells.

    Towns, Roberto / Azhar, Salman / Peegel, Helle / Menon, K M J

    Endocrine

    2005  Volume 27, Issue 3, Page(s) 269–277

    Abstract: Theca-interstitial (T-I) cells synthesize androgens that are converted to estrogen by the granulosa cells. In rat ovary, T-I cells primarily utilize HDL-derived cholesteryl esters (CE) as a precursor for androgen synthesis. The HDL-CE is delivered to ... ...

    Abstract Theca-interstitial (T-I) cells synthesize androgens that are converted to estrogen by the granulosa cells. In rat ovary, T-I cells primarily utilize HDL-derived cholesteryl esters (CE) as a precursor for androgen synthesis. The HDL-CE is delivered to steroidogenic cells by a process termed "selective" uptake in which CE is internalized without the simultaneous uptake of apolipoprotein(s). This process is mediated by an HDL receptor, scavenger receptor class B, type I (SR-BI) and is stimulated by trophic hormone (LH/hCG), which also activates the cAMP cascade. In this study, we tested whether the adenoviral (Ad)-mediated introduction of a dominant-negative analog of cyclic AMP response element binding protein (A-CREB) inhibits the stimulatory effect of LH/hCG on the selective uptake of high-density lipoprotein (HDL)-cholesterol and androgen production in primary cultures of rat T-I cells. Androstenedione production by cultured T-I cells was stimulated by hCG and by the adenoviral overexpression of wtCREB. Additionally, the stimulatory effect observed with hCG was amplified in the presence of HDL. Androgen synthesis was increased 17-fold in the presence of HDL and hCG but the stimulatory effect of hCG was inhibited by Ad A-CREB by approx 70%. In the selective up-take studies, cell-surface association of the labeled HDL was significantly enhanced by hCG treatment, and this effect was inhibited by Ad A-CREB. The selective uptake of HDL-cholesterol was also enhanced by hCG but exposure to Ad A-CREB also abrogated this effect. It is concluded that CREB plays an intermediary role in the stimulatory action of LH/hCG on androgen synthesis and the selective uptake of HDL-cholesterol in T-I cells.
    MeSH term(s) Adenoviridae/genetics ; Androstenedione/biosynthesis ; Androstenedione/metabolism ; Animals ; Cells, Cultured ; Cholesterol, HDL/pharmacokinetics ; Chorionic Gonadotropin/pharmacology ; Cyclic AMP Response Element-Binding Protein/genetics ; Female ; Genetic Vectors ; Luteinizing Hormone/pharmacology ; Membrane Proteins/metabolism ; Rats ; Rats, Sprague-Dawley ; Theca Cells/cytology ; Theca Cells/drug effects ; Theca Cells/physiology
    Chemical Substances Cholesterol, HDL ; Chorionic Gonadotropin ; Cyclic AMP Response Element-Binding Protein ; Membrane Proteins ; Androstenedione (409J2J96VR) ; Luteinizing Hormone (9002-67-9)
    Language English
    Publishing date 2005-10-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 1194484-5
    ISSN 1355-008X ; 0969-711X
    ISSN 1355-008X ; 0969-711X
    DOI 10.1385/ENDO:27:3:269
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  9. Article: Type 2 diabetes with neuropathy: autoantibody stimulation of autophagy via Fas.

    Towns, Roberto / Guo, Chunfang / Shangguan, Yu / Hong, Shuangsong / Wiley, John W

    Neuroreport

    2008  Volume 19, Issue 3, Page(s) 265–269

    Abstract: We reported previously that sera from patients with type 2 diabetes and neuropathy induce autophagy in human neuroblastoma (SH-SY5Y) cells. Here we report that enriched immunoglobulin fractions from a subpopulation of these patients induce autophagy and ... ...

    Abstract We reported previously that sera from patients with type 2 diabetes and neuropathy induce autophagy in human neuroblastoma (SH-SY5Y) cells. Here we report that enriched immunoglobulin fractions from a subpopulation of these patients induce autophagy and colocalization with Fas-activated death domain (FADD), a component of the Fas-activated death domain receptor signaling pathway. These effects were replicated by treatment of SY5Y cells with Fas ligand, tumor necrosis factor alpha and an agonist anti-Fas antibody. Preincubation of these sera with a soluble Fas receptor chimera (extracellular domain) markedly decreased the stimulation of autophagy. The results suggest that sera from subset of individuals with type 2 diabetes and neuropathy contain autoantibodies that activate the Fas cascade.
    MeSH term(s) Adult ; Autoantibodies/immunology ; Autophagy/genetics ; Autophagy/physiology ; Blotting, Western ; Cell Line, Tumor ; Diabetes Mellitus, Type 2/immunology ; Diabetes Mellitus, Type 2/pathology ; Diabetic Neuropathies/immunology ; Diabetic Neuropathies/pathology ; Female ; Fluorescent Antibody Technique ; Humans ; Image Processing, Computer-Assisted ; Immunoglobulin G/biosynthesis ; Immunoglobulin G/genetics ; Immunoglobulin M/biosynthesis ; Immunoglobulin M/genetics ; Male ; Neuroblastoma/pathology ; fas Receptor/genetics ; fas Receptor/physiology
    Chemical Substances Autoantibodies ; Immunoglobulin G ; Immunoglobulin M ; fas Receptor
    Language English
    Publishing date 2008-02-12
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1049746-8
    ISSN 1473-558X ; 0959-4965
    ISSN (online) 1473-558X
    ISSN 0959-4965
    DOI 10.1097/WNR.0b013e3282f4cb50
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: The emerging role of autophagy in the pathophysiology of diabetes mellitus.

    Gonzalez, Claudio D / Lee, Myung-Shik / Marchetti, Piero / Pietropaolo, Massimo / Towns, Roberto / Vaccaro, Maria I / Watada, Hirotaka / Wiley, John W

    Autophagy

    2011  Volume 7, Issue 1, Page(s) 2–11

    Abstract: An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative ... ...

    Abstract An emerging body of evidence supports a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus. Persistent high concentrations of glucose lead to imbalances in the antioxidant capacity within the cell resulting in oxidative stress-mediated injury in both disorders. An anticipated consequence of impaired autophagy is the accumulation of dysfunctional organelles such as mitochondria within the cell. Mitochondria are the primary site of the production of reactive oxygen species (ROS), and an imbalance in ROS production relative to the cytoprotective action of autophagy may lead to the accumulation of ROS. Impaired mitochondrial function associated with increased ROS levels have been proposed as mechanisms contributing to insulin resistance. In this article we review and interpret the literature that implicates a role for autophagy in the pathophysiology of type 1 and type 2 diabetes mellitus as it applies to β-cell dysfunction, and more broadly to organ systems involved in complications of diabetes including the cardiovascular, renal and nervous systems.
    MeSH term(s) Autophagy ; Diabetes Complications/pathology ; Diabetes Mellitus/immunology ; Diabetes Mellitus/pathology ; Diabetes Mellitus/physiopathology ; Diabetes Mellitus/therapy ; Humans ; Insulin Resistance ; Insulin-Secreting Cells/pathology ; Insulin-Secreting Cells/ultrastructure ; Signal Transduction
    Language English
    Publishing date 2011-01-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.4161/auto.7.1.13044
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