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  1. Article ; Online: Metabolic cycles and signals for insulin secretion.

    Merrins, Matthew J / Corkey, Barbara E / Kibbey, Richard G / Prentki, Marc

    Cell metabolism

    2022  Volume 34, Issue 7, Page(s) 947–968

    Abstract: In this review, we focus on recent developments in our understanding of nutrient-induced insulin secretion that challenge a key aspect of the "canonical" model, in which an oxidative phosphorylation-driven rise in ATP production closes ... ...

    Abstract In this review, we focus on recent developments in our understanding of nutrient-induced insulin secretion that challenge a key aspect of the "canonical" model, in which an oxidative phosphorylation-driven rise in ATP production closes K
    MeSH term(s) Adenosine Triphosphate/metabolism ; Glucose/metabolism ; Insulin/metabolism ; Insulin Secretion ; Islets of Langerhans/metabolism
    Chemical Substances Insulin ; Adenosine Triphosphate (8L70Q75FXE) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2022-06-20
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2022.06.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: A peripherally restricted cannabinoid-1 receptor inverse agonist promotes insulin secretion and protects from cytokine toxicity in human pancreatic islets.

    Ghosh, Anindya / Peyot, Marie-Line / Leung, Yat Hei / Ravenelle, François / Madiraju, S R Murthy / Prentki, Marc

    European journal of pharmacology

    2023  Volume 944, Page(s) 175589

    Abstract: The cannabinoid receptor CB1R is expressed in pancreatic β-cells; CB1R increased activity is associated with diabetes, obesity, cardiovascular disorders as well as decreased insulin secretion and insulin resistance. CB1R was shown to signal through G- ... ...

    Abstract The cannabinoid receptor CB1R is expressed in pancreatic β-cells; CB1R increased activity is associated with diabetes, obesity, cardiovascular disorders as well as decreased insulin secretion and insulin resistance. CB1R was shown to signal through G-protein coupling as well as β-arrestins in β-cells. Peripherally restricted CB1R inverse agonists purportedly have beneficial effects on insulin secretion in β-cells, without the unwanted effects in the central nervous system. Here we show that a peripherally restricted CB1R inverse agonist, MRI-1891, augments glucose stimulated insulin secretion in isolated human pancreatic islets and mouse islets. The insulin secretion enhancing effect of MRI-1891 is comparable to exendin-4, an analogue of the glucagon like peptide-1 (GLP1). Moreover, MRI-1891 treatment protects isolated human islet cells against cytokine-induced apoptosis, similar to exendin-4. Thus, MRI-1891, a new class of CB1R inverse agonist, may be considered a potential therapeutic for both type 1 and type 2 diabetes because of its ability to protect pancreatic β-cells from cytokine toxicity and to promote insulin secretion.
    MeSH term(s) Mice ; Animals ; Humans ; Insulin Secretion ; Drug Inverse Agonism ; Insulin/metabolism ; Cytokines/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Exenatide/pharmacology ; Cannabinoid Receptor Agonists/pharmacology ; Islets of Langerhans ; Insulin-Secreting Cells ; Cannabinoids/pharmacology
    Chemical Substances Insulin ; Cytokines ; Exenatide (9P1872D4OL) ; Cannabinoid Receptor Agonists ; Cannabinoids
    Language English
    Publishing date 2023-02-09
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 80121-5
    ISSN 1879-0712 ; 0014-2999
    ISSN (online) 1879-0712
    ISSN 0014-2999
    DOI 10.1016/j.ejphar.2023.175589
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Insulin resistance and insulin hypersecretion in the metabolic syndrome and type 2 diabetes: Time for a conceptual framework shift.

    Nolan, Christopher J / Prentki, Marc

    Diabetes & vascular disease research

    2019  Volume 16, Issue 2, Page(s) 118–127

    Abstract: While few dispute the existence of the metabolic syndrome as a clustering of factors indicative of poor metabolic health, its utility above that of its individual components in the clinical care of individual patients is questioned. This is likely a ... ...

    Abstract While few dispute the existence of the metabolic syndrome as a clustering of factors indicative of poor metabolic health, its utility above that of its individual components in the clinical care of individual patients is questioned. This is likely a consequence of the failure of clinicians and scientists to agree on a unifying mechanism to explain the metabolic syndrome. Insulin resistance has most commonly been proposed for this role and is generally considered to be a root causative factor for not only metabolic syndrome but also for its associated conditions of non-alcoholic fatty liver disease (NAFLD), polycystic ovary syndrome (PCOS), obesity-related type 2 diabetes (T2D) and atherosclerotic cardiovascular disease (ASCVD). An alternative view, for which evidence is mounting, is that hyper-responsiveness of islet β-cells to a hostile environment, such as westernised lifestyle, is primary and that the resulting hyperinsulinaemia drives the other components of the metabolic syndrome. Importantly, within this new conceptual framework, insulin resistance, while always a biomarker and state of poor metabolic health, is not considered to be harmful, but a protective adaptive response of critical tissues including the myocardium against insulin-induced metabolic stress. This major shift in how metabolic syndrome can be considered puts insulin hypersecretion into position as the unifying mechanism. If shown to be correct, this new conceptual framework has major implications for the future prevention and management of the metabolic syndrome, including its associated conditions of NAFLD, PCOS, obesity-related T2D and ASCVD.
    MeSH term(s) Animals ; Biomarkers/blood ; Blood Glucose/metabolism ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/physiopathology ; Diabetes Mellitus, Type 2/blood ; Diabetes Mellitus, Type 2/epidemiology ; Diabetes Mellitus, Type 2/physiopathology ; Diabetes Mellitus, Type 2/therapy ; Female ; Health Status ; Humans ; Insulin/blood ; Insulin Resistance ; Insulin-Secreting Cells/metabolism ; Male ; Metabolic Syndrome/blood ; Metabolic Syndrome/epidemiology ; Metabolic Syndrome/physiopathology ; Metabolic Syndrome/therapy ; Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/epidemiology ; Non-alcoholic Fatty Liver Disease/physiopathology ; Obesity/blood ; Obesity/epidemiology ; Obesity/physiopathology ; Polycystic Ovary Syndrome/blood ; Polycystic Ovary Syndrome/epidemiology ; Polycystic Ovary Syndrome/physiopathology ; Prognosis ; Risk Factors ; Secretory Pathway
    Chemical Substances Biomarkers ; Blood Glucose ; Insulin
    Language English
    Publishing date 2019-02-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2250793-0
    ISSN 1752-8984 ; 1479-1641
    ISSN (online) 1752-8984
    ISSN 1479-1641
    DOI 10.1177/1479164119827611
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  4. Article ; Online: Lipid-associated metabolic signalling networks in pancreatic beta cell function.

    Prentki, Marc / Corkey, Barbara E / Madiraju, S R Murthy

    Diabetologia

    2019  Volume 63, Issue 1, Page(s) 10–20

    Abstract: Significant advances have been made in deciphering the mechanisms underlying fuel-stimulated insulin secretion by pancreatic beta cells. The contribution of the triggering/ATP-sensitive potassium ( ... ...

    Abstract Significant advances have been made in deciphering the mechanisms underlying fuel-stimulated insulin secretion by pancreatic beta cells. The contribution of the triggering/ATP-sensitive potassium (K
    MeSH term(s) Animals ; Fatty Acids, Nonesterified ; Humans ; Insulin ; Insulin-Secreting Cells/metabolism ; Islets of Langerhans/metabolism ; Malonyl Coenzyme A/metabolism ; Monoglycerides
    Chemical Substances Fatty Acids, Nonesterified ; Insulin ; Monoglycerides ; Malonyl Coenzyme A (524-14-1)
    Language English
    Publishing date 2019-08-19
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1694-9
    ISSN 1432-0428 ; 0012-186X
    ISSN (online) 1432-0428
    ISSN 0012-186X
    DOI 10.1007/s00125-019-04976-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Cnidii Fructus: A traditional Chinese medicine herb and source of antiosteoporotic drugs.

    Xu, Tianshu / Yin, Jiyuan / Dai, Xuan / Liu, Tianyuan / Shi, Hanfen / Zhang, Yueyi / Wang, Shan / Yue, Gaiyue / Zhang, Yanfei / Zhao, Dandan / Gao, Sihua / Prentki, Marc / Wang, Lili / Zhang, Dongwei

    Phytomedicine : international journal of phytotherapy and phytopharmacology

    2024  Volume 128, Page(s) 155375

    Abstract: Background: Osteoporosis (OP) is a prevalent chronic metabolic bone disease for which limited countermeasures are available. Cnidii Fructus (CF), primarily derived from Cnidium monnieri (L.) Cusson., has been tested in clinical trials of traditional ... ...

    Abstract Background: Osteoporosis (OP) is a prevalent chronic metabolic bone disease for which limited countermeasures are available. Cnidii Fructus (CF), primarily derived from Cnidium monnieri (L.) Cusson., has been tested in clinical trials of traditional Chinese medicine for the management of OP. Accumulating preclinical studies indicate that CF may be used against OP.
    Materials and methods: Comprehensive documentation and analysis were conducted to retrieve CF studies related to its main phytochemical components as well as its pharmacokinetics, safety and pharmacological properties. We also retrieved information on the mode of action of CF and, in particular, preclinical and clinical studies related to bone remodeling. This search was performed from the inception of databases up to the end of 2022 and included PubMed, China National Knowledge Infrastructure, the National Science and Technology Library, the China Science and Technology Journal Database, Weipu, Wanfang, the Web of Science and the China National Patent Database.
    Results: CF contains a wide range of natural active compounds, including osthole, bergapten, imperatorin and xanthotoxin, which may underlie its beneficial effects on improving bone metabolism and quality. CF action appears to be mediated via multiple processes, including the osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL)/receptor activator of nuclear factor-κB (RANK), Wnt/β-catenin and bone morphogenetic protein (BMP)/Smad signaling pathways.
    Conclusion: CF and its ingredients may provide novel compounds for developing anti-OP drugs.
    MeSH term(s) Humans ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/chemistry ; Drugs, Chinese Herbal/therapeutic use ; Osteoporosis/drug therapy ; Cnidium/chemistry ; Fruit/chemistry ; Animals ; Medicine, Chinese Traditional ; Coumarins/pharmacology ; Coumarins/therapeutic use ; Phytochemicals/pharmacology ; 5-Methoxypsoralen ; Bone Remodeling/drug effects ; Bone Density Conservation Agents/pharmacology ; Bone Density Conservation Agents/therapeutic use ; RANK Ligand
    Chemical Substances Drugs, Chinese Herbal ; Coumarins ; osthol (XH1TI1759C) ; Phytochemicals ; 5-Methoxypsoralen (4FVK84C92X) ; Bone Density Conservation Agents ; RANK Ligand
    Language English
    Publishing date 2024-01-18
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 1205240-1
    ISSN 1618-095X ; 0944-7113
    ISSN (online) 1618-095X
    ISSN 0944-7113
    DOI 10.1016/j.phymed.2024.155375
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  6. Article ; Online: Nutrient-Induced Metabolic Stress, Adaptation, Detoxification, and Toxicity in the Pancreatic β-Cell.

    Prentki, Marc / Peyot, Marie-Line / Masiello, Pellegrino / Madiraju, S R Murthy

    Diabetes

    2020  Volume 69, Issue 3, Page(s) 279–290

    Abstract: Paraphrasing the Swiss physician and father of toxicology Paracelsus (1493-1541) on chemical agents used as therapeutics, "the dose makes the poison," it is now realized that this aptly applies to the calorigenic nutrients. The case here is the ... ...

    Abstract Paraphrasing the Swiss physician and father of toxicology Paracelsus (1493-1541) on chemical agents used as therapeutics, "the dose makes the poison," it is now realized that this aptly applies to the calorigenic nutrients. The case here is the pancreatic islet β-cell presented with excessive levels of nutrients such as glucose, lipids, and amino acids. The short-term effects these nutrients exert on the β-cell are enhanced insulin biosynthesis and secretion and changes in glucose sensitivity. However, chronic fuel surfeit triggers additional compensatory and adaptive mechanisms by β-cells to cope with the increased insulin demand or to protect itself. When these mechanisms fail, toxicity due to the nutrient surplus ensues, leading to β-cell dysfunction, dedifferentiation, and apoptosis. The terms glucotoxicity, lipotoxicity, and glucolipotoxicity have been widely used, but there is some confusion as to what they mean precisely and which is most appropriate for a given situation. Here we address the gluco-, lipo-, and glucolipo-toxicities in β-cells by assessing the evidence both for and against each of them. We also discuss potential mechanisms and defend the view that many of the identified "toxic" effects of nutrient excess, which may also include amino acids, are in fact beneficial adaptive processes. In addition, candidate fuel-excess detoxification pathways are evaluated. Finally, we propose that a more general term should be used for the in vivo situation of overweight-associated type 2 diabetes reflecting both the adaptive and toxic processes to mixed calorigenic nutrients excess: "nutrient-induced metabolic stress" or, in brief, "nutri-stress."
    MeSH term(s) Diabetes Mellitus, Type 2 ; Glucose ; Humans ; Insulin ; Insulin-Secreting Cells ; Nutrients ; Stress, Physiological
    Chemical Substances Insulin ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2020-02-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi19-0014
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  7. Article ; Online: Silencing ANGPTL8 reduces mouse preadipocyte differentiation and insulin signaling.

    Ghosh, Anindya / Leung, Yat Hei / Yu, Jeffrey / Sladek, Robert / Chénier, Isabelle / Oppong, Abel K / Peyot, Marie-Line / Madiraju, S R Murthy / Al-Khairi, Irina / Thanaraj, Thangavel Alphonse / Abubaker, Jehad / Al-Mulla, Fahd / Prentki, Marc / Abu-Farha, Mohamed

    Biochimica et biophysica acta. Molecular and cell biology of lipids

    2024  Volume 1869, Issue 3, Page(s) 159461

    Abstract: ANGPTL8, expressed mainly in the liver and adipose tissue, regulates the activity of lipoprotein lipase (LPL) present in the extracellular space and triglyceride (TG) metabolism through its interaction with ANGPTL3 and ANGPTL4. Whether intracellular ... ...

    Abstract ANGPTL8, expressed mainly in the liver and adipose tissue, regulates the activity of lipoprotein lipase (LPL) present in the extracellular space and triglyceride (TG) metabolism through its interaction with ANGPTL3 and ANGPTL4. Whether intracellular ANGPTL8 can also exert effects in tissues where it is expressed is uncertain. ANGPTL8 expression was low in preadipocytes and much increased during differentiation. To better understand the role of intracellular ANGPTL8 in adipocytes and assess whether it may play a role in adipocyte differentiation, we knocked down its expression in normal mouse subcutaneous preadipocytes. ANGPTL8 knockdown reduced adipocyte differentiation, cellular TG accumulation and also isoproterenol-stimulated lipolysis at day 7 of differentiation. RNA-Seq analysis of ANGPTL8 siRNA or control siRNA transfected SC preadipocytes on days 0, 2, 4 and 7 of differentiation showed that ANGPTL8 knockdown impeded the early (day 2) expression of adipogenic and insulin signaling genes, PPARγ, as well as genes related to extracellular matrix and NF-κB signaling. Insulin mediated Akt phosphorylation was reduced at an early stage during adipocyte differentiation. This study based on normal primary cells shows that ANGPTL8 has intracellular actions in addition to effects in the extracellular space, like modulating LPL activity. Preadipocyte ANGPTL8 expression modulates their differentiation possibly via changes in insulin signaling gene expression.
    MeSH term(s) Mice ; Animals ; Insulin ; Cell Differentiation/genetics ; Adipogenesis/genetics ; Signal Transduction ; RNA, Small Interfering ; Angiopoietin-Like Protein 8
    Chemical Substances Insulin ; RNA, Small Interfering ; ANGPTL8 protein, mouse ; Angiopoietin-Like Protein 8
    Language English
    Publishing date 2024-01-24
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 60-7
    ISSN 1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2618 ; 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbalip.2024.159461
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Glycerol-3-phosphate phosphatase/PGP: Role in intermediary metabolism and target for cardiometabolic diseases.

    Possik, Elite / Madiraju, S R Murthy / Prentki, Marc

    Biochimie

    2017  Volume 143, Page(s) 18–28

    Abstract: Metabolic diseases, including obesity, type 2 diabetes, and metabolic syndrome arise because of disturbances in glucose and fat metabolism, which impact associated physiological events such as insulin secretion and action, fat storage and oxidation. Even ...

    Abstract Metabolic diseases, including obesity, type 2 diabetes, and metabolic syndrome arise because of disturbances in glucose and fat metabolism, which impact associated physiological events such as insulin secretion and action, fat storage and oxidation. Even though, decades of research has contributed to our current understanding of the components involved in glucose and fat metabolism and their regulation, that led to the development of many therapeutics, there are still many unanswered questions. Glycerol-3-phosphate (Gro3P), which is formed during glycolysis, is at the intersection of glucose and fat metabolism, and the availability of this metabolite can regulate energy and intermediary metabolism in mammalian cells. During the course of evolution, mammalian cells are assumed to have lost the capacity to directly hydrolyze Gro3P to glycerol, until the recent discovery from our laboratory showing that a previously known mammalian enzyme, phosphoglycolate phosphatase (PGP), can function as a Gro3P phosphatase (G3PP) and regulate this metabolite levels. Emerging evidence indicates that G3PP/PGP is an evolutionarily conserved "multi-tasking" enzyme that belongs to the superfamily of haloacid dehalogenase-like phosphatase enzymes, and is capable of hydrolyzing Gro3P, an abundant physiologically relevant substrate, as well as other metabolites including 2-phosphoglycolate, 4-phosphoerythronate and 2-phospholactate, which are present in much smaller amounts in cells, under normal conditions. G3PP, by regulating Gro3P levels, plays a critical role in intermediary metabolism, including glycolysis, glucose oxidation, cellular redox and ATP production, gluconeogenesis, esterification of fatty acids towards glycerolipid synthesis and fatty acid oxidation. Because of G3PP's ability to regulate energy and intermediary metabolism as well as physiological functions such as insulin secretion, hepatic glucose production, and fat synthesis, storage and oxidation, the pathophysiological role of this enzyme in metabolic diseases needs to be precisely defined. In this review, we summarize the present knowledge on the structure, function and regulation of G3PP/PGP, and we discuss its potential therapeutic role for cardiometabolic diseases.
    MeSH term(s) Animals ; Cardiovascular Diseases/enzymology ; Diabetes Mellitus, Type 2/enzymology ; Evolution, Molecular ; Glycerophosphates/metabolism ; Humans ; Lipid Metabolism ; Mammals/metabolism ; Metabolic Syndrome/enzymology ; Neoplasms/enzymology ; Phosphoric Monoester Hydrolases/chemistry ; Phosphoric Monoester Hydrolases/genetics ; Phosphoric Monoester Hydrolases/metabolism ; Stress, Physiological/physiology
    Chemical Substances Glycerophosphates ; alpha-glycerophosphoric acid (9NTI6P3O4X) ; glycerol 3-phosphate phosphatase, Mycobacterium tuberculosis (EC 3.1.3.-) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2)
    Language English
    Publishing date 2017-08-05
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 120345-9
    ISSN 1638-6183 ; 0300-9084
    ISSN (online) 1638-6183
    ISSN 0300-9084
    DOI 10.1016/j.biochi.2017.08.001
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  9. Article ; Online: Monoacylglycerol signalling and ABHD6 in health and disease.

    Poursharifi, Pegah / Madiraju, Sri Ramachandra Murthy / Prentki, Marc

    Diabetes, obesity & metabolism

    2017  Volume 19 Suppl 1, Page(s) 76–89

    Abstract: Lipid metabolism dysregulation underlies chronic pathologies such as obesity, diabetes and cancer. Besides their role in structure and energy storage, lipids are also important signalling molecules regulating multiple biological functions. Thus, ... ...

    Abstract Lipid metabolism dysregulation underlies chronic pathologies such as obesity, diabetes and cancer. Besides their role in structure and energy storage, lipids are also important signalling molecules regulating multiple biological functions. Thus, understanding the precise lipid metabolism enzymatic steps that are altered in some pathological conditions is helpful for designing better treatment strategies. Several monoacylglycerol (MAG) species are only recently being recognized as signalling lipid molecules in different tissues. Recent studies indicated the importance of the ubiquitously expressed serine hydrolase α/β-hydrolase domain 6 (ABHD6), which is a MAG hydrolase, in regulating signalling competent MAG in both central and peripheral tissues. The central and peripheral function of the endocannabinoid 2-arachidonoylglycerol, which is a 2-MAG, and its breakdown by both ABHD6 and classical MAG lipase has been well documented. ABHD6 and its substrate MAG appear to be involved in the regulation of various physiological and pathological processes including insulin secretion, adipose browning, food intake, neurotransmission, autoimmune disorders, neurological and metabolic diseases as well as cancer. Diverse cellular targets such as mammalian unc13-1 (Munc13-1), PPARs, GPR119 and CB1/2 receptors, for MAG-mediated signalling processes have been proposed in different cell types. The purpose of this review is to provide a comprehensive summary of the current state of knowledge regarding ABHD6/MAG signalling and its possible therapeutic implications.
    MeSH term(s) Animals ; Arachidonic Acids/metabolism ; Diabetes Mellitus, Type 2/drug therapy ; Diabetes Mellitus, Type 2/enzymology ; Diabetes Mellitus, Type 2/metabolism ; Endocannabinoids/metabolism ; Energy Metabolism/drug effects ; Enzyme Inhibitors/pharmacology ; Enzyme Inhibitors/therapeutic use ; Gene Expression Regulation, Enzymologic/drug effects ; Glycerides/metabolism ; Humans ; Ligands ; Metabolic Syndrome/drug therapy ; Metabolic Syndrome/enzymology ; Metabolic Syndrome/metabolism ; Models, Biological ; Monoacylglycerol Lipases/antagonists & inhibitors ; Monoacylglycerol Lipases/chemistry ; Monoacylglycerol Lipases/genetics ; Monoacylglycerol Lipases/metabolism ; Monoglycerides/metabolism ; Nerve Tissue Proteins/agonists ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Obesity/drug therapy ; Obesity/enzymology ; Obesity/metabolism ; Organ Specificity ; Peroxisome Proliferator-Activated Receptors/agonists ; Peroxisome Proliferator-Activated Receptors/genetics ; Peroxisome Proliferator-Activated Receptors/metabolism ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Second Messenger Systems/drug effects ; Substrate Specificity ; TRPV Cation Channels/agonists ; TRPV Cation Channels/genetics ; TRPV Cation Channels/metabolism
    Chemical Substances Arachidonic Acids ; Endocannabinoids ; Enzyme Inhibitors ; GPR119 protein, human ; Glycerides ; Ligands ; Monoglycerides ; Nerve Tissue Proteins ; Peroxisome Proliferator-Activated Receptors ; Receptors, G-Protein-Coupled ; TRPV Cation Channels ; TRPV1 protein, human ; UNC13B protein, human ; glyceryl 2-arachidonate (8D239QDW64) ; ABHD6 protein, human (EC 3.1.1.23) ; Monoacylglycerol Lipases (EC 3.1.1.23)
    Language English
    Publishing date 2017
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1454944-x
    ISSN 1463-1326 ; 1462-8902
    ISSN (online) 1463-1326
    ISSN 1462-8902
    DOI 10.1111/dom.13008
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  10. Article: New Mammalian Glycerol-3-Phosphate Phosphatase: Role in β-Cell, Liver and Adipocyte Metabolism.

    Possik, Elite / Al-Mass, Anfal / Peyot, Marie-Line / Ahmad, Rasheed / Al-Mulla, Fahd / Madiraju, S R Murthy / Prentki, Marc

    Frontiers in endocrinology

    2021  Volume 12, Page(s) 706607

    Abstract: Cardiometabolic diseases, including type 2 diabetes, obesity and non-alcoholic fatty liver disease, have enormous impact on modern societies worldwide. Excess nutritional burden and nutri-stress together with sedentary lifestyles lead to these diseases. ... ...

    Abstract Cardiometabolic diseases, including type 2 diabetes, obesity and non-alcoholic fatty liver disease, have enormous impact on modern societies worldwide. Excess nutritional burden and nutri-stress together with sedentary lifestyles lead to these diseases. Deranged glucose, fat, and energy metabolism is at the center of nutri-stress, and glycolysis-derived glycerol-3-phosphate (Gro3P) is at the crossroads of these metabolic pathways. Cellular levels of Gro3P can be controlled by its synthesis, utilization or hydrolysis. The belief that mammalian cells do not possess an enzyme that hydrolyzes Gro3P, as in lower organisms and plants, is challenged by our recent work showing the presence of a Gro3P phosphatase (G3PP) in mammalian cells. A previously described phosphoglycolate phosphatase (PGP) in mammalian cells, with no established physiological function, has been shown to actually function as G3PP, under physiological conditions, particularly at elevated glucose levels. In the present review, we summarize evidence that supports the view that G3PP plays an important role in the regulation of gluconeogenesis and fat storage in hepatocytes, glucose stimulated insulin secretion and nutri-stress in β-cells, and lipogenesis in adipocytes. We provide a balanced perspective on the pathophysiological significance of G3PP in mammals with specific reference to cardiometabolic diseases.
    MeSH term(s) Adipocytes/cytology ; Adipocytes/metabolism ; Animals ; Humans ; Insulin Secretion ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/metabolism ; Lipogenesis ; Liver/cytology ; Liver/metabolism ; Membrane Transport Proteins/metabolism
    Chemical Substances Membrane Transport Proteins ; SLC37A1 protein, human (87434-91-1)
    Language English
    Publishing date 2021-07-13
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2021.706607
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