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Article: The Aging Mitochondria.

Theurey, Pierre / Pizzo, Paola

2018 Volume 9, Issue 1

Abstract: Mitochondrial dysfunction is a central event in many pathologies and contributes as well to age-related processes. However, distinguishing between primary mitochondrial dysfunction driving aging and a secondary mitochondrial impairment resulting from ... ...

Abstract	Mitochondrial dysfunction is a central event in many pathologies and contributes as well to age-related processes. However, distinguishing between primary mitochondrial dysfunction driving aging and a secondary mitochondrial impairment resulting from other cell alterations remains challenging. Indeed, even though mitochondria undeniably play a crucial role in aging pathways at the cellular and organismal level, the original hypothesis in which mitochondrial dysfunction and production of free radicals represent the main driving force of cell degeneration has been strongly challenged. In this review, we will first describe mitochondrial dysfunctions observed in aged tissue, and how these features have been linked to mitochondrial reactive oxygen species (ROS)-mediated cell damage and mitochondrial DNA (mtDNA) mutations. We will also discuss the clues that led to consider mitochondria as the starting point in the aging process, and how recent research has showed that the mitochondria aging axis represents instead a more complex and multifactorial signaling pathway. New working hypothesis will be also presented in which mitochondria are considered at the center of a complex web of cell dysfunctions that eventually leads to cell senescence and death.
Language	English
Publishing date	2018-01-09
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes9010022
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Article ; Online: Mitochondria-Associated Membranes Response to Nutrient Availability and Role in Metabolic Diseases.

Theurey, Pierre / Rieusset, Jennifer

Trends in endocrinology and metabolism: TEM

2017 Volume 28, Issue 1, Page(s) 32–45

Abstract: Metabolic diseases are associated with nutrient excess and metabolic inflexibility. Mitochondria and endoplasmic reticulum are important organelles and nutrient sensors, and their dysfunction has been extensively and independently implicated in metabolic ...

Abstract	Metabolic diseases are associated with nutrient excess and metabolic inflexibility. Mitochondria and endoplasmic reticulum are important organelles and nutrient sensors, and their dysfunction has been extensively and independently implicated in metabolic diseases. Both organelles interact at sites known as mitochondria-associated membranes (MAMs), in order to exchange metabolites and calcium. Recent evidence indicates that MAM could be a hub of hepatic insulin signaling and nutrient sensing. In this review, we discuss the roles organelle function and communication play in the cell's adaptation to nutrient availability, in both physiology and metabolic diseases. We highlight how dynamic regulation of MAM affects mitochondria physiology and adaptation of cellular metabolism to nutrient availability, and how chronic MAM disruption participates in the metabolic inflexibility associated with metabolic disorders.
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2016.09.002
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Article ; Online: Glucose dysregulation in pre-clinical Alzheimer's disease.

Connolly, Niamh M C / Theurey, Pierre / Pizzo, Paola

Aging

2019 Volume 11, Issue 15, Page(s) 5296–5297

MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/metabolism ; Alzheimer Disease/psychology ; Cognitive Dysfunction/metabolism ; Glucose/metabolism ; Glycolysis ; Humans ; Middle Aged
Chemical Substances	Glucose (IY9XDZ35W2)
Language	English
Publishing date	2019-08-04
Publishing country	United States
Document type	Editorial ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.102146
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Article ; Online: Phase 2 trial with imeglimin in patients with Type 2 diabetes indicates effects on insulin secretion and sensitivity.

Theurey, Pierre / Thang, Carole / Pirags, Valdis / Mari, Andrea / Pacini, Giovanni / Bolze, Sébastien / Hallakou-Bozec, Sophie / Fouqueray, Pascale

Endocrinology, diabetes & metabolism

2022 Volume 5, Issue 6, Page(s) e371

Abstract: Introduction: The aim of the present study was to evaluate the effect of 18-week monotherapy with imeglimin on glucose tolerance and on insulin secretion/sensitivity in type 2 diabetic (T2D) patients.: Methods: The study was an 18-week, double-blind ... ...

Abstract	Introduction: The aim of the present study was to evaluate the effect of 18-week monotherapy with imeglimin on glucose tolerance and on insulin secretion/sensitivity in type 2 diabetic (T2D) patients. Methods: The study was an 18-week, double-blind clinical trial in T2D subjects previously treated with stable metformin therapy and washed out for 4 weeks. Subjects were randomized 1:1 to receive a 1500 mg bid of imeglimin or placebo. The primary endpoint was the effect of imeglimin vs placebo on changes from baseline to week 18 in glucose tolerance (glucose area under the curve [AUC]) during a 3 h-glucose tolerance test [OGTT]). Secondary endpoints included glycaemic control and calculated indices of insulin secretion and sensitivity. Results: A total of 59 subjects were randomized, 30 receiving imeglimin and 29 receiving placebo. The study met its primary endpoint. Least squares (LS) mean difference between treatment groups (imeglimin - placebo) for AUC glucose from baseline to week 18 was -429.6 mmol/L·min (p = .001). Two-hour post-dose fasting plasma glucose was significantly decreased with LS mean differences of -1.22 mmol/L (p = .022) and HbA1c was improved with LS mean differences of -0.62% (p = .013). The AUC Conclusions: Results are consistent with a mode of action involving insulin secretion as well as improved insulin sensitivity and further support the potential for imeglimin to improve healthcare in T2D patients.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/drug therapy ; Insulin Secretion ; Hypoglycemic Agents/adverse effects ; Insulin Resistance ; Blood Glucose ; Double-Blind Method
Chemical Substances	Hypoglycemic Agents ; imeglimin (UU226QGU97) ; Blood Glucose
Language	English
Publishing date	2022-10-14
Publishing country	England
Document type	Randomized Controlled Trial ; Clinical Trial, Phase II ; Journal Article
ISSN	2398-9238
ISSN (online)	2398-9238
DOI	10.1002/edm2.371
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Article ; Online: Reduced lactic acidosis risk with Imeglimin: Comparison with Metformin.

Theurey, Pierre / Vial, Guillaume / Fontaine, Eric / Monternier, Pierre-Axel / Fouqueray, Pascale / Bolze, Sébastien / Moller, David E / Hallakou-Bozec, Sophie

Physiological reports

2022 Volume 10, Issue 5, Page(s) e15151

Abstract: The global prevalence of type 2 diabetes (T2D) is expected to exceed 642 million people by 2040. Metformin is a widely used biguanide T2D therapy, associated with rare but serious events of lactic acidosis, in particular with predisposing conditions (e.g. ...

Abstract	The global prevalence of type 2 diabetes (T2D) is expected to exceed 642 million people by 2040. Metformin is a widely used biguanide T2D therapy, associated with rare but serious events of lactic acidosis, in particular with predisposing conditions (e.g., renal failure or major surgery). Imeglimin, a recently approved drug, is the first in a new class (novel mode of action) of T2D medicines. Although not a biguanide, Imeglimin shares a chemical moiety with Metformin and also modulates mitochondrial complex I activity, a potential mechanism for Metformin-mediated lactate accumulation. We interrogated the potential for Imeglimin to induce lacticacidosis in relevant animal models and further assessed differences in key mechanisms known for Metformin's effects. In a dog model of major surgery, Metformin or Imeglimin (30-1000 mg/kg) was acutely administered, only Metformin-induced lactate accumulation and pH decrease leading to lactic acidosis with fatality at the highest dose. Rats with gentamycin-induced renal insufficiency received Metformin or Imeglimin (50-100 mg/kg/h), only Metformin increased lactatemia and H
MeSH term(s)	Acidosis, Lactic/chemically induced ; Animals ; Diabetes Mellitus, Type 2/drug therapy ; Dogs ; Humans ; Hypoglycemic Agents/adverse effects ; Hypoglycemic Agents/therapeutic use ; Lactic Acid ; Metformin/adverse effects ; Metformin/therapeutic use ; Mice ; Rats ; Renal Insufficiency ; Triazines
Chemical Substances	Hypoglycemic Agents ; Triazines ; Lactic Acid (33X04XA5AT) ; Metformin (9100L32L2N) ; imeglimin (UU226QGU97)
Language	English
Publishing date	2022-03-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2724325-4
ISSN	2051-817X ; 2051-817X
ISSN (online)	2051-817X
ISSN	2051-817X
DOI	10.14814/phy2.15151
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Article ; Online: The endoplasmic reticulum-mitochondria coupling in health and disease: Molecules, functions and significance.

Filadi, Riccardo / Theurey, Pierre / Pizzo, Paola

Cell calcium

2017 Volume 62, Page(s) 1–15

Abstract: The close apposition between endoplasmic reticulum (ER) and mitochondria represents a key platform, capable to regulate different fundamental cellular pathways. Among these, ... ...

Abstract	The close apposition between endoplasmic reticulum (ER) and mitochondria represents a key platform, capable to regulate different fundamental cellular pathways. Among these, Ca
MeSH term(s)	Alzheimer Disease/metabolism ; Amyotrophic Lateral Sclerosis/metabolism ; Animals ; Calcium/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Metabolic Syndrome/metabolism ; Mitochondria/metabolism ; Parkinson Disease/metabolism
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2017-03
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	757687-0
ISSN	1532-1991 ; 0143-4160
ISSN (online)	1532-1991
ISSN	0143-4160
DOI	10.1016/j.ceca.2017.01.003
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Zs.A 1596: Show issues

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Article ; Online: Therapeutic potential of deuterium-stabilized (R)-pioglitazone-PXL065-for X-linked adrenoleukodystrophy.

Monternier, Pierre-Axel / Singh, Jaspreet / Parasar, Parveen / Theurey, Pierre / DeWitt, Sheila / Jacques, Vincent / Klett, Eric / Kaur, Navtej / Nagaraja, Tavarekere N / Moller, David E / Hallakou-Bozec, Sophie

Journal of inherited metabolic disease

2022 Volume 45, Issue 4, Page(s) 832–847

Abstract: X-linked adrenoleukodystrophy (ALD) results from ABCD1 gene mutations which impair Very Long Chain Fatty Acids (VLCFA; C26:0 and C24:0) peroxisomal import and β-oxidation, leading to accumulation in plasma and tissues. Excess VLCFA drives impaired ... ...

Abstract	X-linked adrenoleukodystrophy (ALD) results from ABCD1 gene mutations which impair Very Long Chain Fatty Acids (VLCFA; C26:0 and C24:0) peroxisomal import and β-oxidation, leading to accumulation in plasma and tissues. Excess VLCFA drives impaired cellular functions (e.g. disrupted mitochondrial function), inflammation, and neurodegeneration. Major disease phenotypes include: adrenomyeloneuropathy (AMN), progressive spinal cord axonal degeneration, and cerebral ALD (C-ALD), inflammatory white matter demyelination and degeneration. No pharmacological treatment is available to-date for ALD. Pioglitazone, an anti-diabetic thiazolidinedione, exerts potential benefits in ALD models. Its mechanisms are genomic (PPARγ agonism) and nongenomic (mitochondrial pyruvate carrier-MPC, long-chain acyl-CoA synthetase 4-ACSL4, inhibition). However, its use is limited by PPARγ-driven side effects (e.g. weight gain, edema). PXL065 is a clinical-stage deuterium-stabilized (R)-enantiomer of pioglitazone which lacks PPARγ agonism but retains MPC activity. Here, we show that incubation of ALD patient-derived cells (both AMN and C-ALD) and glial cells from Abcd1-null mice with PXL065 resulted in: normalization of elevated VLCFA, improved mitochondrial function, and attenuated indices of inflammation. Compensatory peroxisomal transporter gene expression was also induced. Additionally, chronic treatment of Abcd1-null mice lowered VLCFA in plasma, brain and spinal cord and improved both neural histology (sciatic nerve) and neurobehavioral test performance. Several in vivo effects of PXL065 exceeded those achieved with pioglitazone. PXL065 was confirmed to lack PPARγ agonism but retained ACSL4 activity of pioglitazone. PXL065 has novel actions and mechanisms and exhibits a range of potential benefits in ALD models; further testing of this molecule in ALD patients is warranted.
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily D, Member 1/genetics ; ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Adrenoleukodystrophy/drug therapy ; Adrenoleukodystrophy/genetics ; Adrenoleukodystrophy/metabolism ; Animals ; Deuterium/metabolism ; Fatty Acids/metabolism ; Fatty Acids, Nonesterified ; Inflammation ; Mice ; Mice, Knockout ; PPAR gamma/metabolism ; Pioglitazone
Chemical Substances	ATP Binding Cassette Transporter, Subfamily D, Member 1 ; ATP-Binding Cassette Transporters ; Abcd1 protein, mouse ; Fatty Acids ; Fatty Acids, Nonesterified ; PPAR gamma ; Deuterium (AR09D82C7G) ; Pioglitazone (X4OV71U42S)
Language	English
Publishing date	2022-05-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	438341-2
ISSN	1573-2665 ; 0141-8955
ISSN (online)	1573-2665
ISSN	0141-8955
DOI	10.1002/jimd.12510
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Zs.A 1508: Show issues

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Article ; Online: Beneficial Effects of the Direct AMP-Kinase Activator PXL770 in In Vitro and In Vivo Models of X-Linked Adrenoleukodystrophy.

Monternier, Pierre-Axel / Parasar, Parveen / Theurey, Pierre / Gluais Dagorn, Pascale / Kaur, Navtej / Nagaraja, Tavarekere N / Fouqueray, Pascale / Bolze, Sébastien / Moller, David E / Singh, Jaspreet / Hallakou-Bozec, Sophie

The Journal of pharmacology and experimental therapeutics

2022 Volume 382, Issue 2, Page(s) 208–222

Abstract: X-linked adrenoleukodystrophy (ALD) is a severe orphan disease caused by mutations in the ... ...

Abstract	X-linked adrenoleukodystrophy (ALD) is a severe orphan disease caused by mutations in the peroxisomal
MeSH term(s)	AMP-Activated Protein Kinases/metabolism ; ATP Binding Cassette Transporter, Subfamily D, Member 1/genetics ; ATP-Binding Cassette Transporters/genetics ; Adenosine Monophosphate ; Adenylate Kinase/metabolism ; Adrenoleukodystrophy/drug therapy ; Adrenoleukodystrophy/genetics ; Adrenoleukodystrophy/metabolism ; Animals ; Fatty Acids/metabolism ; Mice ; Pyridones/pharmacology ; Tetrahydronaphthalenes/pharmacology
Chemical Substances	2-chloro-3-(1-hydroxy-5,6,7,8-tetrahydronaphthalen-2-yl)-6-oxo-5-phenyl-7H-thieno)(2,3-b)pyridin-4-olate potassium ; ATP Binding Cassette Transporter, Subfamily D, Member 1 ; ATP-Binding Cassette Transporters ; Abcd1 protein, mouse ; Fatty Acids ; Pyridones ; Tetrahydronaphthalenes ; Adenosine Monophosphate (415SHH325A) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Adenylate Kinase (EC 2.7.4.3)
Language	English
Publishing date	2022-06-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3106-9
ISSN	1521-0103 ; 0022-3565
ISSN (online)	1521-0103
ISSN	0022-3565
DOI	10.1124/jpet.122.001208
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Article ; Online: Pharmacodynamic effects of direct AMP kinase activation in humans with insulin resistance and non-alcoholic fatty liver disease: A phase 1b study.

Fouqueray, Pascale / Bolze, Sebastien / Dubourg, Julie / Hallakou-Bozec, Sophie / Theurey, Pierre / Grouin, Jean-Marie / Chevalier, Clémence / Gluais-Dagorn, Pascale / Moller, David E / Cusi, Kenneth

Cell reports. Medicine

2021 Volume 2, Issue 12, Page(s) 100474

Abstract: AMPK is an energy sensor modulating metabolism, inflammation, and a target for metabolic disorders. Metabolic dysfunction results in lower AMPK activity. PXL770 is a direct AMPK activator, ... ...

Abstract	AMPK is an energy sensor modulating metabolism, inflammation, and a target for metabolic disorders. Metabolic dysfunction results in lower AMPK activity. PXL770 is a direct AMPK activator, inhibiting
MeSH term(s)	Adenylate Kinase/metabolism ; Enzyme Activation/drug effects ; Enzyme Activators ; Female ; Glucose/metabolism ; Humans ; Insulin Resistance ; Lipids/blood ; Lipogenesis/drug effects ; Male ; Middle Aged ; Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/enzymology ; Non-alcoholic Fatty Liver Disease/pathology ; Pyridones/adverse effects ; Pyridones/blood ; Pyridones/pharmacokinetics ; Pyridones/pharmacology ; Tetrahydronaphthalenes/adverse effects ; Tetrahydronaphthalenes/blood ; Tetrahydronaphthalenes/pharmacokinetics ; Tetrahydronaphthalenes/pharmacology
Chemical Substances	2-chloro-3-(1-hydroxy-5,6,7,8-tetrahydronaphthalen-2-yl)-6-oxo-5-phenyl-7H-thieno)(2,3-b)pyridin-4-olate potassium ; Enzyme Activators ; Lipids ; Pyridones ; Tetrahydronaphthalenes ; Adenylate Kinase (EC 2.7.4.3) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2021-12-21
Publishing country	United States
Document type	Clinical Trial, Phase I ; Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2021.100474
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Article ; Online: Systems biology identifies preserved integrity but impaired metabolism of mitochondria due to a glycolytic defect in Alzheimer's disease neurons.

Theurey, Pierre / Connolly, Niamh M C / Fortunati, Ilaria / Basso, Emy / Lauwen, Susette / Ferrante, Camilla / Moreira Pinho, Catarina / Joselin, Alvin / Gioran, Anna / Bano, Daniele / Park, David S / Ankarcrona, Maria / Pizzo, Paola / Prehn, Jochen H M

Aging cell

2019 Volume 18, Issue 3, Page(s) e12924

Abstract: Mitochondrial dysfunction is implicated in most neurodegenerative diseases, including Alzheimer's disease (AD). We here combined experimental and computational approaches to investigate mitochondrial health and bioenergetic function in neurons from a ... ...

Abstract	Mitochondrial dysfunction is implicated in most neurodegenerative diseases, including Alzheimer's disease (AD). We here combined experimental and computational approaches to investigate mitochondrial health and bioenergetic function in neurons from a double transgenic animal model of AD (PS2APP/B6.152H). Experiments in primary cortical neurons demonstrated that AD neurons had reduced mitochondrial respiratory capacity. Interestingly, the computational model predicted that this mitochondrial bioenergetic phenotype could not be explained by any defect in the mitochondrial respiratory chain (RC), but could be closely resembled by a simulated impairment in the mitochondrial NADH flux. Further computational analysis predicted that such an impairment would reduce levels of mitochondrial NADH, both in the resting state and following pharmacological manipulation of the RC. To validate these predictions, we utilized fluorescence lifetime imaging microscopy (FLIM) and autofluorescence imaging and confirmed that transgenic AD neurons had reduced mitochondrial NAD(P)H levels at rest, and impaired power of mitochondrial NAD(P)H production. Of note, FLIM measurements also highlighted reduced cytosolic NAD(P)H in these cells, and extracellular acidification experiments showed an impaired glycolytic flux. The impaired glycolytic flux was identified to be responsible for the observed mitochondrial hypometabolism, since bypassing glycolysis with pyruvate restored mitochondrial health. This study highlights the benefits of a systems biology approach when investigating complex, nonintuitive molecular processes such as mitochondrial bioenergetics, and indicates that primary cortical neurons from a transgenic AD model have reduced glycolytic flux, leading to reduced cytosolic and mitochondrial NAD(P)H and reduced mitochondrial respiratory capacity.
MeSH term(s)	Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Animals ; Cells, Cultured ; Female ; Glycolysis ; Male ; Mice ; Microscopy, Fluorescence ; Mitochondria/metabolism ; Neurons/metabolism ; Neurons/pathology ; Systems Biology
Language	English
Publishing date	2019-02-21
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12924
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