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965 results on '"Thorens, Bernard"'

156. Insulin secretion is regulated by the glucose-dependent production of islet beta cell macrophage migration inhibitory factor

Author

Waeber, Gerard, Calandra, Thierry, Roduit, Raphael, Haefliger, Jacques-Antoine, Bonny, Christophe, Thompson, Nancy, Thorens, Bernard, Temler, Evelyne, Meinhardt, Andreas, Bacher, Michael, Metz, Christine N., Picod, Pascal, and Bucala, Richard

Subjects
Type 1 diabetes -- Research, Pancreatic beta cells -- Analysis, Genetic regulation -- Research, Cytokines -- Physiological aspects, Science and technology
Abstract

Macrophage migration inhibitory factor (MIF), originally identified as a cytokine secreted by T lymphocytes, was found recently to be both a pituitary hormone and a mediator released by immune cells in response to glucocorticoid stimulation. We report here that the insulin-secreting [Beta] cell of the islets of Langerhans expresses MIF and that its production is regulated by glucose in a time- and concentration-dependent manner. MIF and insulin colocalize by immunocytochemistry within the secretory granules of the pancreatic islet [Beta] cells, and once released, MIF appears to regulate insulin release in an autocrine fashion. In perifusion studies performed with isolated rat islets, immunoneutralization of MIF reduced the first and second phase of the glucose-induced insulin secretion response by 39% and 31%, respectively. Conversely, exogenously added recombinant MIF was found to potentiate insulin release. Constitutive expression of MIF antisense RNA in the insulin-secreting INS-1 cell line inhibited MIF protein synthesis and decreased significantly glucose-induced insulin release. MIF is therefore a glucose-dependent, islet cell product that regulates insulin secretion in a positive manner and may play an important role in carbohydrate metabolism.

Published
1997

161. Glucose transporters in the regulation of intestinal, renal, and liver glucose fluxes

Author

Thorens, Bernard

Subjects
Glucose metabolism -- Research, Carrier proteins -- Research, Biological sciences
Abstract

The five types of hexose transporters are directly involved in glucose homeostasis and are thus ubiquitously found in all types of tissues. Meanwhile, GLUT-2 is more numerous in liver, intestine and kidney tissues where they regulate extremes in glucose concentration and are, in turn, regulated by hormones. The affinity of GLUT-2 for its substrate is directly influenced by an increase blood glucose.

Published
1996

162. Deletion of Sirt3 does not affect atherosclerosis but accelerates weight gain and impairs rapid metabolic adaptation in LDL receptor knockout mice: implications for cardiovascular risk factor development

Author

Winnik, Stephan, Gaul, Daniel, Preitner, Frédéric, Lohmann, Christine, Weber, Julien, Miranda, Melroy, Liu, Yilei, van Tits, Lambertus, Mateos, José, Brokopp, Chad, Auwerx, Johan, Thorens, Bernard, Lüscher, Thomas, Matter, Christian, Winnik, Stephan, Gaul, Daniel, Preitner, Frédéric, Lohmann, Christine, Weber, Julien, Miranda, Melroy, Liu, Yilei, van Tits, Lambertus, Mateos, José, Brokopp, Chad, Auwerx, Johan, Thorens, Bernard, Lüscher, Thomas, and Matter, Christian

Abstract

Sirt3 is a mitochondrial NAD+-dependent deacetylase that governs mitochondrial metabolism and reactive oxygen species homeostasis. Sirt3 deficiency has been reported to accelerate the development of the metabolic syndrome. However, the role of Sirt3 in atherosclerosis remains enigmatic. We aimed to investigate whether Sirt3 deficiency affects atherosclerosis, plaque vulnerability, and metabolic homeostasis. Low-density lipoprotein receptor knockout (LDLR −/−) and LDLR/Sirt3 double-knockout (Sirt3 −/− LDLR −/−) mice were fed a high-cholesterol diet (1.25% w/w) for 12weeks. Atherosclerosis was assessed en face in thoraco-abdominal aortae and in cross sections of aortic roots. Sirt3 deletion led to hepatic mitochondrial protein hyperacetylation. Unexpectedly, though plasma malondialdehyde levels were elevated in Sirt3-deficient mice, Sirt3 deletion affected neither plaque burden nor features of plaque vulnerability (i.e., fibrous cap thickness and necrotic core diameter). Likewise, plaque macrophage and T cell infiltration as well as endothelial activation remained unaltered. Electron microscopy of aortic walls revealed no difference in mitochondrial microarchitecture between both groups. Interestingly, loss of Sirt3 was associated with accelerated weight gain and an impaired capacity to cope with rapid changes in nutrient supply as assessed by indirect calorimetry. Serum lipid levels and glucose tolerance were unaffected by Sirt3 deletion in LDLR −/− mice. Sirt3 deficiency does not affect atherosclerosis in LDLR −/− mice. However, Sirt3 controls systemic levels of oxidative stress, limits expedited weight gain, and allows rapid metabolic adaptation. Thus, Sirt3 may contribute to postponing cardiovascular risk factor development.

Published
2019

166. Heterogeneous secretion of individual B cells in response to D-glucose and to nonglucidic nutrient secretagogues

Author

Bosco, Domenico, Meda, Paolo, Thorens, Bernard, and Malaisse, Willy J.

Subjects
Insulin -- Research, Glutamate -- Research, Hemolysis and hemolysins -- Research, Biological sciences
Abstract

The response of pancreatic B cells to 2-amino bicyclo(2,2,1)heptane-2-carboxilic acid, glucose and nonmetabolized analogue of L-leucine insinvestigated by using a hemolytic plaque assay. The study reveals that the characterisitics and functioning of B cells are independent of the various stages of glucose metabolism.

Published
1995

170. Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits

Author

Canessa, Cecilia M., Schild, Laurent, Buell, Gary, Thorens, Bernard, Gautschi, Ivan, Horisberger, Jean-Daniel, and Rossier, Bernard C.

Subjects
Sodium channels -- Research, Xenopus -- Research, Absorption (Physiology) -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Alpha, beta and gamma subunits of the rat epithelial sodium channel and mec-4, mec-10 and deg 1 proteins belong to a new gene family which controls cellular volume. The epithelial Na+ channel is sensitive to amiloride and has ion-selective permeability, gating properties and pharmacological profile, decided by the coexpression of component subunits. The gene family may also be crucial for mechano-sensitive ion channels in various organisms and animal cells.

Published
1994

173. GLUT2 surface expression and intracellular transport via the constitutive pathway in pancreatic beta cells and insulinoma: evidence for a block in trans-golgi network exit by brefeldin A

Author

Thorens, Bernard, Gerard, Nadine, and Deriaz, Nathalie

Subjects
Pancreatic beta cells -- Analysis, Glutamate -- Research, Pancreatic tumors, Golgi apparatus -- Observations, Biological transport -- Analysis, Biological sciences
Abstract

An analysis of the biosynthesis, intracellular transport and surface expression of the beta cell glucose transporter GLUT2 in isolated islets and insulinoma cells confirms that the constitutive route effects this expression. Brefeldin A (BFA) can inhibit transport and surface expression of the transporter at two separate stages. The half-time needed for transport from the trans-Golgi networks (TGN) to the plasma membrane was homologous to the 15-minute half-time transport from the endoplasmic reticulum to the TGN.

Published
1993

177. Expression cloning of the pancreatic beta cell receptor for the gluco-incretin hormone glucagon-like peptide 1

Author

Thorens, Bernard

Subjects
Hormone receptors -- Genetic aspects, Pancreatic beta cells -- Physiological aspects, Type 2 diabetes -- Research, G proteins -- Research, Science and technology
Abstract

The isolation of cDNA for the glucagon-like peptide 1 (GLP-1) receptor was performed using transient expression of a rat pancreatic islet cDNA library into COS cells. The receptor binds to GLP-1 with high affinity and is coupled to activation of adenylate cyclase. It is specific for GLP-1 and does not bind glucagon, gastric inhibitory peptide, vasoactive intestinal peptide or secretin. The receptor contains 463 amino acids and seven transmembrane domains.

Published
1992

182. GLP-1(9-36) mediates the glucagonostatic effect of GLP-1 by promiscuous activation of the glucagon receptor

Author

Guida, Claudia, primary, Miranda, Caroline, additional, Asterholm, Ingrid Wernstedt, additional, Basco, Davide, additional, Benrick, Anna, additional, Chanclon, Belen, additional, Chibalina, Margarita V., additional, Harris, Matthew, additional, Kellard, Joely, additional, McCulloch, Laura J., additional, Real, Joana, additional, Rorsman, Nils J.G., additional, Yeung, Ho Yan, additional, Reimann, Frank, additional, Shigeto, Makoto, additional, Clark, Anne, additional, Thorens, Bernard, additional, Rorsman, Patrik, additional, Ladds, Graham, additional, and Ramracheya, Reshma, additional

Published
2019
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185. Hypothalamic CDK4 Regulates Thermogenesis by Modulating the Sympathetic Innervation and Activation of Brown Adipose Tissue

Author

Castillo-Armengol, Judit, primary, Barquissau, Valentin, additional, Ji, Honglei, additional, Severi, Ilenia, additional, Venema, Wiebe, additional, Aria-Fernandez, Eric, additional, Moret, Catherine, additional, Nasrallah, Anita, additional, Martinez-Carreres, Laia, additional, Niederhäuser, Guy, additional, Seoane-Collazo, Patricia, additional, Lagarrigue, Sylviane, additional, López, Miguel, additional, Giordano, Antonio, additional, Croizier, Sophie, additional, Thorens, Bernard, additional, Lopez Mejia, Isabel C., additional, and Fajas, Lluis, additional

Published
2019
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186. A Single Dose of Oral Metformin Reduces the Post-Prandial Glucose Response Through a Transient Modulation of Apical Sodium-Glucose Co-Transporter

Author

Zubiaga, Lorea, primary, Briand, Olivier, additional, Auger, Florent, additional, Touche, Veronique, additional, Hubert, Thomas, additional, Thévenet, Julien, additional, Marciniak, Camille, additional, Quenon, Audrey, additional, Bonner, Caroline, additional, Raverdy, Violeta, additional, Daoudi, Mehdi, additional, Kerr-Conte, Julie, additional, Pasquetti, Gianni, additional, Koepsell, Hermann, additional, Zdzieblo, Daniela, additional, Müehlemanns, Markus, additional, Thorens, Bernard, additional, Delzenne, Nathalie, additional, Bindels, Laure, additional, Deprez, Benoit, additional, Vatyghem, Marie C., additional, Laferrère, Blandine, additional, Staels, Bart, additional, Damien, Huglo, additional, Lestavel, Sophie, additional, and Pattou, Francois, additional

Published
2019
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189. No development of hypertension in the hyperuricemic liver-Glut9 knockout mouse

Author

Preitner Frederic, Pimentel Anabela, Metref Salima, Berthonneche Corinne, Sarre Alexandre, Moret Catherine, Rotman Samuel, Centeno Gabriel, Firsov Dmitri, and Thorens Bernard

Subjects
medicine.medical_specialty, Glucose Transport Proteins, Facilitative, Renal function, Blood Pressure, Hyperuricemia, 030204 cardiovascular system & hematology, Kidney, 03 medical and health sciences, 0302 clinical medicine, Insulin resistance, Heart Rate, Internal medicine, medicine, Animals, Inosine, 030304 developmental biology, Mice, Knockout, 0303 health sciences, biology, business.industry, medicine.disease, 3. Good health, Mice, Inbred C57BL, Disease Models, Animal, Endocrinology, Blood pressure, Nephrology, Echocardiography, Knockout mouse, biology.protein, business, Dyslipidemia, SLC2A9, medicine.drug
Abstract

© 2014 International Society of Nephrology. Urate is the metabolic end point of purines in humans. Although supra physiological plasma urate levels are associated with obesity insulin resistance dyslipidemia and hypertension a causative role is debated. We previously established a mouse model of hyperuricemia by liver specific deletion of Glut9 a urate transporter that provides urate to the hepatocyte enzyme uricase. These LG9 knockout mice show mild hyperuricemia (120 µmol/l) which can be further increased by the urate precursor inosine. Here we explored the role of progressive hyperuricemia on the cardiovascular function. Arterial blood pressure and heart rate were periodically measured by telemetry over 6 months in LG9 knockout mice supplemented with incremental amounts of inosine in a normal chow diet. This long term inosine treatment elicited a progressive increase in uricemia up to 300 µmol/l; however it did not modify heart rate or mean arterial blood pressure in LG9 knockout compared with control mice. Inosine treatment did not alter cardiac morphology or function measured by ultrasound echocardiography. However it did induce mild renal dysfunction as revealed by higher plasma creatinine levels lower glomerular filtration rate and histological signs of chronic inflammation and fibrosis. Thus in LG9 knockout mice inosine induced hyperuricemia was not associated with hypertension despite partial renal deficiency. This does not support a direct role of urate in the control of blood pressure.

Published
2015
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194. Nomenclature of the GLUT/SLC2A family of sugar/polyol transport facilitators

Author

Joost, Hans-Georg, Bell, Graeme I., Best, James D., Birnbaum, Morris J., Charron, Maureen J., Chen, Y.T., Doege, Holger, James, David E., Lodish, Harvey F., Moley, Kelle H., Moley, Jeffrey F., Mueckler, Mike, Rogers, Suzanne, Schurmann, Annette, Seino, Susumu, and Thorens, Bernard

Subjects
Physiology -- Research, Membrane proteins -- Research, Glucose -- Physiological aspects, Biological sciences
Abstract

The recent identification of several additional members of the family of sugar transport facilitators (gene symbol SLC2A, protein symbol GLUT) has created a heterogeneous and, in part, confusing nomenclature. Therefore, this letter provides a summary of the family members and suggests a systematic nomenclature for SLC2A and GLUT symbols. membrane transport; glucose transporters; glucose transporter genes

Published
2002

195. The SLC2 family of facilitated hexose and polyol transporters

Author

Uldry, Marc, Thorens, Bernard, Uldry, Marc, and Thorens, Bernard

Abstract

The SLC2 family of glucose and polyol transporters comprises 13 members, the glucose transporters (GLUT) 1-12 and the H+-myo-inositol cotransporter (HMIT). These proteins all contain 12 transmembrane domains with both the amino and carboxy-terminal ends located on the cytoplasmic side of the plasma membrane and a N-linked oligosaccharide side-chain located either on the first or fifth extracellular loop. Based on sequence comparison, the GLUT isoforms can be grouped into three classes: class I comprises GLUT1-4; class II, GLUT6, 8, 10, and 12 and class III, GLUT5, 7, 9, 11 and HMIT. Despite their sequence similarity and the presence of class-specific signature sequences, these transporters carry various hexoses and HMIT is a H+/myo-inositol co-transporter. Furthermore, the substrate transported by some isoforms has not yet been identified. Tissue- and cell-specific expression of the well-characterized GLUT isoforms underlies their specific role in the control of whole-body glucose homeostasis. Numerous studies with transgenic or knockout mice indeed support an important role for these transporters in the control of glucose utilization, glucose storage and glucose sensing. Much remains to be learned about the transport functions of the recently discovered isoforms (GLUT6-13 and HMIT) and their physiological role in the metabolism of glucose, myo-inositol and perhaps other substrates

Published
2018

196. Cloning, functional expression, and chromosomal localization of the human pancreatic islet glucose-dependent insulinotropic polypeptide receptor

Author

Gremlich, Sandrine, Porret, Andree, Hani, El Habib, Cherif, Dorra, Vionnet, Nathalie, Froguel, Philippe, and Thorens, Bernard

Subjects
Pancreatic beta cells -- Physiological aspects, Insulin -- Physiological aspects, Glucose metabolism -- Physiological aspects, Health, Physiological aspects
Abstract

Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. Here, we present the molecular characterization of the human pancreatic islet GIP receptor. cDNA clones for the GIP receptor were isolated from a human pancreatic islet cDNA library. They encoded two different forms of the receptor, which differed by a 27 amino acid insertion in the COOH-terminal cytoplasmic tail. The receptor protein sequence was 81% identical to that of the rat GIP receptor. When expressed in Chinese hamster lung fibroblasts, both forms of the receptor displayed high-affinity binding for GIP (180 and 600 pmol/l). GIP binding was displaced by, Oral absorption of glucose leads to a much greater insulin secretory response than an intravenous infusion of glucose inducing the same glycemic level (1). This increased insulin secretory response after [...]

Published
1995

197. Cloning and function expression of the human islet GLP-1 receptor: demonstration that exendin-4 is an agonist and exendin-(9-39) an antagonist of the receptor

Author

Thorens, Bernard, Porret, Andree, Buhler, Leo, Morel, Philippe, and Widmann, Christian

Subjects
Pancreas -- Secretions, Glucagon -- Genetic aspects, Health, Genetic aspects
Abstract

A complementary DNA for a glucagon-like peptide-1 receptor was isolated from a human pancreatic islet cDNA library. The isolated clone encoded a protein with 90% identity to the rat receptor. [...]

Published
1993

198. Glucagon-like peptide-I and the control of insulin secretion in the normal state and in NIDDM

Author

Thorens, Bernard and Waeber, Gerard

Subjects
Islands of Langerhans -- Physiological aspects, Pancreatic beta cells -- Physiological aspects, Type 2 diabetes -- Physiological aspects, Health, Physiological aspects
Abstract

Potentiation of glucose-induced insulin secretion by intestinal factors has been described for many years. Today, two major peptides with potent insulinotropic action have been recognized: gastric inhibitory peptide and truncated [...]

Published
1993

199. Recovery of glucose-induced insulin secretion in a rat model of NIDDM is not accompanied by return of the B-cell GLUT2 glucose transporter

Author

Chen, Chuan, Thorens, Bernard, Bonner-Weir, Susan, Weir, Gordon C., and Leahy, John L.

Subjects
Pancreas -- Secretions, Pancreatic beta cells -- Physiological aspects, Biological control systems -- Physiological aspects, Secretion -- Physiological aspects, Type 2 diabetes -- Physiological aspects, Health, Physiological aspects
Abstract

The NSTZ rat model combines loss of glucose-induced insulin secretion with a reduced amount of the high [K.sub.m] B-cell glucose transporter, GLUT2. The purpose of this study was to determine [...]

Published
1992

200. Glutamine Stimulates Biosynthesis and Secretion of Insulin-like Growth Factor 2 (IGF2), an Autocrine Regulator of Beta Cell Mass and Function

Author

Modi Honey, Cornu Marion, and Thorens Bernard

Subjects
medicine.medical_specialty, animal structures, endocrine system diseases, Glutamine, Apoptosis, 030209 endocrinology & metabolism, Biology, Biochemistry, Receptor, IGF Type 1, Mice, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Biosynthesis, Insulin-Like Growth Factor II, Insulin-Secreting Cells, Internal medicine, medicine, Animals, Insulin, Secretion, Phosphorylation, RNA, Small Interfering, Autocrine signalling, Molecular Biology, PI3K/AKT/mTOR pathway, Cell Proliferation, 030304 developmental biology, 0303 health sciences, Cell growth, Cell Biology, female genital diseases and pregnancy complications, body regions, Glucose, Sulfonylurea Compounds, Metabolism, Endocrinology, Gene Expression Regulation, chemistry, Beta cell, Proto-Oncogene Proteins c-akt, Intracellular
Abstract

© 2014 by The American Society for Biochemistry and Molecular Biology Inc. IGF2 is an autocrine ligand for the beta cell IGF1R receptor and GLP 1 increases the activity of this autocrine loop by enhancing IGF1R expression a mechanism that mediates the trophic effects of GLP 1 on beta cell mass and function. Here we investigated the regulation of IGF2 biosynthesis and secretion. We showed that glutamine rapidly and strongly induced IGF2 mRNA translation using reporter constructs transduced in MIN6 cells and primary islet cells. This was followed by rapid secretion of IGF2 via the regulated pathway as revealed by the presence of mature IGF2 in insulin granule fractions and by inhibition of secretion by nimodipine and diazoxide. When maximally stimulated by glutamine the amount of secreted IGF2 rapidly exceeded its initial intracellular pool and tolbutamide and high K+ increased IGF2 secretion only marginally. This indicates that the intracellular pool of IGF2 is small and that sustained secretion requires de novo synthesis. The stimulatory effect of glutamine necessitates its metabolism but not mTOR activation. Finally exposure of insulinomas or beta cells to glutamine induced Akt phosphorylation an effect that was dependent on IGF2 secretion and reduced cytokine induced apoptosis. Thus glutamine controls the activity of the beta cell IGF2/IGF1R autocrine loop by increasing the biosynthesis and secretion of IGF2. This autocrine loop can thus integrate changes in feeding and metabolic state to adapt beta cell mass and function.

Published
2014

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