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Your search keyword '"Berthault, Marie France"' showing total 32 results
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32 results on '"Berthault, Marie France"'

9. Sialylated Form of the Neural Cell Adhesion Molecule (NCAM): A New Tool for the Identification and Sorting of Β-Cell Subpopulations With Different Functional Activity

Author

Bernard-Kargar, Catherine, Kassis, Nadim, Berthault, Marie-France, Pralong, William, and Ktorza, Alain

Subjects
Research, Pancreatic beta cells -- Research, Diabetes research, Cell adhesion molecules -- Research, Diabetes -- Research
Abstract

A New Tool for the Identification and Sorting of Β-Cell Subpopulations With Different Functional Activity To clarify the relationship between variations in Β-cell mass and pancreatic function, we investigated the [...]

Published
2001

12. Improvement of the metabolic state in diabetic Psammomys obesus with S 23521: a new glucagon-like peptide 1 analog

Author

Leibowitz, Gil, Uckaya, Gokhan, Delagrange, Philippe, Chavanieu, Alain, Grassy, Gerard, Berthault, Marie-France, Ktorza, Alain, Cerasi, Erol, and Kaiser, Nurit

Subjects
Diagnosis, Care and treatment, Risk factors, Diabetes research, Diabetes mellitus -- Risk factors -- Diagnosis -- Care and treatment, Diabetes -- Risk factors -- Diagnosis -- Care and treatment -- Research
Abstract

Gil Leibowitz, (1) Gokhan Uckaya, (1) Philippe Delagrange, (2) Alain Chavanieu, (3) Gerard Grassy, (3) Marie-France Berthault, (4) Alain Ktorza, (4,5) Erol Cerasi, (1) Nurit Kaiser (1) From the (1) [...], Glucagon-like peptide (GLP)-1 analogs are considered potential drugs for type 2 diabetes. We studied the effect of a novel GLP-1 analog, S 23521 [([a.sup.8]-des [R.sup..36]) GLP-1-(7-37)-NH], on the progression of diabetes in the Psammomys obesus model of type 2 diabetes. Animals with marked hyperglycemia were given twice-daily injections of 100 µg/kg S 23521 for 15 days. Food intake was decreased in S 23251-treated P. obesus; however, there was no significant difference in body weight from controls. Progressive worsening of hyperglycemia was noted in controls, as opposed to maintenance of pretreatment glucose levels in the S 23521 group. Treated animals had higher serum insulin, insulinogenic index, and leptin, whereas plasma triglyceride and FFA levels were decreased. S 23521 induced a fivefold increase in pancreatic insulin content. Immunohistochemical analysis showed islet degranulation with disrupted morphology in untreated animals, whereas islets from S 23521-treated animals appeared intact and filled with insulin; β-cell apoptosis was ~70% reduced, without change in β-cell proliferation, resulting in a twofold increase in relative β-cell volume. Thus, S 23521 prevented the progression of diabetes in Psammomys obesus with marked improvement of the metabolic profile, pancreatic insulin reserve, and β-cell mass. These effects emphasize the feasibility of preventing metabolic deterioration over time in type 2 diabetes.

Published
2005

15. Dynamic changes in {beta}-cell mass and pancreatic insulin during the evolution of nutrition-dependent diabetes in psammomys obesus: impact of glycemic control.

Author

Kaiser, Nurit, Yuli, Michal, Uçkaya, Gökhan, Oprescu, Andrei I, Berthault, Marie-France, Kargar, Catherine, Donath, Marc Y, Cerasi, Erol, and Ktorza, Alain

Abstract

Recent studies ascribe a major role to pancreatic beta-cell loss in type 2 diabetes. We investigated the dynamics of beta-cell mass during diabetes evolution in Psammomys obesus, a model for nutrition-dependent type 2 diabetes, focusing on the very early and the advanced stages of the disease. P. obesus fed a high-calorie diet for 26 days developed severe hyperglycemia, beta-cell degranulation, and markedly reduced pancreatic insulin content. Reducing calories for 7 days induced normoglycemia in 90% of the animals, restoring beta-cell granulation and insulin content. To dissociate effects of diet from blood glucose reduction, diabetic animals received phlorizin for 2 days, which normalized glycemia and increased the pancreatic insulin reserve to 50% of control, despite a calorie-rich diet. During diabetes progression, beta-cell mass decreased initially but recovered spontaneously to control levels, despite persistent hyperglycemia. Strikingly, however, beta-cell mass did not correlate with degree of hyperglycemia or pancreatic insulin content. We conclude that reduced insulin reserve is the main cause of diabetes progression, whereas irreversible beta-cell mass reduction is a late event in P. obesus. The rapid recovery of the pancreas by phlorizin-induced normoglycemia implies a causal relationship between hyperglycemia and islet dysfunction. Similar mechanisms could be operative during the evolution of type 2 diabetes in humans. [ABSTRACT FROM AUTHOR]

Published
2005
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16. Role of Glucose in IRS Signaling in Rat Pancreatic Islets: Specific Effects and Interplay with Insulin

Author

Maryline Paris, Catherine Bernard-Kargar, Nadim Kassis, Alain Ktorza, José Vilar, Berthault, Marie France, Laboratoire de physiopathologie de la nutrition (LPN), and Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7)

Subjects
Blood Glucose, Male, medicine.medical_specialty, Insulin Receptor Substrate Proteins, medicine.medical_treatment, 030209 endocrinology & metabolism, In Vitro Techniques, Biology, Islets of Langerhans, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, medicine, Diazoxide, Animals, Hypoglycemic Agents, Insulin, RNA, Messenger, Phosphorylation, Rats, Wistar, 030304 developmental biology, 0303 health sciences, Messenger RNA, geography, geography.geographical_feature_category, Pancreatic islets, Osmolar Concentration, Intracellular Signaling Peptides and Proteins, General Medicine, Phosphoproteins, Islet, Rats, Endocrinology, medicine.anatomical_structure, Signal transduction, Research Article, Signal Transduction, medicine.drug
Abstract

We investigated the possible interplay between insulin and glucose signaling pathways in rat pancreaticβ-cell with a special focus on the role of glucose in IRS signalingin vivo. Three groups of rats were constituted by combining simultaneous infusion during 48 h either of glucose and/or insulin, or glucose+diazoxide: Hyperglycemic- Hyperinsulinemic (HGHI), euglycemic-Hyperinsulinemic (eGHI), Hyperglycemic-euinsulinemic (HGeI). Control rats were infused with 0,9% NaCl. In HGHI and HGeI rats plasma glucose levels were maintained at 20-22 mmol/l. In eGHI rats, plasma glucose was not different from that of controls, whereas plasma insulin was much higher than in controls. In HGHI rats, IRS-2 mRNA expression, total protein and phosphorylated protein amounts were increased compared to controls. In HGeI rats, only IRS-2 mRNA expression was increased. No change was observed in eGHI rats whatever the parameter considered. In all groups, mRNA concentration of IRS-1 was similar to that of controls. The quantity of total and phosphorylated IRS- 1 protein was dramatically increased in HGHI rats and to a lesser extent in eGHI rats. Neither mRNA nor IRS-1 protein expression were modified in HGeI rats. The data suggest that glucose and insulin play at once a specific and a complementary role in islet IRSs signaling. Especially, glucose stimulates IRS-2 mRNA expression whatever the insulin status and independently of the secretory process. The differential regulation of IRS-1 and IRS-2 expressions is in agreement with their supposed different involvement in the control ofβ-cell growth and function.

Published
2004
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19. Senseurs d'acide gras et controle nerveux de lhomé

Author

Cruciani-Guglielmacci, C., Migrenne, S., Clément, L., Magnan, Christophe, Laboratoire de physiopathologie de la nutrition (LPN), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), and Berthault, Marie France

Published
2006

20. Lipotoxicité et insulino-résistance

Author

Magnan, Christophe, Laboratoire de physiopathologie de la nutrition (LPN), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), and Berthault, Marie France

Published
2006

21. Contribution d'un disfonctionnement hypo

Author

Cruciani-Guglielmacci, C., christophe magnan, Berthault, Marie France, Laboratoire de physiopathologie de la nutrition (LPN), and Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7)

Published
2005

22. Les circuits cérébraux de l'appétit

Author

Cruciani-Guglielmacci, C., Magnan, Christophe, Laboratoire de physiopathologie de la nutrition (LPN), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), and Berthault, Marie France

Published
2005

23. Quantitative trait locus dissection in congenic strains of the Goto-Kakizaki rat identifies a region conserved with diabetes loci in human chromosome 1q

Author

Stephan C. Collins, Dominique Gauguier, Marie-Thérèse Bihoreau, Alain Ktorza, Karène Argoud, Peng Y. Woon, Karin J. Wallace, Robert H. Wallis, Pamela J. Kaisaki, Laboratoire de physiopathologie de la nutrition (LPN), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), and Berthault, Marie France

Subjects
Male, Transcription, Genetic, Physiology, Sequence analysis, Quantitative Trait Loci, Congenic, 030209 endocrinology & metabolism, Genomics, Biology, Quantitative trait locus, 03 medical and health sciences, 0302 clinical medicine, Inbred strain, Animals, Congenic, Hyperinsulinism, Rats, Inbred BN, Glucose Intolerance, Insulin Secretion, Genetics, Animals, Humans, Insulin, Conserved Sequence, Crosses, Genetic, 030304 developmental biology, 2. Zero hunger, Comparative genomics, 0303 health sciences, Polymorphism, Genetic, Gene Expression Profiling, Body Weight, Chromosome, Rats, Inbred Strains, Sequence Analysis, DNA, Lipids, Rats, Gene expression profiling, Glucose, Phenotype, Diabetes Mellitus, Type 2, Chromosomes, Human, Pair 1, Female
Abstract

Genetic studies in human populations and rodent models have identified regions of human chromosome 1q21–25 and rat chromosome 2 showing evidence of significant and replicated linkage to diabetes-related phenotypes. To investigate the relationship between the human and rat diabetes loci, we fine mapped the rat locus Nidd/ gk2 linked to hyperinsulinemia in an F2 cross derived from the diabetic (type 2) Goto-Kakizaki (GK) rat and the Brown Norway (BN) control rat, and carried out its genetic and pathophysiological characterization in BN.GK congenic strains. Evidence of glucose intolerance and enhanced insulin secretion in a congenic strain allowed us to localize the underlying diabetes gene(s) in a rat chromosomal interval of ∼3–6 cM conserved with an 11-Mb region of human 1q21–23. Positional diabetes candidate genes were tested for transcriptional changes between congenics and controls and sequence variations in a panel of inbred rat strains. Congenic strains of the GK rats represent powerful novel models for accurately defining the pathophysiological impact of diabetes gene(s) at the locus Nidd/ gk2 and improving functional annotations of diabetes candidates in human 1q21–23.

Published
2004

25. Insulinotropic agent ID-1101(4-hydroxyisoleucine)activates insulin signaling in rat

Author

Broca, C., Cruciani-Guglielmacci, C., Manteghetti, M., Rouault, C., Derouet, M., Rizkalla, S., Pau, B., Petit, P., Ribes, G., Rizkalla, G., Ktorza, Alain, Gross, R., Reach, G., Taouis, M., Laboratoire de physiopathologie de la nutrition (LPN), Centre National de la Recherche Scientifique (CNRS)-Université Paris Diderot - Paris 7 (UPD7), and Berthault, Marie France

Published
2004

32. Specific and combined effects of insulin and glucose on functional pancreatic beta-cell mass in vivo in adult rats.

Author

Paris M, Bernard-Kargar C, Berthault MF, Bouwens L, and Ktorza A

Subjects
Age Factors, Animals, Apoptosis drug effects, Blood Glucose, Cell Division drug effects, Cell Size, Drug Interactions, Hyperglycemia chemically induced, Hyperglycemia pathology, Hyperinsulinism chemically induced, Hyperinsulinism pathology, Hypoglycemic Agents analysis, Hypoglycemic Agents blood, In Vitro Techniques, Insulin analysis, Insulin blood, Islets of Langerhans chemistry, Male, Rats, Rats, Wistar, Glucose pharmacology, Hypoglycemic Agents pharmacology, Insulin pharmacology, Islets of Langerhans cytology, Islets of Langerhans metabolism
Abstract

We investigated the specific and associated effects of insulin and glucose on beta-cell growth and function in adult rats. By combining simultaneous infusion either of glucose and/or insulin or glucose and diazoxide, three groups of rats were constituted: hyperglycemic-hyperinsulinemic rats (high glucose-high insulin), hyperglycemic-euinsulinemic rats (high glucose), and euglycemic-hyperinsulinemic rats (high insulin). All the infusions lasted 48 h. Control rats were infused with 0.9% NaCl (saline controls). In all groups, beta-cell mass was significantly increased, compared with controls (by 70% in high glucose-high insulin rats, 65% in high glucose rats, and 50% in high insulin rats). The stimulation of neogenesis was suggested by the high number of islets budding from pancreatic ducts in high glucose-high insulin and high glucose rats and by the presence of numerous clusters of few beta-cells within the exocrine pancreas in high insulin rats. beta-Cell hypertrophy was observed only in high glucose-high insulin rats. The rate of beta-cell proliferation was similar to that of controls in high glucose-high insulin rats after a 48-h glucose infusion, dropped dramatically in high insulin rats, and dropped to a lesser extent in high glucose rats. In high glucose-high insulin and high glucose rats, beta-cell mass increase was related to a higher beta-cell responsiveness to glucose in vitro as measured by islet perifusion studies, whereas in high insulin rats, no significant enhancement of glucose induced insulin secretion could be noticed. The data show that glucose and insulin may have specific stimulating effects on beta-cell growth and function in vivo in adult rats independently of the influence they exert each other on their respective plasma concentration.

Published
2003
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