Добірка наукової літератури з теми "L'homéostatie du glucose"
Оформте джерело за APA, MLA, Chicago, Harvard та іншими стилями
Ознайомтеся зі списками актуальних статей, книг, дисертацій, тез та інших наукових джерел на тему "L'homéostatie du glucose".
Біля кожної праці в переліку літератури доступна кнопка «Додати до бібліографії». Скористайтеся нею – і ми автоматично оформимо бібліографічне посилання на обрану працю в потрібному вам стилі цитування: APA, MLA, «Гарвард», «Чикаго», «Ванкувер» тощо.
Також ви можете завантажити повний текст наукової публікації у форматі «.pdf» та прочитати онлайн анотацію до роботи, якщо відповідні параметри наявні в метаданих.
Статті в журналах з теми "L'homéostatie du glucose":
Vande Walle, J., A. Raes, D. Castillo, and N. Lutz Dettinger. "Dialyse péritonéale aiguë : étude de la combinaison glucose-acides aminés sur l'homéostasie du glucose et la nutrition." Archives de Pédiatrie 4, no. 12 (December 1997): 1275. http://dx.doi.org/10.1016/s0929-693x(97)82651-6.
Fioramonti, X., C. Chrétien, C. Fenech, F. Liénard, S. Grall, R. Bergès, L. Pénicaud, and C. Leloup. "CO-48: Les canaux TRPC3 de l'hypothalamus jouent un rôle fondamental dans la détection cérébrale du glucose et l'homéostasie énergétique." Diabetes & Metabolism 42 (March 2016): A15. http://dx.doi.org/10.1016/s1262-3636(16)30066-0.
Дисертації з теми "L'homéostatie du glucose":
Acosta, Montalvo Ana. "The Role of Hepatocyte-Nuclear-Factor-1-A (HNF1A) in the Regulation of Glucose Homeostasis and Pancreatic Hormone Secretion." Electronic Thesis or Diss., Université de Lille (2022-....), 2022. http://www.theses.fr/2022ULILS043.
Hepatocyte-nuclear-factor-1-alpha (HNF1A) is a key transcription factor that regulates the expression of numerous genes involved in several metabolic processes such as in the liver, intestine, kidney, and pancreas. Heterozygous mutations in the HNF1A gene causes the most frequent form of monogenic diabetes called Maturity-onset-diabetes-of-the-young (MODY), commonly referred to as HNF1A-MODY. HNF1A-MODY mutation carriers develop mild-hyperglycemia in childhood and diabetes later in life due to a progressive loss of beta cell function. However, since HNF1A is not only expressed in pancreatic beta cells, but also in alpha and delta cells, this thesis project was carried out to study the effect of HNF1A deficiency on intra-islet paracrine secretion, accompanied by alterations in genes encoding proteins that control glucose uptake and metabolism. To do so, I used cellular and mouse models of HNF1A-MODYdiabetes.The first cellular model I used was the beta-cell-derived rat insulinoma INS-1 cell line to conditionally overexpress the frameshift P291fsinsC mutation in the HNF1A gene(HNF1A-P291fsinsC), using a reverse tetracycline-dependent transactivator system. The expression of the P291fsinsC mutant protein was maximally induced to a significant level over that of endogenous Hnf1a by treating the cells with 500 ng/ml of doxycycline for (2 to 72 hrs). Non-induced INS-1 cells served as a control. Since INS-1 cells were previously reported to be bi-hormonal and did not express alpha cellmarkers, I utilized this model to study the effect of the HNF1A-P291fsinsC mutation on insulin and glucagon gene and protein expression and secretion. Cytometric and immunofluorescence analysis revealed that INS-1 cells comprised mostly of insulinpositivecells, whereas only a few cells co-expressed insulin and glucagon. However,both mature and immature beta cells secreted insulin and glucagon in response to glucose stimulation. Moreover, the overexpression of the HNF1A-P291fsinsC mutant protein increased proglucagon-derived peptide expression and glucagon secretion inresponse to high-glucose stimulation compared to non-induced INS-1 cells. These findings suggest that Hnf1A is essential to maintain beta cell maturation and function.Although INS-1 cells are a valuable tool to study beta-cell function, they do not resemble human islet cells in terms of paracrine signaling. Therefore, I developed an in vitro model by transfecting human islets with siRNAs targeting HNF1A (siHNF1A). I used islets deficient in HNF1A to investigate its effects on glucose transport and hormone secretion, simultaneously from the same donor islet preparations. siHNF1A transfections significantly decreased HNF1A protein levels compared to scrambled controls, observed by Western Blot analysis. siHNF1A also reduced insulin protein expression and secretion in response to high-glucose stimulation. This coincided with reduction in SGLT2 protein levels, with no changes in SGLT1, but a slight decrease inGLUT2. The decrease in SGLT2 was also associated with a significant increase inglucagon protein expression and secretion. These findings highlighted that HNF1A is also a key regulator of alpha cell function.Two HNF1A-MODY mouse models have previously been developed to study the pathogenesis of HNF1A-MODY in vivo. The first was a global Hnf1a-/- knock-out (KO) mouse and the second was a transgenic mouse that overexpresses the dominant-negative human mutant protein specifically in pancreatic beta cells, under the rat insulin promoter [...]
Lanfray, Damien. "Rôle des endozépines dans la régulation hypothalamique de l'homéostasie énergétique." Rouen, 2010. http://www.theses.fr/2010ROUENR11.
Diazepam-binding inhibitor (DBI) is a polypeptide exclusively produced by astroglials cells in CNS. DBI and its maturation products including the octadecaneuropeptide (ODN) are collectively termed endozepines. ODN is a potent anorexigenic factor which exerts opposite actions on hypothalamic NPY and POMC neurons. We show that a 18-h fasting markedly reduce mRNA DB1 levels in hypothalamic astroglials cells. This effect cannot be reversed by peripheral injection of insulin or leptin. In contrast, central administration of glucose partially reverses food deprivation-induced decrease of DB1 expression. In addition, glucose induces endozepine release from hypothalamic explants. Anorexigenic effect of central or peripheral administration of glucose is relayed by activation of ODN metabotropic receptor and stimulation of POMC neurons. Hyperphagic effect of central glucoprivation, mimicked by 2-deoxyglucose, is abolished by injection of ODN analogue. Moreover, show for the first time that central endozepines exert an hypoglycemic tonus. Finally, in vitro preliminary studies suggest that glucose induces an increase of DBI gene promoter activity through activation of the hexosamine biosynthetic pathway, a branch pathway of glycolysis which is strongly active in hypothalamus. Altogether these data suggest that endozepines produced by hypothalamic astroglial cells are essential for central glucosensing and are involved in control of whole-body glucose homeostasis
Steiler, Tatiana L. "Cascades de signalisation dans la régulation de l'homéostasie du glucose." Paris 6, 2005. http://www.theses.fr/2005PA066111.
Cruciani-Guglielmacci, Céline. "Régulation de l'homéostasie glucidique par les lipides : effets centraux et périphériques." Paris 7, 2004. http://www.theses.fr/2004PA077042.
Marsollier, Nicolas. "Rôle des lipides et du monoxyde d'azote dans la régulation hypothalamique de l'homéostasie glucidique chez le rat : aspects adaptatifs et physiologiques." Paris 7, 2009. http://www.theses.fr/2009PA077253.
The control of energy homeostasis- determinate as steady-state between energy expenditure and energy intake/stored- is essential in survival of an organism. Therefore several parameters have to be intimately regulated on short and long term period, to maintain energy balance. Homeostasis depends on existence of a whole neural network, informing central nervous System on environmental and nutritional status variations. Hypothalamus is one of cerebral structure that integrates peripheral signals, partly through detection of circulating nutrients, and hormones. There are nutrients sensing neurons inserted in neural circuit of energy homeostasis regulation, and the study of mechanisms involved in nutrient detection, and the outcome of an overload, is decisive in the comprehension of central metabolic disorders onset. In the frame of this work we focus on hypothalamic lipid sensing, and we dispose of an animal model where only brain micro circulation lipids concentration is increased. This allows us to discriminate between peripheral and central effects. In this model, we show that nitric oxide (NO) production is an intermediary of central lipid effects on energy homeostasis. In a second part of this work, we study the role of plasma-elevated lipid concentration in physiological situation of 24hr fasting-induced lipolysis. We observed that a systemic inhibition of lipolysis increases food intake after refeeding and modifies insulin sensitivity, and that restoration of central circulating lipids is sufficient to reverse lipolysis inhibition effects. Descriptions of central mechanisms and molecular actors highlighted could permit, at least, to find new therapeutic targets
O'Connor, Sarah. "L'effet d'une consommation augmentée de produits laitiers sur l'homéostasie du glucose et les profils métabolomiques chez des sujets hyperinsulinémiques." Master's thesis, Université Laval, 2019. http://hdl.handle.net/20.500.11794/35722.
Observational evidences suggest an association between dairy product intake and a reduced risk of developing type 2 diabetes. However, results from clinical studies remain controversial, notably due to large interindividual variability in response to dairy products. Further, clinical studies using objective dietary biomarkers to assess dietary intake are missing. Serum metabolite analysis using metabolomics could be a novel strategy to identify new biomarkers of dairy product intake and thus, improving accuracy of nutritional evaluations in clinical studies. The main objective of this research was to observe the effects of increased dairy product intake on type 2 diabetes related risk factors such as glycemic and insulinemic parameters, along with metabolomic profiles in hyperinsulinemic subjects. Interindividual variability in response to dairy products was also assessed as a specific objective. Results from a cross-over randomized controlled trial undertaken among 27 hyperinsulinemic adults suggest that consuming 4 servings or more of dairy products daily for 6 weeks does not affect glycemic and insulinemic parameters compared to a standard intake of dairy products (2 servings or less per day). Yet, increasing dairy intake to 4 servings or more per day increased insulin resistance compared with baseline values, without affecting insulin secretion of β-cells function. However, large inter-individual variability in response to dairy products was denoted for insulin resistance, suggesting that higher intake of dairy products might be unfavorable or beneficial depending on the individual. Further, consuming 4 servings or more of dairy products daily affected serum metabolomic profiles distinctly from consuming ≤2 servings per day, suggesting specific metabolite signature to increased dairy product intake. Additional long-term trials studying interindividual variability and using objective biomarkers of dairy intake are required to identify which individuals may really benefit from increasing dairy intake to prevent type 2 diabetes.
Turcotte, Anne-Frédérique. "Impact de la dérivation biliopancréatique sur le métabolisme osseux et son association avec les changements hormonaux et l'homéostasie du glucose." Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/40343.
Bariatric surgery is gaining in popularity as a treatment of severe obesity in Quebec and across Canada. While more than one third of patients have type 2 diabetes before bariatric surgery, a large meta-analysis reported type 2 diabetes resolution in 80% of patients after sleeve gastrectomy and Roux-in-Y gastric bypass, and in 95% of patients after biliopancreatic diversion (BPD). However, despite clear health benefits, recent evidence showed that bariatric procedures, especially Roux-in-Y gastric bypass and BPD, are associated with an increased risk of fracture. Assessment of circulating biochemical markers of bone formation and resorption after bariatric surgery could provide insight into the pathophysiology of bone fragility after surgery. More over, several mechanisms have been put forward to explain resolution of type 2 diabetes after bariatric surgery. While preclinical studies have reported that a bone-derived hormone, uncarboxylated osteocalcin (ucOCN), is involved in glucose metabolism, no study has evaluated whether changes in this hormone are associated with improvement in glucose homeostasis after bariatric surgery. Our study aimed at evaluating the early- and medium-term changes in bone remodeling markers after BPD, and whether these changes are associated with changes in whole-body (total) bone mineral density (BMD) and in hormonal factors. Furthermore, we assessed if changes in ucOCN are associated with changes in glucose homeostasis indices after BPD. We used data and frozen plasma samples from a one-year prospective cohort study where blood was drawn at 3 days, 3 months and 12 months after BPD. We showed that BPD is associated with an increase in the bone resorption marker C-telopeptide as early as 3 days after surgery, and that it continued to rise up to one year after surgery, with a greater increase in bone resorption over bone formation markers. Furthermore, a significant decrease in the bone formation marker osteocalcin was seen at 3 days after BPD, which was followed by an increase up to one year after surgery. Moreover, an inverse association between the change in bone resorption marker and the change in total BMD, as well as significant associations between the changes in several bone turnover markersand changes in hormonal factors after BPD were observed. Finally, there was a strong correlation between the increase in ucOCN and the improvement in several indices of glucose homeostasis after BPD, independent of weight loss, suggesting a link between bone and glucose metabolism.
Dumont, Martine. "Étude des changements de la tension artérielle chez la femme, associations avec les lipides plasmatiques et certains indices de l'homéostasie du glucose et de l'insuline plasmatiques." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq25303.pdf.
Perilhou, Anaïs. "Le facteur de transcription COUP-TFII, un nouvel acteur dans le contrôle de l'homéostasie glucidique dans le foie et le pancréas." Paris 5, 2008. http://www.theses.fr/2008PA05T028.
Metabolic pathways concerned in the regulation of glucose homeostasis in liver and pancreas are precisely controlled at gene level. We showed that COUP-TFII (Chicken ovalbumin upstream promoter transcription factor II) deletion from pancreatic beta cells in heterozygous mice led to abnormal insulin secretion. This work reveals that 1) COUP-TFII expression is negatively controlled by glucose and insulin in pancreatic beta cells and hepatocytes, in vivo and in vitro, via ChREBP and Foxo-1 signaling; 2) COUP-TFII inhibates insulin genes transcription, as well as insulin content and insulin secretion in beta 832/13 ENS-1 cell line, and decreases the fatty acid esterification capacity in these cells; 3) COUP-TFII and HNF-4alpha (MODY-1) activate one another their expression in pancreatic beta cells. These results conduct and argue to propose an important contribution of COUP-TFII hi the control of glucose homeostasis in the fasted state, and potentially in pathologies as type 2 diabetes
Rabhi, Nabil. "Régulation de l'homéostasie du glucose et de la sécrétion d'inuline par le cofacteur transcriptionnel KAT2B - implication dans le développement du diabète de type II : rôle de KAT2B dans la cellule β pancréatique". Thesis, Lille 2, 2016. http://www.theses.fr/2016LIL2S058.
The Endoplasmic Reticulum (ER) unfolded protein response (UPRer) pathway plays an important role for pancreatic p cells to adapt their cellular responses to environmental cues and metabolic stress. Although altered UPRer gene expression appears in rodent and human type 2 diabetic (T2D) islets, the underlying molecular mechanisms remain unknown. We show here that germ-line and p-cell specific disruption of the lysine acetyltransferase 2B (Kat2b) gene in mice leads to impaired insulin secretion and glucose intolerance. Genome wide analysis of Kat2b-regulated genes and functional assays revealed a critical role for Kat2b in maintaining UPRer gene expression and subsequent p-cell function. Importantly, Kat2b expression was decreased in db/db and in human T2D islets and correlated with UPRer genes in normal human islets. In conclusion, Kat2b is a crucial transcriptional regulator for adaptive P-cell function during metabolic stress by controlling UPRer and represents a promising target for T2D prevention and treatment