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Nurit Kaiser - One of the best experts on this subject based on the ideXlab platform.
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diet induced diabetes in the sand rat Psammomys obesus
Methods of Molecular Biology, 2012Co-Authors: Nurit Kaiser, Erol Cerasi, Gil LeibowitzAbstract:Insulin deficiency is the underlying cause of hyperglycemia in type 2 diabetes. The gerbil Psammomys obesus (P. obesus) is a naturally insulin resistant rodent with tendency to develop diet-induced hyperglycemia associated with obesity. P. obesus does not exhibit hyperglycemia in its natural desert habitat, feeding on low caloric vegetation. However, when fed regular laboratory chow containing higher caloric density, the animals develop moderate obesity and hyperglycemia. Diabetes development and progression is very fast in P. obesus. The animals reach the irreversible hypoinsulinemic stage of the disease, in which a marked reduction of β-cell mass is apparent, within 4-6 weeks of high caloric diet. The present review describes the P. obesus of the Hebrew University colony, with emphasis on its use for the study of β-cell dysfunction in type 2 diabetes.
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Psammomys obesus a model for environment gene interactions in type 2 diabetes
Diabetes, 2005Co-Authors: Nurit Kaiser, Rafael Nesher, Erol Cerasi, Marc Y Donath, Merav Fraenkel, Vered Behar, Christophe Magnan, Alain Ktorza, Gil LeibowitzAbstract:Type 2 diabetes is characterized by insulin resistance and progressive beta-cell failure. Deficient insulin secretion, with increased proportions of insulin precursor molecules, is a common feature of type 2 diabetes; this could result from inappropriate beta-cell function and/or reduced beta-cell mass. Most studies using tissues from diabetic patients are retrospective, providing only limited information on the relative contribution of beta-cell dysfunction versus decreased beta-cell mass to the "beta-cell failure" of type 2 diabetes. The gerbil Psammomys obesus is a good model to address questions related to the role of insulin resistance and beta-cell failure in nutritionally induced diabetes. Upon a change from its natural low-calorie diet to the calorie-rich laboratory food, P. obesus develops moderate obesity associated with postprandial hyperglycemia. Continued dietary load, superimposed on its innate insulin resistance, results in depletion of pancreatic insulin stores, with increased proportions of insulin precursor molecules in the pancreas and the blood. Inadequate response of the preproinsulin gene to the increased insulin needs is an important cause of diabetes progression. Changes in beta-cell mass do not correlate with pancreatic insulin stores and are unlikely to play a role in disease initiation and progression. The major culprit is the inappropriate insulin production with depletion of insulin stores as a consequence. Similar mechanisms could operate during the evolution of type 2 diabetes in humans.
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dynamic changes in β cell mass and pancreatic insulin during the evolution of nutrition dependent diabetes in Psammomys obesus impact of glycemic control
Diabetes, 2005Co-Authors: Nurit Kaiser, Erol Cerasi, Marc Y Donath, Michal Yuli, Gokhan Uckaya, Andrei I Oprescu, Mariefrance Berthault, Catherine Kargar, Alain KtorzaAbstract:Recent studies ascribe a major role to pancreatic β-cell loss in type 2 diabetes. We investigated the dynamics of β-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, β-cell degranulation, and markedly reduced pancreatic insulin content. Reducing calories for 7 days induced normoglycemia in 90% of the animals, restoring β-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, β-cell mass decreased initially but recovered spontaneously to control levels, despite persistent hyperglycemia. Strikingly, however, β-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 β-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.
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Increased glucose sensitivity of stimulus-secretion coupling in islets from Psammomys obesus after diet induction of diabetes.
Diabetes, 2002Co-Authors: Jose A.g. Pertusa, Rafael Nesher, Nurit Kaiser, Erol Cerasi, Jean-claude Henquin, Jean-christophe JonasAbstract:When fed a high-energy (HE) diet, diabetes-prone (DP) Psammomys obesus develop type 2 diabetes with altered glucose-stimulated insulin secretion (GSIS). Beta-cell stimulus-secretion coupling was investigated in islets isolated from DP P. obesus fed a low-energy (LE) diet (DP-LE) and after 5 days on a HE diet (DP-HE). DP-LE islets cultured overnight in 5 mmol/l glucose displayed glucose dose-dependent increases in NAD(P)H, mitochondrial membrane potential, ATP/(ATP + ADP) ratio, cytosolic calcium concentration ([Ca(2+)](c)), and insulin secretion. In comparison, DP-HE islets cultured overnight in 10 mmol/l glucose were 80% degranulated and displayed an increased sensitivity to glucose at the level of glucose metabolism, [Ca(2+)](c), and insulin secretion. These changes in DP-HE islets were only marginally reversed after culture in 5 mmol/l glucose and were not reproduced in DP-LE islets cultured overnight in 10 mmol/l glucose, except for the 75% degranulation. Diabetes-resistant P. obesus remain normoglycemic on HE diet. Their beta-cell stimulus-secretion coupling was similar to that of DP-LE islets, irrespective of the type of diet. Thus, islets from diabetic P. obesus display an increased sensitivity to glucose at the level of glucose metabolism and a profound beta-cell degranulation, both of which may affect their in vivo GSIS.
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ipf1 pdx1 deficiency and β cell dysfunction in Psammomys obesus an animal with type 2 diabetes
Diabetes, 2001Co-Authors: Gil Leibowitz, Erol Cerasi, David J Gross, Sarah Ferber, Asa Apelqvist, Helena Edlund, Danielle Melloul, Nurit KaiserAbstract:The homeodomain transcription factor IPF1/PDX1 is required in beta-cells for efficient expression of insulin, glucose transporter 2, and prohormone convertases 1/3 and 2. Psammomys obesus, a model of diet-responsive type 2 diabetes, shows markedly depleted insulin stores when given a high-energy (HE) diet. Despite hyperglycemia, insulin mRNA levels initially remained unchanged and then decreased gradually to 15% of the basal level by 3 weeks. Moreover, insulin gene expression was not increased when isolated P. obesus islets were exposed to elevated glucose concentrations. Consistent with these observations, no functional Ipf1/Pdx1 gene product was detected in islets of newborn or adult P. obesus using immunostaining, Western blot, DNA binding, and reverse transcriptase-polymerase chain reaction analyses. Other beta-cell transcription factors (e.g., ISL-1, Nkx2.2, and Nkx6.1) were expressed in P. obesus islets, and the DNA binding activity of the insulin transcription factors RIPE3b1-Act and IEF1 was intact. Ipf1/Pdx1 gene transfer to isolated P. obesus islets normalized the defect in glucose-stimulated insulin gene expression and prevented the rapid depletion of insulin content after exposure to high glucose. Taken together, these results suggest that the inability of P. obesus islets to adapt to dietary overload, with depletion of insulin content as a consequence, results from IPF1/PDX1 deficiency. However, because not all animals become hyperglycemic on HE diet, additional factors may be important for the development of diabetes in this animal model.
Erol Cerasi - One of the best experts on this subject based on the ideXlab platform.
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diet induced diabetes in the sand rat Psammomys obesus
Methods of Molecular Biology, 2012Co-Authors: Nurit Kaiser, Erol Cerasi, Gil LeibowitzAbstract:Insulin deficiency is the underlying cause of hyperglycemia in type 2 diabetes. The gerbil Psammomys obesus (P. obesus) is a naturally insulin resistant rodent with tendency to develop diet-induced hyperglycemia associated with obesity. P. obesus does not exhibit hyperglycemia in its natural desert habitat, feeding on low caloric vegetation. However, when fed regular laboratory chow containing higher caloric density, the animals develop moderate obesity and hyperglycemia. Diabetes development and progression is very fast in P. obesus. The animals reach the irreversible hypoinsulinemic stage of the disease, in which a marked reduction of β-cell mass is apparent, within 4-6 weeks of high caloric diet. The present review describes the P. obesus of the Hebrew University colony, with emphasis on its use for the study of β-cell dysfunction in type 2 diabetes.
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Psammomys obesus a model for environment gene interactions in type 2 diabetes
Diabetes, 2005Co-Authors: Nurit Kaiser, Rafael Nesher, Erol Cerasi, Marc Y Donath, Merav Fraenkel, Vered Behar, Christophe Magnan, Alain Ktorza, Gil LeibowitzAbstract:Type 2 diabetes is characterized by insulin resistance and progressive beta-cell failure. Deficient insulin secretion, with increased proportions of insulin precursor molecules, is a common feature of type 2 diabetes; this could result from inappropriate beta-cell function and/or reduced beta-cell mass. Most studies using tissues from diabetic patients are retrospective, providing only limited information on the relative contribution of beta-cell dysfunction versus decreased beta-cell mass to the "beta-cell failure" of type 2 diabetes. The gerbil Psammomys obesus is a good model to address questions related to the role of insulin resistance and beta-cell failure in nutritionally induced diabetes. Upon a change from its natural low-calorie diet to the calorie-rich laboratory food, P. obesus develops moderate obesity associated with postprandial hyperglycemia. Continued dietary load, superimposed on its innate insulin resistance, results in depletion of pancreatic insulin stores, with increased proportions of insulin precursor molecules in the pancreas and the blood. Inadequate response of the preproinsulin gene to the increased insulin needs is an important cause of diabetes progression. Changes in beta-cell mass do not correlate with pancreatic insulin stores and are unlikely to play a role in disease initiation and progression. The major culprit is the inappropriate insulin production with depletion of insulin stores as a consequence. Similar mechanisms could operate during the evolution of type 2 diabetes in humans.
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dynamic changes in β cell mass and pancreatic insulin during the evolution of nutrition dependent diabetes in Psammomys obesus impact of glycemic control
Diabetes, 2005Co-Authors: Nurit Kaiser, Erol Cerasi, Marc Y Donath, Michal Yuli, Gokhan Uckaya, Andrei I Oprescu, Mariefrance Berthault, Catherine Kargar, Alain KtorzaAbstract:Recent studies ascribe a major role to pancreatic β-cell loss in type 2 diabetes. We investigated the dynamics of β-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, β-cell degranulation, and markedly reduced pancreatic insulin content. Reducing calories for 7 days induced normoglycemia in 90% of the animals, restoring β-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, β-cell mass decreased initially but recovered spontaneously to control levels, despite persistent hyperglycemia. Strikingly, however, β-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 β-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.
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Increased glucose sensitivity of stimulus-secretion coupling in islets from Psammomys obesus after diet induction of diabetes.
Diabetes, 2002Co-Authors: Jose A.g. Pertusa, Rafael Nesher, Nurit Kaiser, Erol Cerasi, Jean-claude Henquin, Jean-christophe JonasAbstract:When fed a high-energy (HE) diet, diabetes-prone (DP) Psammomys obesus develop type 2 diabetes with altered glucose-stimulated insulin secretion (GSIS). Beta-cell stimulus-secretion coupling was investigated in islets isolated from DP P. obesus fed a low-energy (LE) diet (DP-LE) and after 5 days on a HE diet (DP-HE). DP-LE islets cultured overnight in 5 mmol/l glucose displayed glucose dose-dependent increases in NAD(P)H, mitochondrial membrane potential, ATP/(ATP + ADP) ratio, cytosolic calcium concentration ([Ca(2+)](c)), and insulin secretion. In comparison, DP-HE islets cultured overnight in 10 mmol/l glucose were 80% degranulated and displayed an increased sensitivity to glucose at the level of glucose metabolism, [Ca(2+)](c), and insulin secretion. These changes in DP-HE islets were only marginally reversed after culture in 5 mmol/l glucose and were not reproduced in DP-LE islets cultured overnight in 10 mmol/l glucose, except for the 75% degranulation. Diabetes-resistant P. obesus remain normoglycemic on HE diet. Their beta-cell stimulus-secretion coupling was similar to that of DP-LE islets, irrespective of the type of diet. Thus, islets from diabetic P. obesus display an increased sensitivity to glucose at the level of glucose metabolism and a profound beta-cell degranulation, both of which may affect their in vivo GSIS.
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ipf1 pdx1 deficiency and β cell dysfunction in Psammomys obesus an animal with type 2 diabetes
Diabetes, 2001Co-Authors: Gil Leibowitz, Erol Cerasi, David J Gross, Sarah Ferber, Asa Apelqvist, Helena Edlund, Danielle Melloul, Nurit KaiserAbstract:The homeodomain transcription factor IPF1/PDX1 is required in beta-cells for efficient expression of insulin, glucose transporter 2, and prohormone convertases 1/3 and 2. Psammomys obesus, a model of diet-responsive type 2 diabetes, shows markedly depleted insulin stores when given a high-energy (HE) diet. Despite hyperglycemia, insulin mRNA levels initially remained unchanged and then decreased gradually to 15% of the basal level by 3 weeks. Moreover, insulin gene expression was not increased when isolated P. obesus islets were exposed to elevated glucose concentrations. Consistent with these observations, no functional Ipf1/Pdx1 gene product was detected in islets of newborn or adult P. obesus using immunostaining, Western blot, DNA binding, and reverse transcriptase-polymerase chain reaction analyses. Other beta-cell transcription factors (e.g., ISL-1, Nkx2.2, and Nkx6.1) were expressed in P. obesus islets, and the DNA binding activity of the insulin transcription factors RIPE3b1-Act and IEF1 was intact. Ipf1/Pdx1 gene transfer to isolated P. obesus islets normalized the defect in glucose-stimulated insulin gene expression and prevented the rapid depletion of insulin content after exposure to high glucose. Taken together, these results suggest that the inability of P. obesus islets to adapt to dietary overload, with depletion of insulin content as a consequence, results from IPF1/PDX1 deficiency. However, because not all animals become hyperglycemic on HE diet, additional factors may be important for the development of diabetes in this animal model.
Yuval Heled - One of the best experts on this subject based on the ideXlab platform.
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physical exercise increases the expression of tnfα and glut 1 in muscle tissue of diabetes prone Psammomys obesus
Life Sciences, 2005Co-Authors: Yuval Heled, Daniel S Moran, S R Sampson, Y Dror, Tovit Rosenzweig, Yoram Epstein, Joseph MeyerovitchAbstract:Abstract Introduction Tumor necrosis factor-α (TNFα) is a major mediator of insulin resistance. On the other hand, it has been suggested that TNFα may facilitate glucose uptake through GLUT 1 expression. We recently found that physical exercise prevented the progression to type 2 diabetes mellitus in diabetes prone Psammomys obesus (sand rat). Aim The aim of the present study was to characterize the influence of physical exercise on the expression of TNFα, its receptor R1 and GLUT 1 in muscle tissue of this animal model. Methods Animals were assigned for 4 weeks to four groups: high-energy diet (HC), high-energy diet and exercise (HE), low-energy diet (LC), low-energy diet and exercise (LE). TNFα, R1 and GLUT 1 expression were analyzed using Western blot technique. Results None of the animals in the HE group became diabetic while all the animals in the HC group became diabetic. TNFα, its receptor (R1) and GLUT 1 expressions were significantly higher in the two exercising groups (LE and HE) and significantly lower in the HC group compared to the control LC group. Conclusions Physical exercise augments the expression of TNFα, its receptor R1 and the glucose transporter GLUT 1 in muscle tissue. We suggest that this mechanism may improve glucose uptake through pathways parallel and unrelated to insulin signaling that may include MAPK and/or NO. These biochemical processes contribute to the beneficial effects of physical exercise on the prevention of type 2 diabetes mellitus.
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physical exercise enhances hepatic insulin signaling and inhibits phosphoenolpyruvate carboxykinase activity in diabetes prone Psammomys obesus
Metabolism-clinical and Experimental, 2004Co-Authors: Yuval Heled, Lea Langzam, Yoav Shani, Y Shapiro, Daniel S Moran, Varda Barash, S R Sampson, Joseph MeyerovitchAbstract:We have shown that physical exercise enhances insulin sensitivity of skeletal muscle in diabetes-prone Psammomys-obesus. In this study, we examined the effect of physical exercise on the liver of these animals. Three groups of animals were exposed to a 4-week protocol; high-energy diet (CH), high-energy diet and exercising (EH), and low-energy diet (CL). Different groups were studied either in a fed state or after an overnight fast, 30 minutes after intraperitoneal (IP) injection of 1 U insulin. Hepatic phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) activity was measured. Insulin signaling response was examined after insulin injection in the fast state by analyzing tyrosine phosphorylation of insulin receptor (IR) and the association between insulin receptor substrate-1 (IRS-1) and IRS-2 with phosphatidylinositol 3 kinase (PI3-K). After 4 weeks, none of the EH animals became diabetic, whereas all the CH animals became diabetic. PEPCK activity in the fed state was higher in the CH group compared with the CL and EH groups (480 +/- 28 nmol/min/mg protein, 280 +/- 30 nmol/min/mg protein, and 208 +/- 13 nmol/min/mg protein, respectively) (P < .02). G6Pase activity was higher in the CH and EH groups compared with the CL group (261 +/- 54 nmol/min/mg protein, 251 +/- 34 nmol/min/mg protein, and 75 +/- 32 nmol/min/mg protein, respectively) (P < .01). After insulin administration in the fast state, tyrosine phosphorylation of IR and association of IRS-2 with PI3-K were higher in the EH and CL groups than in the CH group. We conclude that exercise improves in vivo hepatic insulin sensitivity in diabetes-prone Psammomys-obesus.
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physical exercise enhances protein kinase c δ activity and insulin receptor tyrosine phosphorylation in diabetes prone Psammomys obesus
Metabolism-clinical and Experimental, 2003Co-Authors: Yuval Heled, Yair Shapiro, Dani S. Moran, Lea Langzam, Yoav ShaniAbstract:We recently reported that physical exercise prevents the progression of type 2 diabetes mellitus in Psammomys obesus, an animal model of nutritionally induced type 2 diabetes mellitus. In the present study we characterized the effect of physical exercise on protein kinase C δ (PKCδ) activity, as a mediator of the insulin-signaling cascade in vivo. Three groups of Psammomys obesus were exposed to a 4-week protocol: high-energy diet (HE/C), high-energy diet and exercise (HE/EX), or low-energy diet (LE/C). None of the animals in the HE/EX group became diabetic, whereas all the animals in the HE/C group became diabetic. After overnight fast, intraperitoneal (IP) insulin (1U) caused a greater reduction in blood glucose levels in the HE/EX and LE/C groups compared to the HE/C group. Tyrosine phosphorylation of insulin receptor (IR), insulin receptor substrate-1 (IRS-1), and phosphatidylinositol 3 kinase (PI3 kinase) was significantly higher in the HE/EX and LE/C groups compared with the HE/C group. Finally, IR-associated PKCδ was higher in the HE/EX and LE/C groups compared to the HE/C group. Coprecipitation of PKCδ with IR was higher in the HE/EX and LE/C groups compared to the HE/C group. Thus, we suggest that 4 weeks of physical exercise results in improved insulin-signaling response in Psammomys obesus accompanied by a direct connection between PKCδ and IR. We conclude that this mechanism may be involved in the preventive effect of exercise on type 2 diabetes mellitus in Psammomys obesus.
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Physical exercise prevents the development of type 2 diabetes mellitus in Psammomys obesus.
American Journal of Physiology-endocrinology and Metabolism, 2002Co-Authors: Yuval Heled, Yair Shapiro, Yael Shani, Dani S. Moran, Lea Langzam, Liora Braiman, Sanford R. Sampson, Joseph MeyerovitchAbstract:We hypothesized that exercise training might prevent diabetes mellitus in Psammomys obesus. Animals were assigned to three groups: high-energy diet (CH), high-energy diet and exercise (EH), and low...
Ken Walder - One of the best experts on this subject based on the ideXlab platform.
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Psammomys obesus a natural diet controlled model for diabetes and cardiovascular diseases
Current Atherosclerosis Reports, 2018Co-Authors: Ken Walder, Rajneesh Chaudhary, Christoph E Hagemeyer, Jagat R KanwarAbstract:This review specifically summarises and reports terrestrial mammals of the gerbil subfamily, known as Israeli sand rats or Psammomys obesus (P. obesus) as a diet-controlled, unique, polygenic rodent model for research in the areas of obesity, type 2 diabetes, and cardiovascular diseases. The animal model closely mimics phenotypic and pathophysiological resemblance with human populations. The physiological status and biochemical composition in P. obesus can be manipulated effectively by controlling its nutritional intake, making it a natural model for cardiovascular and diabetic research. Humans exhibit remarkable disparity in physiology and pathology, which are inter-dependent factors. However, variations in these factors in most animal models currently being used for cardiovascular/diabetes research are insignificant. Consequently, it is a necessity to identify and develop animal models exhibiting physiological variations mimicking human pathological conditions. We have compiled research developments conducted with this rodent model manifesting pathophysiology, closely mimicking that in human beings, thereby enabling better translation of novel therapeutic and diagnostic discoveries.
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the small leucine rich proteoglycan biglycan is highly expressed in adipose tissue of Psammomys obesus and is associated with obesity and type 2 diabetes
Biologics: Targets & Therapy, 2012Co-Authors: Kristy Bolton, David J Segal, Ken WalderAbstract:We have previously demonstrated that the small leucine-rich proteoglycan decorin may play a role in adipose tissue homeostasis and the pathophysiology of obesity. Biglycan is highly similar in structure to decorin, therefore we hypothesized it would have a similar expression profile and role to decorin in adipose tissue. Real time polymerase chain reaction was used to measure biglycan mRNA levels in adipose tissue from normal glucose tolerant and impaired glucose tolerant and type 2 diabetic (T2D) Psammomys obesus. Biglycan mRNA was found to be highly expressed in adipose tissue, and gene expression was significantly higher in visceral compared to subcutaneous adipose tissue, with elevated levels in obese, T2D compared to lean normal glucose tolerant P. obesus (P < 0.04). Biglycan mRNA was predominantly expressed by stromal/vascular cells of fractionated adipose tissue (P = 0.023). Biglycan expression in adipose tissue, particularly in the obese state, was markedly upregulated. Collectively, our data suggest that the small leucine-rich proteoglycan family proteins biglycan and decorin may play a role in the development of obesity and T2D, possibly by facilitating expansion of adipose tissue mass.
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Effects of rosiglitazone on intramyocellular lipid accumulation in Psammomys obesus
Biochimica et biophysica acta, 2009Co-Authors: Juan Carlos Molero, Scott Lee, Ilit Leizerman, Ayelet Chajut, Adrian Cooper, Ken WalderAbstract:Objective: To examine the effects of rosiglitazone in intramyocellular lipid (IMCL) content in diabetic Psammomys obesus using novel electron microscopy technologies. Background: P. obesus is an unique polygenic model of obesity and type 2 diabetes. Male diabetic P. obesus were treated daily with 5 mg/Kg Rosiglitazone by oral gavage for 14 days. Data were compared with a group of age-matched diabetic P. obesus treated with saline vehicle. Methods: Assessment of insulin resistance and adiposity were determine before and after the treatment period by oral glucose tolerance test (oGTT) and dual energy X-ray absorptiometry (DEXA) analysis. We used a new scanning electron microscopy technology, (WETSEM) to investigate the effects of rosiglitazone administration on IMCL content, size and distribution in red gastrocnemius muscle. Results: Rosiglitazone treatment improved glucose tolerance in P. obesus with no difference in the overall body fat content although a significant reduction in subscapular fat mass was observed. Rosiglitazone changed the distribution of lipid droplet size in skeletal muscle. Treated animals tended to have smaller lipid droplets compared with saline-treated controls. Conclusions: Since smaller IMCL droplets are associated with improvements in insulin sensitivity, we propose that this may be an important mechanism by which rosiglitazone affects glucose tolerance.
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localization and expression of selenoprotein s in the testis of Psammomys obesus
Journal of Molecular Histology, 2007Co-Authors: Kelly Windmill, Ken Walder, Janette Tennebrown, Richard Bayles, James L Trevaskis, Yuan Gao, Greg R CollierAbstract:Selenium is an essential trace element and selenoprotein S is a member of the selenoprotein family that has the non-standard amino acid selenocysteine incorporated into the polypeptide. Dietary selenium has been shown to play an important protective role in a number of diseases including cancer, immune function and the male reproductive system. In this study, we have observed high levels of selenoprotein S gene expression in the testis from Psammomys obesus. Real-time PCR and immunofluorescence demonstrate that selenoprotein S expression is low in testes from 4-week-old animals but increases significantly by 8 weeks of age and remains high until 17 weeks of age. Selenoprotein S protein is detected in primary spermatocytes, Leydig and Sertoli cells of 8, 12 and 17-week-old animals. These results suggest that selenoprotein S may play a role in spermatogenesis.
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identification of hypothalamic genes implicated in the development of obesity in Psammomys obesus using differential display pcr
Comparative Biochemistry and Physiology B, 2003Co-Authors: James L Trevaskis, Ken Walder, Kelly Windmill, Janine Mcmillan, Greg R CollierAbstract:The hypothalamus is a key central controller of energy homeostasis and is the source and/or site of action of many neuropeptides involved in this process. The aim of this study was to isolate hypothalamic genes differentially expressed between lean and obese Psammomys obesus, a polygenic animal model of obesity and type 2 diabetes. Differential display PCR was used to compare hypothalamic gene expression profiles of lean and healthy, obese and hyperinsulinemic, and obese, diabetic P. obesus in both the fed and fasted states. We conducted differential display with 180 separate primer combinations to amplify approximately 9000 expressed transcripts. Sixty differentially expressed bands were excised. Taqman PCR was performed on 36 of these transcripts to confirm differential gene expression in a larger sample population. Of these 36 transcripts, 9 showed homology to known genes, and 27 were considered to be novel sequences. Gene expression profiles for two of these genes are presented here. In conclusion, differential display PCR was successfully used to isolate several transcripts that may be involved in the central regulation of energy balance. We are currently conducting numerous studies to further investigate the role of these genes in the development of obesity in P. obesus.
F Khammar - One of the best experts on this subject based on the ideXlab platform.
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androgen receptor mediated regulation of adrenocortical activity in the sand rat Psammomys obesus
Journal of Comparative Physiology B-biochemical Systemic and Environmental Physiology, 2014Co-Authors: Abdelouafi Benmouloud, Jean-marie Exbrayat, F Khammar, Zaina Amirat, Alexandre V Patchev, Osborne F X AlmeidaAbstract:The wild sand rat, Psammomys obesus, displays seasonal variations in adrenocortical activity that parallel those of testicular activity, indicating functional cross-talk between the hypothalamo-pituitary-adrenal and hypothalamo-pituitary–gonadal axes. In the present study, we examined androgen receptor (AR)-mediated actions of testicular steroids in the regulation of adrenocortical function in the sand rat. Specifically, we examined the expression of AR in the adrenal cortex, as well as adrenal apoptosis in male sand rats that had been surgically castrated or castrated and supplemented with testosterone; biochemical indices of adrenocortical function and hormone profiles were also measured. Orchiectomy was followed by an increase in adrenocorticotropic hormone secretion from the anterior pituitary and subsequently, increased adrenocortical activity; the latter was evidenced by orchiectomy-induced increases in the adrenal content of cholesterol and lipids as well as adrenal hypertrophy (seen as an elevation of the RNA/DNA ratio). Further, androgen deprivation respectively up- and downregulated the incidence of apoptosis within the glucocorticoid-producing zona fasciculata and sex steroid-producing zona reticularis. Interestingly, orchiectomy resulted in increased expression of AR in the zona fasciculata. All of the orchiectomy-induced cellular and biochemical responses were reversible after testosterone substitution therapy. Together, these data suggest that adrenocortical activity in the sand rat is seasonally modulated by testicular androgens that act through AR located in the adrenal cortex itself.
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variations saisonnieres comparees des activites testiculaire et thyroidienne chez deux especes de rongeurs deserticoles la gerbille gerbillus gerbillus et le rat des sables Psammomys obesus
Sciences & Technologie. C Biotechnologies, 2014Co-Authors: R Boufermes, Z Amirat, F KhammarAbstract:Une etude comparative des variations saisonnieres des activites testiculaire et thyroidienne a ete realisee sur deux especes de rongeurs deserticoles de la famille des gerbillides : Gerbillus gerbillus (nocturne granivore) et Psammomys obesus (diurne herbivore). Pour l’espece nocturne, la fonction testiculaire est caracterisee par un minimum en automne, une reprise en hiver, un maximum au debut du printemps et une regression en ete. Pour l’espece diurne, il existe un cycle saisonnier de la fonction endocrine du testicule, faible au printemps-ete et eleve en automne-hiver. La fonction thyroidienne de l’espece nocturne varie dans des proportions faibles et semble active tout au long de l’annee alors que celle du rat du sable, espece diurne, est de moindre activite au printemps et en ete. Chez le rat des sables, les variations saisonnieres de la fonction thyroidienne semblent plus nettes.
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etude comprative des variations saisonnieres des activites testiculaire et thyroidienne chez deux especes de rongeurs deserticoles la gerbille gerbillus gerbillus et le rat des sables Psammomys obesus
Sciences & Technologie. C Biotechnologies, 2013Co-Authors: R Boufermes, Z Amirat, F KhammarAbstract:Une etude comparative des variations saisonnieres des activites testiculaire et thyroidienne a ete realisee sur deux especes de rongeurs deserticoles de la famille des gerbillides : Gerbillus gerbillus (nocturne granivore) et Psammomys obesus (diurne herbivore). Pour l’especes nocturne, la fonction testiculaire est caracterisee par un minimum en automne, une reprise en hiver, un maximum au debut du printemps et une regression en ete. Chez l’espece diurne, il existe un cycle saisonnier de la fonction endocrine du testicule, faible au printemps-ete et eleve en automne-hiver. La fonction thyroidienne de l’especes nocturne varie dans des proportions faibles et semble active tout au long de l’annee. La thyroide du rat des sables, espece diurne, est cependant, de moindre activite au printemps et en ete. Chez le rat des sables, les variations saisonnieres de la fonction thyroidienne semblent plus nettes.
