{"id":84,"date":"2020-06-09T05:20:10","date_gmt":"2020-06-09T09:20:10","guid":{"rendered":"https:\/\/islets.ca\/?page_id=84"},"modified":"2022-05-05T11:05:09","modified_gmt":"2022-05-05T17:05:09","slug":"member-labs","status":"publish","type":"page","link":"https:\/\/islets.ca\/member-labs\/","title":{"rendered":"Member Labs"},"content":{"rendered":"
[et_pb_section fb_built=”1″ custom_padding_last_edited=”on|desktop” module_id=”features” _builder_version=”4.4.8″ custom_padding=”40px||54px|||” custom_padding_tablet=”50px|0|50px|0″ custom_padding_phone=”” transparent_background=”off” padding_mobile=”off” make_fullwidth=”off” use_custom_width=”off” width_unit=”on” global_colors_info=”{}”][et_pb_row padding_mobile=”on” column_padding_mobile=”on” disabled_on=”off|off|off” _builder_version=”4.4.8″ background_size=”initial” background_position=”top_left” background_repeat=”repeat” custom_padding=”20px||5px|” make_fullwidth=”off” use_custom_width=”off” width_unit=”on” global_colors_info=”{}”][et_pb_column type=”4_4″ _builder_version=”3.25″ custom_padding=”|||” global_colors_info=”{}” custom_padding__hover=”|||”][et_pb_text admin_label=”About our member labs” _builder_version=”4.5.1″ header_2_letter_spacing=”4px” background_size=”initial” background_position=”top_left” background_repeat=”repeat” text_orientation=”center” module_alignment=”center” hover_enabled=”0″ use_border_color=”off” border_color=”#ffffff” border_style=”solid” global_colors_info=”{}” sticky_enabled=”0″]<\/p>\n
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Our laboratory is interested in harnessing stem cell biology to recapitulate beta cell development and the islet niche in a dish, to study beta cell function and dysfunction, and develop cell therapies for T1D.<\/p>\n<\/div>\n
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The Bruin lab is particularly interested in how environmental factors, such as exposure to pollutants, impact the endocrine pancreas during critical windows of fetal development and periods of metabolic stress in adulthood. Current projects we are investigating: a) the role of xenobiotic metabolism enzymes in islets; b) how environmental pollutants impact adult beta cell function and survival; c) the long-term impact of fetal and neonatal pollutant exposure on diabetes risk; d) effects of pollutants on human stem cell differentiation into pancreatic endocrine cells; and e) off-target effects of chemotherapeutic drugs on islets.<\/p>\n<\/div>\n
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Our research efforts are aimed at identifying novel molecular mechanisms that govern beta-cell differentiation, proliferation, and survival. The overall goal is to harness the therapeutic potential of these newly discovered targets to stimulate the generation of new beta-cells and to expand and protect the functional beta-cells that still reside in the pancreas of patients with diabetes.<\/p>\n<\/div>\n
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CIRTN-R2FIC is saddened by the loss of member, collaborator, and friend, Susie Clee. Highlights of her work include discovery and functional analysis of genes involved in type 2 diabetes and obesity. Follow this link<\/a> for more on Susie and her life\u2019s work.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Research in the Dhanvantari Laboratory is focused on investigating the mechanisms of glucagon intracellular trafficking and secretion. To this end, we utilize techniques such as molecular imaging of islet function and heart failure. We are also dedicated to and interested in promoting equity, diversity, and inclusion in STEM.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Our lab has two main interests. First is understanding the circadian regulation of insulin secretion. Insulin secretion capacity varies throughout the day and we are interested in understanding the intrinsic mechanisms of the beta cell that regulate dynamic cycles of insulin secretion capacity and how this is impacted by circadian disruption, contributing to diabetes risk. Secondly, we are studying gene-environment interactions and impact on islet function. Indigenous children of Manitoba are disproportionately affected by type 2 diabetes. We have several ongoing projects to examine how genes and environment relevant to these children interact to impact islet function and diabetes development.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Our research focuses on understanding the pathogenesis of diabetes at the molecular level. We know that metabolic abnormalities in one tissue often impact the health of another (organ cross-talk), adding layers of complexity. In our lab, we strive to understand the molecular events in each tissue that trigger disease in the islet, and identify new ways to prevent, diagnosis, or reverse the metabolic abnormalities associated with insulin resistance and beta-cell dysfunction \/ death. To achieve our goals, we use tools in genetic engineering, molecular biology and physiology in vitro cell models to pre-clinical animal and small clinical studies.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Ferdaoussi lab is interested in understanding the molecular and cellular mechanisms involved in the etiology of pancreatic \u00df cell failure and death in type 2 Diabetes. We are also interested in designing and generating novel molecules and peptides to preserve pancreatic islets and stem-derived \u03b2 cells during transplantation protocol. We are also engaged in promoting bilingual research in the French-Canadian Minority Communities as part of our EDI commitment.<\/p>\n — <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n In our lab, we are studying the function and regulation of the bone-derived hormone osteocalcin. This hormone controls insulin secretion and beta cell proliferation, as well as insulin sensitivity in peripheral organs. We are currently studying how the post-translational modifications of osteocalcin (glycosylation, carboxylation, etc.) regulate its activity in mice and humans. In addition, we are investigating the mechanism of vitamin K in beta cell and how this influences the development of diabetes. We are examining the function of vitamin K-dependent proteins in insulin secretion and beta cells adaptation to ER stress. Also, we are characterizing novel vitamin K-dependent proteins.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n At the uOttawa Immunometabolab (see what we did? Immune + Metabolism + Lab = so clever…) we use mice and cells as biological models to uncover how specific metabolic and\/or immune pathways are linked. Our BIG PICTURE GOALS are to understand how these molecular, metabolic and immune pathways work in hopes that our research will translate to humans and lead to new ways to prevent and\/or treat chronic metabolic diseases including diabetes and atherosclerosis. <\/span><\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Gaisano lab focuses on SNARE proteins\u2019 regulation of exocytosis in pancreatic beta and acinar cells, elucidating how their dysregulated exocytosis underlie T2D insulin secretory defects and pancreatitis, respectively. His lab pioneered the thinking that SNARE proteins directly bind and regulate membrane depolarizing (KATP) and repolarizing (Kv) potassium channels that control beta-cell excitability to regulate secretion. Current projects include investigating the role of glucagon-secreting alpha-cell and islet paracrine control and their dysfunction that underlie T1D islet dysfunction. Secondly, we are studying the role of intestinal microbiome in metabolic syndrome.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n The primary theme of our research is the investigation of the effects of excess circulating energy substrates, in particular free fatty acids, on insulin action, secretion and kinetics, and the implication of these effects for the pathogenesis of diabetes. Secondary themes of research are the studies of the effects of nutrient and insulin excess in animal models of atherosclerosis and cancer.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Intra-islet and endocrine signaling resulting in beta-cell plasticity during metabolic stress, such as pregnancy. Early life programming of pancreatic development resulting in islet cell dysfunction in later life and risk of diabetes. Origins and prevention of gestational diabetes using both rodent models and interventional clinical trials as part of the DALI clinical trials consortium.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n The Hoesli Stem Cell Bioprocessing Lab develops devices and cell culture methods for cellular therapy – in particular for islet transplantation. We have upscaled islet encapsulation processes using stirred or microchannel emulsification to produce large amounts (L volumes) of microencapsulated islets cells in less than an hour. Using 3D bioprinting, we are engineering 3D vascularized tissues to study islet interactions with endothelial cells and other vascular cells. These vascularized tissue constructs could one day be used for transplantation. Overall, we are using our knowledge of bioprocess engineering and materials engineering to service the islet biology and diabetes community.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n We study how histone modifications and transcription factors mediate gene expression during pancreas development and to control beta-cell function.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Our lab is interested in understanding the molecular mechanisms that regulate beta cell mass and function. We use pregnancy as a physiologic model of increased insulin demand to understand how pancreatic beta cells adapt to stress. Our current research focus is on 1) identification of novel signalling pathways that regulates \u03b2-cell function and survival during pregnancy, 2) identification of non-cell autonomous function of prolactin receptor in \u03b2-cell function, 3) mechanism underlying fetal programming of \u03b2-cells in the context of prenatal exposure to mild hyperglycemia.<\/p>\n<\/div>\n <\/p>\n <\/div>\n <\/div>\n <\/div>\n <\/div>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n <\/div>\n <\/p>\n <\/p>\n Our laboratory uses a variety of technical approaches, from live-cell imaging to integrated physiology to multi-omics, to study islet biology and the roles of insulin throughout the body. Ongoing projects include sex differences in insulin production and ER stress, examining beta-cell stress and insulin production in early stage T1D, beta-cell stress adaptation, role of specific Ca release in beta-cell function, Scn9a<\/em> in T1D, autocrine insulin action in beta-cell specific insulin resistance, role of macro-nutrient as secretagogues in human islets, spatio-temporal dynamics of insulin gene transcription, and the role of insulin in metabolic dysfunction.<\/p>\n<\/div>\n <\/p>\n
\nLe laboratoire Ferdaoussi s’int\u00e9resse \u00e0 \u00e9tudier les m\u00e9canismes mol\u00e9culaires et cellulaires impliqu\u00e9s dans l’\u00e9tiologie de la dysfonction et la mort des cellules \u00df pancr\u00e9atiques dans le diab\u00e8te de type 2. Nous sommes \u00e9galement int\u00e9ress\u00e9s par le design et la g\u00e9n\u00e9ration de nouvelles mol\u00e9cules et peptides pour pr\u00e9server les \u00eelots pancr\u00e9atiques et les cellules \u03b2 d\u00e9riv\u00e9es de cellules souches pour am\u00e9liorer le protocole de transplantation. Nous sommes aussi engag\u00e9s \u00e0 promouvoir la recherche bilingue dans les communaut\u00e9s minoritaires canadiennes francophones comme un des engagements du laboratoire envers EDI.<\/em><\/p>\n<\/div>\n