{"id":{"repo_id":"utswmed","oai_identifier":"oai:utswmed-ir.tdl.org:2152.5/384"},"canonical_url":"https://search.dev.ndltd.org/etd/utswmed/oai:utswmed-ir.tdl.org:2152.5/384","repository":{"repo_id":"utswmed","name":"University of Texas Southwestern Medical Center","base_url":"https://utswmed-ir.tdl.org/server/oai/request"},"display":{"title":"Loss of Ventromedial Hypothalamic Leptin Receptors Results in Increased Adiposity and a Metabolic Syndrome","abstract":"Obesity is a leading health problem here in the United States and in other developing countries. Obesity is a risk factor for several life-threatening conditions including Type II diabetes, hypertension, and cardiovascular disease. Given the growing obesity epidemic, understanding the mechanisms whereby the central nervous system monitors and regulates energy homeostasis has become a major focus of scientific research in the last several decades. The discovery that mice fed a low fat diet exhibit significantly increased adipose mass with no difference in weight compared to wild-type littermates. Further, these mice exhibit a metabolic syndrome including mild steatosis, dyslipidemia, and hyperleptinemia. From a young age, Lepr KOleptin, an adipocyte-derived hormone, acts on the brain to suppress appetite and stimulate energy expenditure greatly extended our understanding of such mechanisms. The leptin receptor is expressed in a number of hypothalamic nuclei known to play a role in energy homeostasis. While much work has focused on leptin's actions in the arcuate nucleus, other sites have received substantially less attention. Here, I report that mice lacking leptin receptors within the ventromedial hypothalamic nucleus (Lepr KOVMH) develop increased adiposity and a metabolic syndrome. Lepr KOVMH mice fed high fat rodent chow show an increased sensitivity to diet-induced obesity, while Lepr KOVMH mice are hyperinsulinemic and eventually become glucose intolerant. These data demonstrate that Lepr KOVMH mice are a novel genetic model of obesity and may be used for the study of energy partitioning, lipogenesis, and central leptin signaling.","abstract_html":"Obesity is a leading health problem here in the United States and in other developing countries. Obesity is a risk factor for several life-threatening conditions including Type II diabetes, hypertension, and cardiovascular disease. Given the growing obesity epidemic, understanding the mechanisms whereby the central nervous system monitors and regulates energy homeostasis has become a major focus of scientific research in the last several decades. The discovery that mice fed a low fat diet exhibit significantly increased adipose mass with no difference in weight compared to wild-type littermates. Further, these mice exhibit a metabolic syndrome including mild steatosis, dyslipidemia, and hyperleptinemia. From a young age, Lepr KOleptin, an adipocyte-derived hormone, acts on the brain to suppress appetite and stimulate energy expenditure greatly extended our understanding of such mechanisms. The leptin receptor is expressed in a number of hypothalamic nuclei known to play a role in energy homeostasis. While much work has focused on leptin's actions in the arcuate nucleus, other sites have received substantially less attention. Here, I report that mice lacking leptin receptors within the ventromedial hypothalamic nucleus (Lepr KOVMH) develop increased adiposity and a metabolic syndrome. Lepr KOVMH mice fed high fat rodent chow show an increased sensitivity to diet-induced obesity, while Lepr KOVMH mice are hyperinsulinemic and eventually become glucose intolerant. These data demonstrate that Lepr KOVMH mice are a novel genetic model of obesity and may be used for the study of energy partitioning, lipogenesis, and central leptin signaling.","abstract_has_math":false,"creators":["Bingham, Nathan Christian"],"institution":null,"degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Parker, Keith L."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2010,"date_issued":"2010-07-12T17:51:35Z","date_published":"2010-07-12T17:51:35Z","updated_at":"2026-07-24T05:52:11Z","subjects":["Mice","Receptors, Leptin","Adiposity","Ventromedial Hypothalamic Nucleus"],"languages":["en"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["421114695"],"render_values":[{"text":"421114695","href":null,"code":true}]}]},"links":{"outbound_url":"https://hdl.handle.net/2152.5/384","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Parker, Keith L."]},{"key":"dc:creator","label":"Author","values":["Bingham, Nathan Christian"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2010-07-12T17:51:35Z","2008-05-12"]},{"key":"dc:type","label":"Dc Type","values":["Thesis","Text","dissertation"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Mice","Receptors, Leptin","Adiposity","Ventromedial Hypothalamic Nucleus"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["en"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["https://hdl.handle.net/2152.5/384","421114695"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["Obesity is a leading health problem here in the United States and in other developing countries. Obesity is a risk factor for several life-threatening conditions including Type II diabetes, hypertension, and cardiovascular disease. Given the growing obesity epidemic, understanding the mechanisms whereby the central nervous system monitors and regulates energy homeostasis has become a major focus of scientific research in the last several decades. The discovery that mice fed a low fat diet exhibit significantly increased adipose mass with no difference in weight compared to wild-type littermates. Further, these mice exhibit a metabolic syndrome including mild steatosis, dyslipidemia, and hyperleptinemia. From a young age, Lepr KOleptin, an adipocyte-derived hormone, acts on the brain to suppress appetite and stimulate energy expenditure greatly extended our understanding of such mechanisms. The leptin receptor is expressed in a number of hypothalamic nuclei known to play a role in energy homeostasis. While much work has focused on leptin's actions in the arcuate nucleus, other sites have received substantially less attention. Here, I report that mice lacking leptin receptors within the ventromedial hypothalamic nucleus (Lepr KOVMH) develop increased adiposity and a metabolic syndrome. Lepr KOVMH mice fed high fat rodent chow show an increased sensitivity to diet-induced obesity, while Lepr KOVMH mice are hyperinsulinemic and eventually become glucose intolerant. These data demonstrate that Lepr KOVMH mice are a novel genetic model of obesity and may be used for the study of energy partitioning, lipogenesis, and central leptin signaling."]},{"key":"dc:format","label":"Dc Format","values":["Electronic","application/pdf","born digital"]},{"key":"dc:title","label":"Title","values":["Loss of Ventromedial Hypothalamic Leptin Receptors Results in Increased Adiposity and a Metabolic Syndrome"]}]}],"canonical_facts":{"dc:contributor":["Parker, Keith L."],"dc:creator":["Bingham, Nathan Christian"],"dc:date":["2010-07-12T17:51:35Z","2008-05-12"],"dc:description":["Obesity is a leading health problem here in the United States and in other developing countries. Obesity is a risk factor for several life-threatening conditions including Type II diabetes, hypertension, and cardiovascular disease. Given the growing obesity epidemic, understanding the mechanisms whereby the central nervous system monitors and regulates energy homeostasis has become a major focus of scientific research in the last several decades. The discovery that mice fed a low fat diet exhibit significantly increased adipose mass with no difference in weight compared to wild-type littermates. Further, these mice exhibit a metabolic syndrome including mild steatosis, dyslipidemia, and hyperleptinemia. From a young age, Lepr KOleptin, an adipocyte-derived hormone, acts on the brain to suppress appetite and stimulate energy expenditure greatly extended our understanding of such mechanisms. The leptin receptor is expressed in a number of hypothalamic nuclei known to play a role in energy homeostasis. While much work has focused on leptin's actions in the arcuate nucleus, other sites have received substantially less attention. Here, I report that mice lacking leptin receptors within the ventromedial hypothalamic nucleus (Lepr KOVMH) develop increased adiposity and a metabolic syndrome. Lepr KOVMH mice fed high fat rodent chow show an increased sensitivity to diet-induced obesity, while Lepr KOVMH mice are hyperinsulinemic and eventually become glucose intolerant. These data demonstrate that Lepr KOVMH mice are a novel genetic model of obesity and may be used for the study of energy partitioning, lipogenesis, and central leptin signaling."],"dc:format":["Electronic","application/pdf","born digital"],"dc:identifier":["https://hdl.handle.net/2152.5/384","421114695"],"dc:language":["en"],"dc:subject":["Mice","Receptors, Leptin","Adiposity","Ventromedial Hypothalamic Nucleus"],"dc:title":["Loss of Ventromedial Hypothalamic Leptin Receptors Results in Increased Adiposity and a Metabolic Syndrome"],"dc:type":["Thesis","Text","dissertation"]},"updated_at":"2026-07-24T05:52:11Z"}