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Recent Clinical trialsII

  • 작성자한진
  • 작성일2006-09-10 09:56:42
  • 조회수2298
  • 첨부파일첨부파일
(Recruiting) Sponsor(s): University of Pittsburgh ;NIH/NIDDK Conditions to be treated: Diabetes; Obesity Purpose: This investigation is being carried out to learn more about research findings from a study that was completed last year. Those findings revealed that within the skeletal muscle cells of individuals with type 2 diabetes, there was often damage to the mitochondria (the muscle cell’s power source or the machinery of the muscle cell that produces energy). In individuals with type 2 diabetes, the liver continues to release sugar even when sugar levels are normal; the pancreas is not able to produce and release insulin normally; and the muscle and fat cells no longer respond as effectively to insulin. These defects lead to an abnormal rise of sugar in the blood. In this study, we want both to look more closely at the mitochondria and see if there is potential for improving mitochondrial functioning (improving the machinery of the muscle cell that produces energy) and reversing mitochondrial damage through a weight loss or a combined exercise/weight loss program. The program you get assigned to will be determined by a process called randomization (like a flip of a coin). Interventions: Behavior:weight loss/ exercise Study type: Interventional Study Design Overview: Treatment Randomized Open Label Uncontrolled Factorial Assignment Age limit of subjects: 30 to 55 years of age Genders eligible for study: Both Official title: Primary Outcomes: To measure the functional capacity of mitochondria in skeletal muscle of those with T2DM and those at increased risk of developing T2DM Secondary Outcomes: To assess whether exercise and diet can improve mitochondrial function and morphology. Expected Total Enrollment: 49 Important dates: Start Date: 2003-12-01 Expected Completion Date: 2007-12-01 Last Followup: 2006-12-01Data Entry Closure: 2007-12-01 Contact information for recruiting centers: University of Pittsburgh, Pittsburgh, Pennsylvania, 15213, United States; Recruiting Carol A Kelley, RN 412-692-2973 KelleyC@dom.pitt.edu David E. Kelley, MD, Principal Investigator
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No. 제목 작성자 작성일 조회수
241 Mitochondrial Damage Impairs Oxygen Metabolism After Intracerebral Hemorrhage 2007.01.11 한진 2007.01.11 2,141
240 Weight Loss Improves Heart Rate Recovery in Overweight and Obese Men With Features of the Metabolic Syndrome 2007.01.11 한진 2007.01.11 2,128
239 Metabolic Syndrome Independently Predicts Vascular Complications in Diabetes 2007.01.11 한진 2007.01.11 1,925
238 Metabolic Syndrome Helps Predict Cardiovascular Disease and Diabetes Risk 2007.01.11 한진 2007.01.11 4,116
237 미토콘드리아 DNA의 복제 첨부파일 2007.01.10 한진 2007.01.10 3,232
236 미토콘드리아에 관심 집중 2007.01.10 한진 2007.01.10 2,177
235 미토콘드리아 산화 스트레스로 인한 파킨슨병 기전 동정 2007.01.10 한진 2007.01.10 2,730
234 미토콘드리아 이동 변화에 따른 신경세포 기능 이상 동정 2007.01.10 한진 2007.01.10 2,170
233 세포의 기능에 영향을 주는 미토콘드리아 DNA 발견 2007.01.10 한진 2007.01.10 2,817
232 미토콘드리아 DNA조절 부위 변이가 알츠하이머병과 연관 2007.01.10 한진 2007.01.10 4,206
231 미토콘드리아 돌연변이가 혈압 및 콜레스테롤 이상과 관련 2007.01.10 한진 2007.01.10 2,371
230 암세포의 아킬레스腱은 미토콘드리아 2007.01.10 한진 2007.01.10 2,064
229 Inadequate cytoplasmic antioxidant enzymes response contributes to the oxidative stress in human hypertension. 2007.01.06 한진 2007.01.06 3,717
228 A comparison of arteries and veins in oxidative stress: producers, destroyers, function, and disease. 2007.01.06 한진 2007.01.06 2,198
227 Uncoupling protein-3: clues in an ongoing mitochondrial mystery. 2007.01.06 한진 2007.01.06 2,508
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