This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The Insulin Resistant Syndrome provides the 'common soil' for the development of Type 2 Diabetes & Cardiovascular Disease. Insulin stimulates glucose transport via translocation of intracellular GLUT4 glucose transporters to the cell surface. IR in NIDDM is caused by profound depletion of GLUT4 in fat, but normal in muscle, suggesting that GLUT4 translocation to plasma membrane may be defective.
Aim of this hypothesis is that IR is due to defects in GLUT4 trafficking which impair insulin-mediated GLUT4 translocation in skeletal muscle. To accomplish this multiple sub-groups will be studied: healthy subjects before and during intralipid infusion, type 2 diabetics before and after intensive insulin therapy, subjects before and after short-term dexamethasone administration, and subjects before and during treatment with insulin sensitizing medications (pioglitazone/rosiglitazone). Subjects will be admitted to GCRC for medical history, physical examnation, KEG, blood pressure, laboratory blood/urine tests to determine eligibility. Qualified persons will undergo metabolic studies to characterize body compositon, energy expenditure, glucose tolerance, in vivo insulin sensitivity and glucose metabolism, insulin secretion, & lipid metabolism. Studies include OGTT, 24 hr urine, V02MAX, indirect and room calorimetry, DEXA, Leg NMR, muscle biopsy of thigh, subcutaneous fat biopsy of lower abdominal wall, and intravenous glucose tolerance test or hyperinsulinemic euglycemic infusion (clamp).
|Yu, Alan S L; Shen, Chengli; Landsittel, Douglas P et al. (2018) Baseline total kidney volume and the rate of kidney growth are associated with chronic kidney disease progression in Autosomal Dominant Polycystic Kidney Disease. Kidney Int 93:691-699|
|Askie, Lisa M; Darlow, Brian A; Finer, Neil et al. (2018) Association Between Oxygen Saturation Targeting and Death or Disability in Extremely Preterm Infants in the Neonatal Oxygenation Prospective Meta-analysis Collaboration. JAMA 319:2190-2201|
|McKenzie, Katelyn A; El Ters, Mirelle; Torres, Vicente E et al. (2018) Relationship between caffeine intake and autosomal dominant polycystic kidney disease progression: a retrospective analysis using the CRISP cohort. BMC Nephrol 19:378|
|Srinivasan, Lakshmi; Page, Grier; Kirpalani, Haresh et al. (2017) Genome-wide association study of sepsis in extremely premature infants. Arch Dis Child Fetal Neonatal Ed 102:F439-F445|
|Morrison, Shannon A; Goss, Amy M; Azziz, Ricardo et al. (2017) Peri-muscular adipose tissue may play a unique role in determining insulin sensitivity/resistance in women with polycystic ovary syndrome. Hum Reprod 32:185-192|
|Shen, Chengli; Landsittel, Douglas; Irazabal, María V et al. (2017) Performance of the CKD-EPI Equation to Estimate GFR in a Longitudinal Study of Autosomal Dominant Polycystic Kidney Disease. Am J Kidney Dis 69:482-484|
|Denson, Lee A; McDonald, Scott A; Das, Abhik et al. (2017) Early Elevation in Interleukin-6 is Associated with Reduced Growth in Extremely Low Birth Weight Infants. Am J Perinatol 34:240-247|
|Kline, Timothy L; Korfiatis, Panagiotis; Edwards, Marie E et al. (2017) Image texture features predict renal function decline in patients with autosomal dominant polycystic kidney disease. Kidney Int 92:1206-1216|
|James, Jennifer; Munson, David; DeMauro, Sara B et al. (2017) Outcomes of Preterm Infants following Discussions about Withdrawal or Withholding of Life Support. J Pediatr 190:118-123.e4|
|Younge, Noelle; Goldstein, Ricki F; Bann, Carla M et al. (2017) Survival and Neurodevelopmental Outcomes among Periviable Infants. N Engl J Med 376:617-628|
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