This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.There is increasing evidence that insulin resistance, chronic subclinical inflammation, and Thrombosis/impaired fibrinolysis play a role in the development and progression of coronary heart disease (CHD) and type 2 diabetes mellitus. These processes are particularly accelerated inoverweight/obese individuals. Although insulin resistance, hyperinsulinemia, and some markers of inflammation and thrombosis/impaired fibrinolysis are greater among African Americans (AA) compared to Caucasians (C), the possibility that these factors are related to greater disease prevalence in AA is unknown. Early intervention aimed at the reduction of these processes may be crucial for disease risk reduction. Diets differing in glycemic index (GI) and glycemic load (GL), referring to the glycemic responses induced by foods and the accompanying insulin secretion, could be beneficial in this context, because they may have an effect on circulating insulin and/or improve insulin sensitivity (Si). There is a lack of randomized, controlled trial evaluating the effects of dietary interventions differing in GI and GL on insulin resistance. inflammation, and thrombosis/fibrinolysis.Therefore, we propose to conduct a randomized, cross-over controlled feeding study of low- and high-GI/GL diets (4 weeks each) in 25 overweight or obese AA and C men to investigate these effects. The objectives of this study are 1) to compare the effects of matched diets differing only in GI and GL inoverweight/obese men on insulin sensitivity (Si), markers of inflammation, and markers of thrombosis and fibrinolysis; 2) to assess whether the responses to low- and high- GVGL dietary interventions are predicted by baseline insulin concentration and/or Si; 3) to assess the effects of the low-and high-GI/GL dietary interventions on satiety.The study design includes 1) conducting a randomized, cross-over controlled feeding study of low- and high-GI/GL diets (4 weeks each) in 25 overweight/ obese AA and C men; 2) measuring baseline and post-intervention fasting serum concentrations of insulin and glucose. and comparing these in low- and high-GI/GL diets; 3) measuring baseline and post-intervention Si and the acute insulin response to glucose (AIRg), and comparing these in low- and high-GI/GL diets; 4) and measuring baseline and postintervention satiety scores, and comparing these in the low- and high-GI/GL diets.We hypothesize that 1) a low-GI/GL diet will result in lower fasting insulin and AIRg and higher Si relative to the high-GI/GL diet; 2) a low-GI/GL diet will result in lower plasma concentrations of markers of inflammation relative to the high-GI/GL diet; 3) a low GI/GL diet will result in lower plasma concentrations of PAI-1 and fibrinogen relative to the high-GI/GL diet; 4) the low-GI/GL diet will be greater in subjects with higher baseline insulin concentrations and/or lower Si, primarily AA; 5) and the low-GI/GL diet will result in greater satietv than the high-GI/GL diet.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
General Clinical Research Centers Program (M01)
Project #
5M01RR000032-47
Application #
7603254
Study Section
National Center for Research Resources Initial Review Group (RIRG)
Project Start
2007-03-01
Project End
2008-02-29
Budget Start
2007-03-01
Budget End
2008-02-29
Support Year
47
Fiscal Year
2007
Total Cost
$65,323
Indirect Cost
Name
University of Alabama Birmingham
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
063690705
City
Birmingham
State
AL
Country
United States
Zip Code
35294
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
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
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

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