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CIRCULATING LACTATE IS ELEVATED IN PREDIABETES PHENOTYPES COMPARED WITH NORMAL GLUCOSE TOLERANT COUNTERPARTS

Presenters Name: 
Brielle Dotson
Co Presenters Name: 
Primary Research Mentor: 
Steve Malin
Secondary Research Mentor: 
Time: 
12:30 - 1:45
Time of Presentation: 
2019 - 12:30pm to 1:45pm
Session: 
3
Location: 
Newcomb Hall Ballroom
Presentation Type: 
Poster
Presentations Academic Category: 
Science
Grant Program Recipient: 
USOAR Program
Abstract: 

Purpose: Prediabetes can be characterized as impaired fasting glucose (IFG) with or without impaired glucose tolerance (IGT; 2-hr blood glucose). However, whether people with IFG and/or IFG+IGT have elevated lactate concentrations compared to normal glucose tolerant (NGT) controls is unclear. We hypothesized that individuals with IFG and IFG+IGT would have higher lactate levels than NGT controls in relation to glucose metabolism. Methods: Forty-one obese adults (Age: 54.8±2.0yrs; BMI: 36.0±1.0kg/m2; 34F/7M) were screened for NGT, IFG, or IFG+IGT (75g OGTT, ADA criteria) following an overnight fast. Plasma lactate, glucose, and insulin were measured during a 120min 75g OGTT. The oral minimal model was used as an estimate for insulin sensitivity. Aerobic fitness (VO2peak), fasting substrate oxidation (respiratory exchange ratio (RER), indirect calorimetry) and body composition (bioelectrical impedance) were tested. Results: There were no differences in VO2peak, body fat or fasting RER across groups. Individuals with IFG+IGT had lower insulin sensitivity compared with IFG and NGT (P<0.01). However, both IFG and IFG+IGT had increased lactate tAUC compared to NGT (P<0.01 and P=0.01, respectively). Increased lactate tAUC correlated with fasting glucose (r=0.33, P=0.03) and reduced VO2peak (r=-0.34, P=0.03). Fasting lactate also related to fasting RER (r=0.31, P=0.04). Conclusion: Despite no differences between prediabetes phenotypes, adults with IFG and IFG+IGT have elevated lactates compared to NGT controls. Lactate tAUC directly associates with fasting glucose and fitness. These data suggest that fitness may mediate lactate metabolism via the liver. Future work is warranted to determine the mechanism by which lactate influences type 2 diabetes risk.