Effect of Progressive Weight Loss on Lactate Metabolism: A Randomized Controlled Trial

Effect of Progressive Weight Loss on Lactate Metabolism: A Randomized Controlled Trial
Title:
Effect of Progressive Weight Loss on Lactate Metabolism: A Randomized Controlled Trial
Other Titles:
Obesity
Publication Date:
24 February 2018
Citation:
Chondronikola M, Magkos F, Yoshino J, et al. Effect of Progressive Weight Loss on Lactate Metabolism: A Randomized Controlled Trial. Obesity (Silver Spring). 2018;26(4):683‐688. doi:10.1002/oby.22129
Abstract:
Objective: Lactate is an intermediate of glucose metabolism that has been implicated in the pathogenesis of insulin resistance. This study evaluated the relationship between glucose kinetics and plasma lactate concentration ([LAC]) before and after manipulating insulin sensitivity by progressive weight loss. Methods: Forty people with obesity (BMI = 37.9 ± 4.3 kg/m2 ) were randomized to weight maintenance (n = 14) or weight loss (n = 19). Subjects were studied before and after 6 months of weight maintenance and before and after 5%, 11%, and 16% weight loss. A hyperinsulinemic-euglycemic clamp procedure in conjunction with [6,6-2 H2 ]glucose tracer infusion was used to assess glucose kinetics. Results: At baseline, fasting [LAC] correlated positively with endogenous glucose production rate (r = 0.532; P = 0.001) and negatively with insulin sensitivity, assessed as the insulin-stimulated glucose disposal (r = -0.361; P = 0.04). Progressive (5% through 16%) weight loss caused a progressive decrease in fasting [LAC], and the decrease in fasting [LAC] after 5% weight loss was correlated with the decrease in endogenous glucose production (r = 0.654; P = 0.002) and the increase in insulin sensitivity (r = -0.595; P = 0.007). Conclusions: This study demonstrates the interrelationships among weight loss, hepatic and muscle glucose kinetics, insulin sensitivity, and [LAC], and it suggests that [LAC] can serve as an additional biomarker of glucose-related insulin resistance.
License type:
PublisherCopyrights
Funding Info:
This study was supported by National Institutes of Health grants DK 104995, DK 56341 (Nutrition Obesity Research Center), DK20579 (Diabetes Research Center), DK052574 (Digestive Disease Research Center),and RR024992 (Clinical and Translational Science Award), and grants from the Pershing Square Foundation and the Longer Life Foundation. MC is supported by a postdoctoral fellowship from the American Heart Association (17POST33060003).
Description:
The full paper is available for download at the publisher's URL: https://doi.org/10.1002/oby.22129
ISSN:
1930-7381
1930-739X
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