In vivo association of adipose tissue function and High Density Lipoprotein Metabolism in humans

Program: Late-Breaking Abstracts
Session: SUN-LB-Late-Breaking Poster Session 2
Bench to Bedside
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-LB-08
Demidmaa Tuvdendorj*1, Alejandro Olano Munoz2, Jean-Marc Schwarz3, Giuseppe Montalto4, Manisha Chandalia5, Manfredi Rizzo4, Elizabeth J Murphy6 and Nicola Abate5
1University of Texas Medical Bran, Galveston, TX, 2UTMB Galveston, Galveston, TX, 3University of California in San Francisco, San Francisco, CA, 4University of Palermo, Italy, 5University of Texas Medical Branch, Galveston, TX, 6UCSF, San Francisco General Hospital, San Francisco, CA
Low concentration of plasma high density lipoprotein (HDL) is an independent predictor of coronary heart disease (CHD). Pre-clinical studies reported that impaired function of adipose tissue (AT) results in inability of HDL particles to mature, higher rates of breakdown and lower HDL concentration. In the current study we aimed to explore if an in vivo association exists between the function of subcutaneous (s.q.) AT and HDL metabolism in humans. Method: The fractional synthesis of triglyceride (TGf) in s.q. AT, a marker of AT function, was measured using Mass Isotopomer Distribution Analysis approach after 12 weeks of deuterium labeling in 12 obese normoglycemic adults (Age:50±22 years; BMI:33±2 kg•m-2; Fasting Plasma Glucose:92±8 mg•dl-1). Plasma concentration of HDL was measured in Clinical Laboratory, The University of Texas Medical Branch, Galveston, TX. The HDL particles were separated using Non-denaturing, linear polyacrylamide gel electrophoresis and HDL subclasses, including Large (L-HDL), Intermediate (I-HDL) and Small (S-HDL), were measured using the LipopPrint© system (Quantimetrix Corporation, Redondo Beach, CA, USA). Association analyses were performed using linear and multiple regression analyses. The p value less than 0.05 was considered statistically significant. Results: The TGf in s.q. AT varied between 7 and 29 %; the HDL concentration varied between 30 and 69 mg•dl-1. L-HDL, I-HDL and S-HDL particles comprised 26±6, 50±3, 24±6 %, respectively, of total HDL. Linear regression analysis demonstrated a significant positive association between TGf and HDL concentration (r = 0.65; p < 0.05). There was no association between TGf and L-HDL (r = 0.37, p = NS) or S-HDL (r = 0.13, p = NS). Although due to lack of power, an association between TGf and I-HDL did not reach statistical significance (r= 0.47, p = 0.122), the multiple regression analysis demonstrated that TGf association with plasma HDL concentration improved with addition of I-HDL as an independent variable (r = 0.71, p <  0.05). No association between plasma concentration of HDL and I-HDL was observed (r= 0.32, p = NS). Conclusion: Our data, for the first time, demonstrate in vivo association between the function of s.q. AT, represented by TGf, and HDL metabolism in humans. AT dysfunction may be a target to maintain plasma concentration of HDL. Further interventional studies to explore the mechanisms of this association, to ameliorate the risks of development of CHD, are warranted.

Nothing to Disclose: DT, AOM, JMS, GM, MC, MR, EJM, NA

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