학술논문

Relationship of postprandial nonesterified fatty acids, adipokines, and insulin across gender in human immunodeficiency virus-positive patients undergoing highly active antiretroviral therapy
Document Type
Report
Source
Metabolic Syndrome and Related Disorders. June 2009, Vol. 7 Issue 3, p199, 6 p.
Subject
United States
Language
English
ISSN
1540-4196
Abstract
Introduction The use of highly active antiretroviral therapy (HAART) in human immunodeficiency virus (HIV) infection has been associated with a constellation of metabolic risk factors, including insulin resistance, dyslipidemia, visceral [...]
Background: Metabolic derangements are common in human immunodeficiency virus (HIV)-positive subjects undergoing antiretroviral therapy, but little is known about postprandial conditions. Methods: We investigated the relationship between leptin, adiponectin, nonesterified fatty acids (NEFA), and insulin in response to a day-long meal pattern and evaluated gender differences in HIV-positive men (n = 12) and women (n = 13) undergoing highly active antiretroviral therapy (HAART). Results: For both men and women, a significant decrease in postprandial NEFA levels was observed following breakfast (0.53 vs. 0.22 mmol/L, P < 0.001, baseline and at 3 hours, respectively), whereas day-long postprandial leptin and adiponectin levels showed small nonsignificant oscillations. In contrast to NEFA and adiponectin, postprandial leptin levels were significantly higher among women compared to men (P < 0.05). Postprandial NEFA levels correlated positively with fasting insulin levels ([r.sup.2] = 0.25, P = 0.016), and the postbreakfast decrease in NEFA levels correlated significantly with the postbreakfast increase in insulin levels ([r.sup.2] = 0.17, P = 0.038). No significant association between postprandial adipokines and insulin was observed. Conclusions: In HAART-treated, HIV-infected men and women, levels of NEFA, but not adipokines, showed significant postprandial variation. Furthermore, food intake resulted in significant NEFA suppression in proportion to the food-stimulated insulin increase.