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Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy.
Am J Physiol Endocrinol Metab. 2008 Jul; 295(1):E85-91.AJ

Abstract

In this cross-sectional study, we sought to determine whether gene expression of macrophage markers and inflammatory chemokines in lipoatrophic subcutaneous abdominal adipose tissue and liver fat content are increased and interrelated in human immunodeficiency virus (HIV)-1-positive, highly active antiretroviral therapy (HAART)-treated patients with lipodystrophy (HAART+LD+; n = 27) compared with those without (HAART+LD-; n = 13). The study groups were comparable with respect to age, gender, and body mass index. The HAART+LD+ group had twofold more intra-abdominal (P = 0.01) and 1.5-fold less subcutaneous (P = 0.091) fat than the HAART+LD- group. As we have reported previously, liver fat was 10-fold higher in the HAART+LD+ compared with the HAART+LD- group (P = 0.00003). Inflammatory gene expression was increased in HAART-lipodystrophy: CD68 4.5-fold (P = 0.000013), tumor necrosis factor (TNF)-alpha 2-fold (P = 0.0094), chemokine (C-C motif) ligand (CCL) 2 2.5-fold (P = 0.0024), CCL3 7-fold (P = 0.0000017), integrin alphaM (ITGAM) 3-fold (P = 0.00067), epidermal growth factor-like module containing, mucin-like, hormone receptor-like (EMR)1 2.5-fold (P = 0.0038), and a disintegrin and metalloproteinase domain (ADAM)8 3.5-fold (P = 0.00057) higher in the HAART+LD+ compared with the HAART+LD- group. mRNA concentration of CD68 (r = 0.37, P = 0.019), ITGAM (r = 0.35, P = 0.025), CCL2 (r = 0.39, P = 0.012), and CCL3 (r = 0.54, P = 0.0003) correlated with liver fat content. In conclusion, gene expression of markers of macrophage infiltration and adipose tissue inflammation is increased in lipoatrophic subcutaneous abdominal adipose tissue of patients with HAART-associated lipodystrophy compared with those without. CD68, ITGAM, CCL2, and CCL3 expression is significantly associated with accumulation of liver fat.

Authors+Show Affiliations

Minerva Institute for Medical Research, Helsinki, Finland. ksenia.sevastianova@helsinki.fiNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18430964

Citation

Sevastianova, Ksenia, et al. "Adipose Tissue Inflammation and Liver Fat in Patients With Highly Active Antiretroviral Therapy-associated Lipodystrophy." American Journal of Physiology. Endocrinology and Metabolism, vol. 295, no. 1, 2008, pp. E85-91.
Sevastianova K, Sutinen J, Kannisto K, et al. Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy. Am J Physiol Endocrinol Metab. 2008;295(1):E85-91.
Sevastianova, K., Sutinen, J., Kannisto, K., Hamsten, A., Ristola, M., & Yki-Järvinen, H. (2008). Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy. American Journal of Physiology. Endocrinology and Metabolism, 295(1), E85-91. https://doi.org/10.1152/ajpendo.90224.2008
Sevastianova K, et al. Adipose Tissue Inflammation and Liver Fat in Patients With Highly Active Antiretroviral Therapy-associated Lipodystrophy. Am J Physiol Endocrinol Metab. 2008;295(1):E85-91. PubMed PMID: 18430964.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Adipose tissue inflammation and liver fat in patients with highly active antiretroviral therapy-associated lipodystrophy. AU - Sevastianova,Ksenia, AU - Sutinen,Jussi, AU - Kannisto,Katja, AU - Hamsten,Anders, AU - Ristola,Matti, AU - Yki-Järvinen,Hannele, Y1 - 2008/04/22/ PY - 2008/4/24/pubmed PY - 2008/8/30/medline PY - 2008/4/24/entrez SP - E85 EP - 91 JF - American journal of physiology. Endocrinology and metabolism JO - Am. J. Physiol. Endocrinol. Metab. VL - 295 IS - 1 N2 - In this cross-sectional study, we sought to determine whether gene expression of macrophage markers and inflammatory chemokines in lipoatrophic subcutaneous abdominal adipose tissue and liver fat content are increased and interrelated in human immunodeficiency virus (HIV)-1-positive, highly active antiretroviral therapy (HAART)-treated patients with lipodystrophy (HAART+LD+; n = 27) compared with those without (HAART+LD-; n = 13). The study groups were comparable with respect to age, gender, and body mass index. The HAART+LD+ group had twofold more intra-abdominal (P = 0.01) and 1.5-fold less subcutaneous (P = 0.091) fat than the HAART+LD- group. As we have reported previously, liver fat was 10-fold higher in the HAART+LD+ compared with the HAART+LD- group (P = 0.00003). Inflammatory gene expression was increased in HAART-lipodystrophy: CD68 4.5-fold (P = 0.000013), tumor necrosis factor (TNF)-alpha 2-fold (P = 0.0094), chemokine (C-C motif) ligand (CCL) 2 2.5-fold (P = 0.0024), CCL3 7-fold (P = 0.0000017), integrin alphaM (ITGAM) 3-fold (P = 0.00067), epidermal growth factor-like module containing, mucin-like, hormone receptor-like (EMR)1 2.5-fold (P = 0.0038), and a disintegrin and metalloproteinase domain (ADAM)8 3.5-fold (P = 0.00057) higher in the HAART+LD+ compared with the HAART+LD- group. mRNA concentration of CD68 (r = 0.37, P = 0.019), ITGAM (r = 0.35, P = 0.025), CCL2 (r = 0.39, P = 0.012), and CCL3 (r = 0.54, P = 0.0003) correlated with liver fat content. In conclusion, gene expression of markers of macrophage infiltration and adipose tissue inflammation is increased in lipoatrophic subcutaneous abdominal adipose tissue of patients with HAART-associated lipodystrophy compared with those without. CD68, ITGAM, CCL2, and CCL3 expression is significantly associated with accumulation of liver fat. SN - 0193-1849 UR - https://www.unboundmedicine.com/medline/citation/18430964/Adipose_tissue_inflammation_and_liver_fat_in_patients_with_highly_active_antiretroviral_therapy_associated_lipodystrophy_ L2 - http://www.physiology.org/doi/full/10.1152/ajpendo.90224.2008?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -