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Salsalate treatment improves glycemia without altering adipose tissue in nondiabetic obese hispanics
Author(s) -
Alderete Tanya L.,
Sattler Fred R,
Richey Joyce M.,
Allayee Hooman,
Mittelman Steven D.,
Sheng Xia,
Tucci Jonathan,
Gyllenhammer Lauren E.,
Grant Edward G.,
Goran Michael I.
Publication year - 2015
Publication title -
obesity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.438
H-Index - 199
eISSN - 1930-739X
pISSN - 1930-7381
DOI - 10.1002/oby.20991
Subject(s) - medicine , adipose tissue , adiponectin , endocrinology , adipokine , insulin resistance , inflammation , insulin
Objective Salsalate treatment has well‐known effects on improving glycemia, and the objective of this study was to examine whether the mechanism of this effect was related to changes in adipose tissue. Methods A randomized double‐blind and placebo‐controlled trial in obese Hispanics (18‐35 years) was conducted. The intervention consisted of 4 g day −1 of salsalate ( n = 11) versus placebo ( n = 13) for 4 weeks. Outcome measures included glycemia, adiposity, ectopic fat, and adipose tissue gene expression and inflammation. Results In those receiving salsalate, plasma fasting glucose decreased by 3.4% ( P < 0.01), free fatty acids decreased by 42.5% ( P = 0.06), and adiponectin increased by 27.7% ( P < 0.01). Salsalate increased insulin AUC by 38% ( P = 0.01) and HOMA‐B by 47.2% ( P < 0.01) while estimates of insulin sensitivity/resistance were unaffected. These metabolic improvements occurred without changes in total, abdominal, visceral, or liver fat. Plasma markers of inflammation/immune activation were unchanged following salsalate. Salsalate had no effects on adipose tissue including adipocyte size, presence of crown‐like structures, or gene expression of adipokines, immune cell markers, or cytokines downstream of NF‐κB with the exception of downregulation of IL‐1β ( P < 0.01). Conclusions Findings suggest that metabolic improvements in response to salsalate occurred without alterations in adiposity, ectopic fat, or adipose tissue gene expression and inflammation.