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Repeated Binge‐Like Alcohol Intoxication Dysregulates Mesenteric Perilymphatic Adipose Tissue Lipogenic Gene Expression
Author(s) -
SouzaSmith Flavia M.,
Song Kejing,
Molina Patricia E
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1292.5
Subject(s) - adiponectin , endocrinology , medicine , adipose tissue , adipokine , insulin resistance , white adipose tissue , leptin , biology , insulin , obesity
Visceral adipose tissue (VAT) inflammation is an important mediator of local insulin resistance (IR) and the consequent secretion of cytokines and adipokines may contribute to systemic IR. Repeated binge‐like alcohol intoxication (RBAI) episodes induce whole‐body IR and may potentially increase the risk for metabolic syndrome and type 2 diabetes. Previously we showed that RBAI promotes lymphatic vessels hyperpermeability leading to perilymphatic adipose tissue (PLAT – VAT isolated from blood vessels and lymphatic vessels) inflammatory milieu, impairs PLAT insulin signaling, and decreases circulating adiponectin levels. Based on a recognized shift from the traditional ‘glucocentric’ view of IR to a ‘lipocentric’ viewpoint we hypothesized that RBAI promotes impairment of PLAT lipid metabolism. Male Sprague‐Dawley rats received an intragastric bolus (intragastric catheter) of 2.5 g/kg/day of alcohol (12.5% alcohol w/v) or isocaloric dextrose in Vanilla Ensure (116 kcal/kg/day) for 3 days. PLAT was isolated 30 min or 24 h after the last alcohol or dextrose administration. PLAT gene expression of markers for peroxisome proliferator–activated receptor (PPAR‐γ), Diacylglycerol O‐AcylTransferase 1 (DGAT1), Fatty Acid Synthase (FAS), and Hormone‐Sensitive Lipase (HSL) was determined by Real Time PCR. PLAT isolated from RBAI rats at 24 h had decreased PPAR‐γ, DGAT1, and FAS but no significant alteration in HSL expression compared to dextrose‐treated time‐matched control animals. These results may suggest that RBAI impairs critical steps involved in PLAT lipid synthesis, which may in turn contribute to suppressed circulating adiponectin levels previously observed. We speculate that gut‐derived toxins leaking from lymphatic vessels into PLAT directly mediate these early alterations, reflecting lymphatic/PLAT crosstalk contributing to alcohol‐induced metabolic dysregulation. Support or Funding Information Supported by LSUHSC Department of Physiology.