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Increase in visceral fat per se does not induce insulin resistance in the canine model
Author(s) -
Castro Ana V.B.,
Woolcott Orison O.,
Iyer Malini S.,
Kabir Morvarid,
Ionut Viorica,
Stefanovski Darko,
Kolka Cathryn M.,
Szczepaniak Lidia S.,
Szczepaniak Edward W.,
AsareBediako Isaac,
Paszkiewicz Rebecca L.,
Broussard Josiane L.,
Kim Stella P.,
Kirkman Erlinda L.,
Rios Hernan C.,
Mkrtchyan Hasmik,
Wu Qiang,
Ader Marilyn,
Bergman Richard N.
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.20906
Subject(s) - insulin resistance , medicine , endocrinology , visceral fat , insulin
Objectives To determine whether a selective increase of visceral adipose tissue content will result in insulin resistance. Methods Sympathetic denervation of the omental fat was performed under general inhalant anesthesia by injecting 6‐hydroxydopamine in the omental fat of lean mongrel dogs ( n = 11). In the conscious animal, whole‐body insulin sensitivity was assessed by the minimal model ( S I ) and the euglycemic hyperinsulinemic clamp (SI CLAMP ). Changes in abdominal fat were monitored by magnetic resonance. All assessments were determined before (Wk0) and 2 weeks (Wk2) after denervation. Data are medians (upper and lower interquartile). Results Denervation of omental fat resulted in increased percentage (and content) of visceral fat [Wk0: 10.2% (8.5‐11.4); Wk2: 12.4% (10.4‐13.6); P < 0.01]. Abdominal subcutaneous fat remained unchanged. However, no changes were found in S I [Wk0: 4.7 (mU/l) −1 min −1 (3.1‐8.8); Wk2: 5.3 (mU/l) −1 min −1 (4.5‐7.2); P = 0.59] or SI CLAMP [Wk0: 42.0 × 10 −4 dl kg −1 min −1 (mU/l) −1 (41.0‐51.0); Wk2: 40.0 × 10 −4 dl kg −1 min −1 (mU/l) −1 (34.0‐52.0); P = 0.67]. Conclusions Despite a selective increase in visceral adiposity in dogs, insulin sensitivity in vivo did not change, which argues against the concept that accumulation of visceral adipose tissue contributes to insulin resistance.