Increase in visceral fat per se does not induce insulin resistance in the canine model

OBJECTIVE: To determine whether a selective increase of visceral adipose tissue content will result in insulin resistance. DESIGN AND 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, we found no changes 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 sensitivityin vivo does not change, which argues against the concept that accumulation of visceral adipose tissue contributes to insulin resistance.